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The Learning Curve - Part 3: The Natural Miticides
The Learning Curve: Part 3 Randy Oliver ScientificBeekeeping.com First Published in ABJ in July 2009 I added a number of updates on May 2015, marking 15 years of successful commercial beekeeping in my operation without the use of synthetic miticides. "It is not the strongest of the species that survives, nor the most intelligent [...]
Read More | Varroa Management Archives - Page 8 of 8 - Scientific Beekeeping | https://scientificbeekeeping.com/varroa-management/page/8/ |
Pesticide exposure pathways
Sorry for the low resolution of this snip of this Powerpoint slide that I created for a presentation. I've color coded the ellipses and arrows. Red is the pesticide active ingredient. Blue is the initial mode of exposure. Orange are the ages/temporal tasks of the bees involved. Green are the contaminated foods or combs.
Note how colony organization is set up to avoid exposing the queen and brood to toxins (whether natural or manmade). Note the special case (the pollen hogs at the lower right) in which newly emerged workers and drones get killed by planting dust.
Category: Topics | Pesticide exposure pathways - Scientific Beekeeping | https://scientificbeekeeping.com/pesticide-exposure-pathways/ |
The Short Version
The Major Problems Facing Bees and Beekeepers
Number one is varroa. Varroa changed the virus dynamics within the colony. If either the bees or the beekeeper don't keep the varroa infestation rate down to fewer than 5 mites per 100 bees, colonies start to suffer. At about 15 mites per 100, viruses go epidemic, and the colony will generally die. Lack of varroa management is the number one reason that colonies die, other than from sheer neglect (see Feeding).
Many recreational beekeepers want to go "natural" and "treatment free." I commend you on those sentiments, and hold that as a goal to reach (it is much harder to do so if you are making your living from your bees). But keep this in mind: you wouldn't expect a broiler-type chicken bred for living under controlled conditions to survive in the wild. And you can't expect commercial bee stock bred for living under intense beekeeper management to survive in the wild just because you want to be Mr. or Ms. Natural. I strongly suggest that beginning beekeepers make life easier on themselves and their bees by first following standard practices until you get the hang of beekeeping; then you can try going treatment free (see Varroa Management or Treatment Free).
Feeding
It is not necessary to feed a colony. I ran hundreds of healthy colonies for years without ever feeding a drop of syrup or a single pollen patty. But that was only possible because I moved my hives to good forage throughout the year.
It became far more difficult to keep bees healthy after the arrival of varroa. In my traditional yards in the dry Sierra foothills during summer, colonies went downhill without supplemental protein. In order to cut out my summer migration to better forage, I learned to feed pollen supplement, with fantastic results!
And then I learned how sugar syrup, fed at critical times, could also greatly improve colony buildup, health, and wintering. The short version is to feed light syrup for stimulation, heavy syrup for winter stores. Feeding nucs, packages, or even overwintered colonies during spring buildup really helps them. In our dry late summers, light syrup along with protein patties encourages broodrearing and greatly improves colony health.
Caution: if you are growing a new colony, it is possible to overfeed syrup to the extent that you plug out the broodnest, leaving the queen no place to lay eggs! You can kill a colony with kindness. Don't keep feeding unless you are inspecting the broodnest from time to time.
I normally leave enough natural honey on the hives for them to winter on (in my moderately cold area, I want a strong double-deep hive to weigh about 120-130 lbs total. However, if the bees put on dark honeydew as winter stores, it may help to replace the combs of honeydew directly above the cluster with dark drawn combs, and then feed heavy syrup for the bees to refill those combs with.
The type of sugar does not appear to be critical. Cane or beet sugar work fine. Commercial sucrose/HFCS blends may even be better. Some beekeepers feel that inverting the sugars also helps, but that is beyond the scope of this short version.
The one clear responsibility that a beekeeper has is to make sure that his colonies don't starve! There is no excuse for allowing animals in your care to starve. Starvation usually happens in late winter/early spring. Heft your hives regularly to make sure that the bees always have a reserve of honey or syrup honey. In a pinch you can even feed dry sugar poured over a piece of newspaper laid on the top bars.
If you live in an area with pollen dearths, feeding high-quality pollen supplements can make all the difference in the world to your bees. I know, it's not natural, but neither is the food that you feed your dog or cat, or even your children. Get over it!
Varroa Management
Treatment Free
Nosema
AFB
Small Cell
Although the use of small cell foundation to help the bees control varroa has an impassioned following, there is little empirical evidence that it actually helps (see http://www.elgon.es/diary/?p=37 for a review). However, in the single trial in which I tested it, the results appeared to be positive, so I keep an open mind. I can say this-many have tried it, sometimes at large scale, and were disappointed in the results. Others find that mite resistant stocks do not necessarily require small cell to be successful at controlling the mite.
If I wanted to practice truly "natural" beekeeping, I'd allow the bees to build their own combs in foundationless frames, rather than trying to force them into any specific cell size. In my own operation, we keep a single foundationless drone frame in each hive (in the upper brood chamber, to the outside of the broodnest), as I feel that it is completely unreasonable to expect the bees to maintain 20 brood combs without any drone brood! See "Drone Trap Frames."
Drone Trap Frames
Summer Nucs
See Mike Palmer's video https://www.youtube.com/watch?v=nznzpiWEI8A
Category: Topics | The Short Version - Scientific Beekeeping | https://scientificbeekeeping.com/the-short-version/ |
IPM 6 Fighting Varroa The Arsenal: Our Choice of Chemical Weapons
IPM 6 Fighting Varroa The Arsenal: Our Choice of Chemical Weapons Randy Oliver ScientificBeekeeping.com First Published in ABJ in June 2007 I'm clearly in the "minimal chemical" camp, yet all my commercial buddies, without exception, depend upon "off label" use of agricultural miticides to keep their colonies alive. These are top-notch beekeepers, and I [...]
Read More | Varroa Management Archives - Page 7 of 8 - Scientific Beekeeping | https://scientificbeekeeping.com/varroa-management/page/7/ |
Pesticide exposure pathways
Sorry for the low resolution of this snip of this Powerpoint slide that I created for a presentation. I've color coded the ellipses and arrows. Red is the pesticide active ingredient. Blue is the initial mode of exposure. Orange are the ages/temporal tasks of the bees involved. Green are the contaminated foods or combs. Note [...]
Read More | Topics Archives - Page 4 of 4 - Scientific Beekeeping | https://scientificbeekeeping.com/topics/page/4/ |
Mite Washer; Still Improving
First published in: American Bee Journal, August 2015
Mite Washer; Still Improving Randy Oliver ScientificBeekeeping.com First Published in ABJ in August 2015 The quickest and most accurate way to monitor varroa levels is by the alcohol wash. After the publication of my "improved" washer design, I've gotten some great suggestions from readers. Unless you monitor for varroa, you have no idea as to [...]
Read More | Varroa Management Archives - Page 6 of 8 - Scientific Beekeeping | https://scientificbeekeeping.com/varroa-management/page/6/ |
General public presentation
Here is a slide show for general public presentation. Contains some old 35mm photos, which I hope to soon replace.
Public general presentationPublic general presentation
Category: Topics | General public presentation - Scientific Beekeeping | https://scientificbeekeeping.com/general-public-presentation/ |
DWV sampling instructions
Dear U.S. beekeeper,
Recent studies by Dr. Stephen Martin and associates have found that there is apparently a benign form of DWV that can out compete the virulent form, thus allowing colonies to survive despite varroa infestation.
If this is true, it raises the possibility that we may be able to minimize the effect of varroa by inoculating our colonies with the benign form of DWV.
We obtained funding from Project Apism to survey bee colonies across the U.S. to determine the distribution of the strains of DWV. We're especially interested in adult bee samples from feral and survivor stock that have survived for some time without treatment. We also need reference samples from "normal" managed apiaries.
If you are interested in contributing samples, please write to Randy at randy@randyoliver.com, with the word "kit" in the subject line, the sort(s) of hive(s) that you're able to sample, and the state in which the hives are located. Please also include your mailing address.
I will reply, and send a postpaid sampling kit. It should take less than an hour of your time to contribute to this research.
Please print out these sampling instructions
Sampling Instructions PDF
Category: Topics | DWV sampling instructions - Scientific Beekeeping | https://scientificbeekeeping.com/dwv-sampling-instructions/ |
Building a Better Mite Washer
Building a Better Mite Washer - Larry Clamp
Notes from Randy:
Tinkerer Larry Clamp put together a very nice set up illustrated instructions for building mite washer cups, and is generously sharing them. Thanks, Larry!
The thin black screen from package bee cages (or some older veils) is easier to work with than hardware cloth, and
Depending upon the type of plastic cup, some expensive glues intended for plastics may work (I found that the alcohol may eventually work under the silicone). Brion Dunbar tells me that he's had good luck with 3M ScotchWeld High Performance Industrial Plastic Adhesive 4693H.
Category: Topics | Building a Better Mite Washer - Scientific Beekeeping | https://scientificbeekeeping.com/building-a-better-mite-washer/ |
What's Happening with the Bees 2015
2015 What's Happening Auburn
Category: Topics | What's Happening with the Bees 2015 - Scientific Beekeeping | https://scientificbeekeeping.com/whats-happening-with-the-bees-2015/ |
International Websites of Interest
I'm open to suggestions for interesting websites on beekeeping in countries other than the U.S. to link to-please email me suggestions.
Ukraine:A commercial honey sales website, but with a nice summary of the history of beekeeping in that country http://www.honey-export.com/
Category: Topics | International Websites of Interest - Scientific Beekeeping | https://scientificbeekeeping.com/international-websites-of-interest/ |
Donze 1998 A look under the cap
donze-1998-a-look-under-the-cap
Category: Topics | Donze 1998 A look under the cap - Scientific Beekeeping | https://scientificbeekeeping.com/donze-1998-a-look-under-the-cap/ |
Extended-Release Oxalic Acid Progress Report - Part 1
First published in: American Bee Journal, July 2017
Extended-Release Oxalic Acid Progress Report Part 1 Randy Oliver ScientificBeekeeping.com First published in ABJ July 2017 In January I wrote about an exciting extended-release application method for oxalic acid [[1]]. I'm currently collaborating with the USDA Agricultural Research Service and the EPA to get this application method added to the current label for oxalic acid. [...]
Read More | Varroa Management Archives - Page 5 of 8 - Scientific Beekeeping | https://scientificbeekeeping.com/varroa-management/page/5/ |
K.I.S.S. Breeding for varroa resistance
Open the link below to view the annotated pictorial presentation. 2017 KISS Breeding and if you want to see us doing smokin' hot mite washin' in real time, Rachel surprised me by figuring out how to prop up her cell phone to take a video of us washing a yard-to see the 36-second video, click [...]
Read More | Topics Archives - Page 3 of 4 - Scientific Beekeeping | https://scientificbeekeeping.com/topics/page/3/ |
2019 EcoFarm
Beekeeping is more difficult today than it used to be.
Our changing agricultural landscape provides less forage, and growers still apply pesticides to freely (although the pesticide situation for bees today is far better than it used to be in the '60s and '70s).
The main problem for honey bees worldwide is the recent invasion of the varroa mite, which acts as a vector for Deformed Wing Virus.
The long-term solution is to breed bees naturally resistant to the mite. In this presentation I offer a brief version of how to go about doing it. There is more information at my website.
Until such bee stock is more widely available, good bee husbandry requires occasional treatments to control the mite. My sons and I run a successful commercial beekeeping operation, and have used only organically-approved treatments since 2001.
I also give a progress report on our registration of extended-release oxalic acid for mite control. This organic treatment will help us to keep healthy, thriving bees.
You can find instructions for keeping bees healthy at https://scientificbeekeeping.com/first-year-care-for-your-nuc/
The slides for my presentation can be viewed at 2019 EcoFarm short (this is a large file with many photos, so may take a while to download).
Happy beekeeping!
Randy
Category: Topics | 2019 EcoFarm - Scientific Beekeeping | https://scientificbeekeeping.com/2019-ecofarm-2/ |
Being Part of The Solution
Click on the link below to view a ppt presentation.
Being Part of the Solution
Category: Topics | Being Part of The Solution - Scientific Beekeeping | https://scientificbeekeeping.com/being-part-of-the-solution/ |
Guessing our future with varroa
Category: Topics | Guessing our future with varroa - Scientific Beekeeping | https://scientificbeekeeping.com/guessing-our-future-with-varroa/ |
Glyphosate fact checking
This is a very contentious subject, but how much of the media alarm over glyphosate is based upon actual risk assessment?
Having run my garden and orchard organically for many years, I was faced with invasive Vinca major and Himalaya blackberries that were taking an excessive amount of my time to control. Weed whacking, horticultural vinegar, or ammoniated soaps would kill the aboveground foliage, but the vines would sprout right back up and laugh at me. I'm anything but a corporate shill for spraying unnecessary or dangerous chemicals, so I researched, for my own health concern, about the safety of using a glyphosate herbicide (which also meant that I could no longer consider my property as "organic").
I found that my own independent review of the literature did not support glyphosate as being of risk to me. Keep in mind that the label instructs the applicator to wear normal protective gear anyway! So I don't use it in my garden beds, but have now used it in other areas on my property, spot-treating only those two specific invasives (with impressive results). That said, I am not a proponent of widespread use of glyphosate on landscapes, as eliminating all native vegetation and "weeds" eliminates the food plants necessary for pollinators and wildlife, and good soil structure is dependent upon vegetation coverage that provides plenty of plant roots. Any pesticide should be used only sparingly and in a sustainable manner.
I also must point out that we citizens hire the scientists at EPA to perform risk assessments for us. The EPA risk assessors also have families that they wish to protect. I have the honor of knowing the head of risk assessment personally from informal meetings and meals at conferences, as well as many phone and email conversations about protecting bees from pesticides. EPA knows how to do risk assessment, and can better analyze the data from any published or unpublished study better than any can layman or activist group. Bottom line: I have no reason to question EPA's risk assessments, summarized at https://www.epa.gov/ingredients-used-pesticide-products/glyphosate
For an excellent and objective scientific review, read (of interest, search the word "honey"): Residues of glyphosate in food and dietary exposure https://ift.onlinelibrary.wiley.com/doi/10.1111/1541-4337.12822
For a very good review of glyphosate residues in off-the-shelf foods, the CFIA (Canadian Food Inspection Agency) analyzed 7955 samples of foods to determine the level of compliance of foods in the Canadian marketplace against established MRLs. Read the full report here: https://pubs.acs.org/doi/10.1021/acs.jafc.9b07819
That said, the best layman's review of glyphosate was recently published at https://geneticliteracyproject.org/gmo-faq/is-glyphosate-roundup-dangerous/?mc_cid=527d29e2df&mc_eid=dc9006049b
I've snipped three informative graphics from the above article, since in my own prior research, they were three data sets that I had already graphed out myself:
Money-hungry, fear-provoking "activist groups" such as the Environmental Working Group, hire skilled marketers and lawyers to generate and post scary correlations about glyphosate and cancer. But correlation does not imply causality, as evidenced by the graph below:
For more humorous spurious correlations, see https://www.tylervigen.com/spurious-correlations
I had previously checked the databases of countries that had kept track of incidence of Non-Hodgkin's Lymphoma and glyphosate use, and had found that although glyphosate use has skyrocketed over the years, the incidence of NHL has remained flat, which does not support a link between the two. Take a look at the two graphs below (from the GLP article):
If there was really any evidence that glyphosate caused NHL, we'd see it in the farmers who get it splashed all over their jeans all day long when applying it.
The maps below would clearly indicate if there was any connection between glyphosate application and NHL. There doesn't appear to be one.
Bottom line: I'm far more likely to harm myself from picking, digging, and pulling out blackberries than I am from spraying them (once is usually enough) with glyphosate. I you have hard data that indicates that I should revisit my current assessment, please forward it to me!
Category: Topics | Glyphosate fact checking - Scientific Beekeeping | https://scientificbeekeeping.com/glyphosate-fact-checking/ |
About Randy
About me
To start with, among other things, I'm a honey bee researcher, so if you're not comfortable with honey bees being around, read no more
I'm a healthy, youthful, happy, high-energy, and loving guy, finally over the heartache of losing my beloved wife. So I'm now looking for a new life partner and soul mate with whom to share my exciting, productive, and joyful days.
I am a biologist, nature lover, family man, teacher, inventor, writer, gardener, and builder. My friends would describe me as the busiest guy they know, and the guy who gets things done. The answer man to any question. Playful and funny. My joy is sharing with others - I've always been a teacher and giver. Helpful, loving, sharing. Widely loved by many.
I maintain amicable relationships with those with whom I've been in previous relationships. They, and the women that I work with, will all vouch for my loving good nature, honesty, and trustworthiness. And if you're familiar with the five love languages, mine is clearly touch -- hugs and intimacy warm my soul.
Disclaimer: My eharmony photo is from 2018 , but it best captures my essence. Here are some more from this year.
Possible Incompatibilities
Since I'm not in any way trying to seduce you (and have no desire to waste our time), please let me share some things about me and my lifestyle that might suggest incompatibility:
I'm a honey bee researcher (writer and international invited speaker). You'd need to be OK with being around honey bees.
If you're looking for a quiet life in front of the TV, read no more. I'm a high-energy, high IQ, vibrant, scientifically-minded guy, biologically about 10 years younger than my chronological age, lean and very active, and I work nonstop -- so am not the right partner for a low self-esteem or low-energy lady (although I'm an intense and focused hard worker, I'm also very happy and humorous, always smiling, laughing, and joking).
I've got many skills. And just like the cobbler who can't find time to shoe his children, my houses are in various stages of remodeling and disarray.
Although I'm financially set up, I live a simple, rustic, eco-friendly lifestyle, and wear my jeans for more than one day at a time.
I am looking for someone who wants to move to my place. I've got a rural property in the California foothills (Grass Valley), where we get a bit of snow in the winter. I grow a large garden and orchard, and am looking for a partner who would enjoy being involved and engaged in the garden and the property (woodsy with a lovely view).
I'm more of a cat person than a dog person. I like the wildlife around my home, and don't want a dog scaring everything off.
I'm not the right person for someone who is intimidated by intelligence, or put off by me being so engaged in my research, writing, shop work, and property maintenance. I can also be kinda messy, since I always have so many projects in the works.
As far as a partner, I'd prefer an energetic, physically active, preferably lean, and affectionate woman who enjoys a simple rustic, eco-friendly lifestyle. I follow the Golden Rule, but have no interest in organized religion.
More about me
I'm likeable, happy, and appreciated by others. I've got no issues or traumas, and am responsible and caring. I exemplify the Scout Laws (I'm the inverse of our ex-president). You will never hear an untruth cross my lips.
I'm an ex hippy child of the '60s, now a responsible, environmental, fiscally-conservative, socially-liberal adult. I was raised to honor and respect women, and have no desire to dominate a relationship.
I've got many skills, and am highly competent, capable, and accomplished. I'm always happy, free of stress, loving, generous, and looking for a soul mate and partner to share the everyday joys of life with -- like a new flower blooming, or the taste of the first fruits from my orchard, or a beautiful sunset.
I live on a dream property with garden, orchard, and a view, am in good health, and financially stable. I've got two houses next to each other (one vacant since my mother passed away), and I'd be happy to remodel either one to my new partner's likings.
I've handed my sons our beekeeping business, so am now free to follow my passion of performing honey bee research and providing scientific information to beekeepers worldwide. My sons run the business from my property (one lives next door), so we often have visitors and things going on at the property.
I lead a simple, frugal, rustic life, in an older house - nothing fancy (other than traveling to speak). I'm early to bed, early to rise. In my office before sunrise, cranking data, writing, email correspondence, and reading scientific papers. After breakfast, in and out for the rest of the day. Other than the news, I watch very little TV. Back in for dinner, which I enjoy cooking. I love spending evenings watching a movie together with the one I love.
I'm home or nearby most days, and don't go to town much, but do travel to speaking engagements, which I try to limit to no more than once a month.
I respect and honor women, and have worked with ladies most of my life. I'm well liked and loved - any of my ex's or female coworkers will give me a thumbs up.
The partner I'm looking for
My previous relationships have been based upon love, attractiveness, and intimacy, but after signing up for eharmony, I realize that I'd be wise to find someone whose energy and personality traits match mine. I'm a likeable guy, so I'm not desperate or trying to sell myself, seduce or mislead you, so I will be honest and straightforward. I do not want to waste your time or mine.
As far as relationship, since I'm a brainy, strong guy, I want an equally strong, self-assured partner who can stand up for herself, and communicate and articulate her feelings and wants. I don't argue or criticize, and have zero desire to dominate or always get my way.
Although I very much love doing things together, I need a partner who also has her own interests and hobbies to happily entertain herself while I'm working on my own projects. I'm far more interested in an active tomboy "country girl" in dirty jeans than a beauty queen in high heels. I want a gal who doesn't mind getting dirt on her hands, and will enjoy working in the garden and orchard with me, and be my third hand when I'm working on projects (and ditto for me helping with yours).
I ain't perfect, and don't expect you to be either. I want my partner to accept me in full as I am, and I will do the same in return. I don't want to merely love my partner, I want to be in love with her every moment of my life!
Category: Topics | About Randy - Scientific Beekeeping | https://scientificbeekeeping.com/about-randy/ |
Fair demo cage
Category: Topics | Fair demo cage - Scientific Beekeeping | https://scientificbeekeeping.com/fair-demo-cage/ |
The Varroa Problem: Part 16b - Bee Drift and Mite Dispersal (cont.)
First published in: American Bee Journal, May 2018
Contents Bee Drift and Mite Dispersal (continued) 1 So why do colonies allow bees to drift in?. 1 The sheer numbers involved. 4 The amount of mite drift into other hives. 5 Collapse and Robbing. 7 What happens to all the mite-infested bees when a colony collapses?. 8 Swarms coming back to bite you in [...]
Read More | Varroa Management Archives - Page 4 of 8 - Scientific Beekeeping | https://scientificbeekeeping.com/varroa-management/page/4/ |
Screenshots of hive weights
Supplementary material for A Study on Bee and Mite Drift, Part 5
Due to unfamiliarity with data preservation for the scale hives, we lost all our raw data when we removed the batteries from the scales at the end of the trial. Luckily, I had been following the weight data during the course of the trial, and had taken a few screenshots. I fully expected to see evidence of robbing correlating with mite immigration, but did not.
A screenshot of scale data for the Donors.The only sudden weight losses that we observed were for Donors D6 and D8 (not shown in this chart) -- the rest of the Donors showed no indication of getting robbed during their collapse. But the bulk of those weight reductions may well have simply represented the body mass of the workers that abandoned the hive (the bees covering 8 combs weigh roughly 4 pounds).
A screenshot of typical scale data for the Receivers, with weight gains by R4 and R7.
Category: Topics | Screenshots of hive weights - Scientific Beekeeping | https://scientificbeekeeping.com/screenshots-of-hive-weights/ |
Sick Bees - Part 14: An Update on the "Nosema Cousins"
Contents
Worldwide Status and Distribution
Ceranae vs. apis
Coinfection
Seasonality
Sample Interpretation
What if You're Dealing with N. apis?
Seasonality
Recommendations
Acknowledgements
References
Sick Bees 14:
An Update On The "Nosema Cousins"
First published in ABJ December 2011
Randy Oliver
ScientificBeekeeping.com
In my last article, I described how to quickly sample for nosema. So what do the spore counts actually mean as far as colony health is concerned? I wrote an article a little over two years ago with the tongue in cheek title "Nosema ceranae: Kiss of Death, or Much Ado about Nothing." Well, N. ceranae is still an enigma, but it appears that the answer lies somewhere in between.
Dr. Mariano Higes (2005, 2006) was the first to raise the flag to alert beekeepers worldwide that a new species of nosema had invaded Europe, and appeared to be the cause of the unusual colony collapses that plagued Spain (a major beekeeping country) in 2003 and 2004. Then in 2007, just as Colony Collapse Disorder was rampaging through our own bee operations, we found out that Nosema ceranae had somehow spread throughout the U.S. right under our eyes!
Drs. Diana Cox-Foster and Ian Lipkin (2007) then published a paper suggesting that a newly-described virus was involved in CCD, but later research indicated that IAPV wasn't the only culprit, leaving N. ceranae as a leading suspect.
Shortly afterward, Higes (2008) described in great detail the progression of N. ceranae infection (in his Spanish apiaries) through four stages: Asymptomatic, Replacement, False Recovery, and finally the dreaded Depopulation. The logic, the numbers, and the devastating final result were all clear and compelling. The specter of N. ceranae ravaging our hives resulted in unnerved beekeepers boosting the sales of fumagillin to the point that supplies ran short.
I had never previously worried about nosema, but I pulled out a microscope and found out that N. ceranae was indeed widespread in my operation. I ran trials, and found out that the danged parasite could flourish despite being drowned in fumagillin (Oliver 2008a), but more surprisingly, that colonies here at Comedy of Errors Apiaries thrived despite exhibiting spore counts in the millions. To try to reconcile the differences between the very different outcomes of N. ceranae infection in my operation with those reported for Spain, I began an ongoing correspondence with Dr. Higes, which continues to this day.
To be frank, some other Spanish researchers dispute Higes' conclusions (debate leads to better science), so I have often questioned and challenged him on details of methodology and interpretation, which he and his team of collaborators have generally clarified with additional research. In this series of articles I will be citing a number of the Higes team's papers, since they have clearly led the pack in N. ceranae research, meticulously investigating nearly every aspect of this pathogen's effects upon bees.
I've previously written at length about N. ceranae in my "Nosema Twins" series (all available at ScientificBeekeeping.com), but feel that there has been so much recent research completed that it would benefit the reader for me to write a digest of our current state of knowledge. I've scoured the literature for every relevant research paper (including a number still in press), and have discussed as well current findings with many of the world's nosema researchers. I wish that at this time I could say that I have the answers to all your questions about Nosema ceranae, but unfortunately, in many aspects this parasite still remains an enigma.
Worldwide Status And Distribution
Nosema ceranae has now spread into the European honey bee populations of most areas of the world, roughly concurrent with the spread of varroa (and its altering of virus dynamics), which greatly confuses analysis of the effect of these two novel parasites upon bee health. It is difficult to tell in which countries N. ceranae has already reached equilibrium, and in which it is still invading.
Since the first invasive wave of a novel parasite into naive hosts is generally that most damaging, it would be helpful to know when ceranae actually arrived in various countries. For example, we know from analysis of archived bee samples that N. ceranae has been present on the East Coast for at least two decades (Chen 2008). Unfortunately, any initial effects of its invasion may have been masked by our focus upon the massive impact of the arrival of varroa at about the same time.
Since no one was looking for N. ceranae in the U.S. until 2007, we obviously didn't start studying it until long after it was well established and likely homogenized throughout the bee population via migratory beekeeping practices. And it is also likely that by the time we started studying the impact of N. ceranae upon the health of colonies, natural selection may have already weeded out the bees least tolerant of the emergent pathogen.
In Europe, however, N. ceranae only recently invaded bee populations already suffering from varroa and viruses, miticide failure and comb contamination, extreme weather events, plus changes in agricultural practices and pesticide use--the combination of which likely factor into colony losses in that region.
In a fresh study (Botias 2011), the Higes team analyzed archived Spanish honey samples (frozen) and adult bee samples (in alcohol) dating back to 1998. They found that N. ceranae first appeared beginning in 2000 and increased in prevalence through 2009 (the latest samples analyzed), concurrent with a decrease in the prevalence of N. apis. It is noteworthy that Spain concurrently suffered from devastating drought during much of that period, which led to serious colony stress.
N. ceranae is still in the process of extending its range worldwide, and appears to be most successful in warmer climates. It is of interest that in varroa-free Australia, its invasion does not appear to be causing significant colony losses. Interestingly, although it is well-established in Canada, it is not yet common in some northern European countries, but this may be due to restrictions upon bee imports (Fries 2010).
N. ceranae is widely distributed throughout the U.S., but surprisingly, there were great differences in the percent of colonies infected in a recent state-by-state survey (Fig. 1).
Figure 1. Prevalence (percent of samples infected) of N. ceranae in various states as determined by PCR analysis (more sensitive than spore counts) of aggregate samples collected from 8 randomly selected colonies per apiary, 4 apiaries per state. Note that in some states over 70% of samples were infected! From Rennich, K, et al (2011) 2010-2011 National Honey Bee Pests and Diseases Survey Report.
Ceranae Vs. Apis
In a widely cited paper by Martin-Hernandez (2007), her arresting graph of nosema positive samples over time clearly shows a definite shift over the period from 1999 to 2005--there initially were only spikes in spring and fall (ostensibly from apis), transitioning to nearly 100% of samples being positive every month of the year (due to ceranae). Of note is that her data has an inherent bias, in that the samples were voluntarily sent to the lab by beekeepers for diagnosis of problems, suggesting that the data may reflect the change in nosema loads in sick hives. Also of note, is that despite this graph being widely cited, it is often misunderstood--it did not plot spore levels, but rather only the yes/no detection of nosema spores.
What the graph did strongly indicate was that N. ceranae rapidly and thoroughly invaded Spain over a period of only a few years! This initial finding has now been confirmed by Botias (2011). Likely, a similar phenomenon occurred in the U.S., since Chen (2008) found N. ceranae to already be widespread in archived U.S. bee samples dating back to 1995.
The general trend appears to be that N. ceranae now predominates in warmer countries, whereas N. apis is better adapted to colder areas. It has been often stated that N. ceranae has displaced N. apis, but more careful analysis suggests that that may not actually be the case!
When Dr. Robb Cramer asked me in 2007 to send him infected bees so that he could culture pure N. ceranae, he found that the samples often contained some N. apis as a "contaminant." In Dr. Diana Cox-Foster's (2007) analysis of CCD colonies, they also found both species of nosema. Later studies by Bourgeois (2010) and Runckel (2011) of commercial operations in the U.S. also found N. apis, but in far fewer hives than its cousin, only in spring and/or fall, and notably, at much lower spore levels than N. ceranae.
The differences between the detectability of the two nosema species (N. apis typically produces much lower spore counts and is generally only seen in spring and fall) may lead "to an increased chance of detecting N. ceranae over N. apis, which could have biased the impression that N. apis has been displaced" (Higes 2010).
So, has ceranae actually displaced apis, or have we merely been overlooking its cousin? In order to answer that question, Dr. Raquel Martin-Hernandez (2011) carefully analyzed over 2000 bee samples from all across Spain. She found ceranae and apis coexisting throughout country, with ceranae clearly predominant (in roughly 40% of hives), apis hanging in there (in up to 15%), and occasional mixed infections (below 7%). She also found that infection by ceranae was favored in hotter areas of the country, whereas apis succeeded better where winters are colder.
I'm seeing similar indications from other countries (e.g., Gisder 2010), which are appearing to confirm that apis is the more cold-adapted species. As far as seasonality, Martin-Hernandez found apis only in the spring and fall, whereas ceranae could be found all year, and notably, once ceranae infects a colony, it almost always persists (detectable with PCR, even if not obvious via spore counts).
Practical note: these studies indicate that N. ceranae remains present as an infection in a colony throughout the year, even if it is not detectable by microscopy. But we don't know whether these inapparent infections affect colony health.
I found one last study to be of special interest: Dr. Judy Chen (2009) looked at nosema invasion from the other direction--in a turn of the tables, N. apis appears to have been introduced from the Western honey bee (Apis mellifera) into the Eastern honey bee (Apis cerana) in Asia, and is now an emergent parasite in that species, which had historically been infected only by N. ceranae! She analyzed bee samples from China, Taiwan, and Japan. Her findings:
"N. apis was detected in 31% of examined bees and N. ceranae was detected in 71% of examined bees and that the copy number of N. ceranae was 100-fold higher than that of N. apis in co-infected bees, showing that N. ceranae is the more abundant of two Nosema species in the Eastern honey bees."
This study suggests that N. apis can not only hold its own against N. ceranae, but can actually invade into ceranae's turf! Interestingly, in the Eastern honey bee, despite its long coevolution with N. ceranae, ceranae still produces higher spore counts than its invading cousin.
Coinfection
This brings up the question of what happens when bees are infected simultaneously by both species of nosema? Dr. Zachary Huang (pers comm) found that in both cage trials and field observations that longevity was substantially shorter for coinfected bees as opposed to those infected by either species of nosema alone (unpublished data).
Note that in Cox-Foster's (2007) CCD study that they found "a trend for increased CCD risk in samples positive for N. apis" (100% of CCD colonies tested positive for ceranae and 90% for apis, but remember that apis is easy to miss when samples consist of house bees). As Jim Fischer noted in a post to Bee-L, "What was striking was that every hive showing CCD symptoms tested positive for BOTH Nosema apis and Nosema ceranae, and this correlation was better than the correlation between CCD and IAPV that was the focus of the paper."
These findings leave me very curious about the impact of coinfection by two nosema species upon colony health!
Seasonality
Spore counts of N. ceranae generally reach a peak in May, then drop spontaneously during summer, and may spike sporadically in fall and winter. But there is more to the picture than this. Dr. Ingemar Fries (2010), who has studied nosema for decades, explains thusly:
"The typical pattern for N. apis infections in temperate climates is low prevalence or hardly detectable levels during the summer with a small peak in the fall. During the winter there is a slight increased prevalence with a large peak in the spring before the winter bees are replaced by young bees... The pattern is similar both in the southern and northern hemisphere... Unfortunately, very few data exist for N. apis on the seasonal prevalence from tropical or subtropical conditions. The only published year round sampling under conditions where bees could fly all year round, revealed detectable levels of N. apis with no seasonal pattern of prevalence."
Along that line, Dr. Denis Anderson in Australia (pers comm) tells me that, "there are also many unseasonal occurrences of N. apis -- I get many samples sent in in the mid summer here that are loaded with N. apis." This could well be happening in the U.S., where, as far as I can tell, there have been few studies on N. apis in warmer areas, other than the fact that it was commonly found in package bees produced in the southern states.
Practical application: we need to learn more about the prevalence and seasonality of N. apis in the warmer parts of our country!
I've now seen data and presentations on N. ceranae seasonal prevalence from researchers from all over the world. Since a picture is worth a thousand words, I've summarized them in a crude graph below (Fig. 2).
Figure 2. A generic graph of typical N. ceranae spore counts over the course of the year in my operation. Important note: Counts of house bees would follow the same trend, but at much lower levels. The late-season spikes are often sporadic flare ups that spontaneously "go away."
Practical application: It is not unusual to see high nosema spore counts in April and May. Counts will typically drop in summer whether you treat or not. I'll cover treatments in a subsequent article.
But new technology is showing something surprising about nosema sampling--that spore counts do not necessarily reflect degree of actual nosema infection (Meana 2010)! Look at the following graph (Fig. 3), from a recent nationwide study of pathogens in U.S. bees--instead of measuring spore counts, the blue bars indicate the percentage of colonies infected by N. ceranae as determined by DNA analysis (PCR).
Figure 3. The blue bars indicate the percentage prevalence of N. ceranae in sampled colonies (e.g., 0.7 = present in 70% of hives). Note that even though spore counts suggest that N. ceranae disappears for much of the year (previous graph), a substantial proportion of colonies actually remain infected to some degree by the parasite. Also note how closely the coinfection with another intestinal parasite (the presumably opportunistic trypanosomes) tracks nosema infection. No one is sure whether there is a causal relationship, or whether the simple explanation is that both parasites flourish in stressed bees. Graph from Rennich, K, et al (2011) 2010-2011 National Honey Bee Pests and Diseases Survey Report.
As opposed to the above graph, Runckel (2011) also measured the amount of nosema DNA in samples, which presumably correlates with the intensity of the infection. They found high levels of N. ceranae transcripts in midsummer, at a time when spore counts are generally quite low (Fig. 5)! Their data indicated that N. apis was only present in spring and fall (which does correspond to spore counts). Go figure!
So what's up with high levels of N. ceranae DNA transcripts without correspondingly high spore counts? No one to my knowledge has answered that important question. What we do know is that N. ceranae can exist in the vegetative stage for a while before it produces spores (Martin-Hernandez 2009). But we're not clear on to what extent N. ceranae produces "autoinfective spores," as opposed to the "environmental" spores that are discharged into the gut contents (Cali 1999), and whether such autoinfective spores show up under microscopy. What is clear, however, is that N. ceranae appears to be able to reproduce within a bee without producing spores that are observable by microscopy.
Practical note: although N. ceranae spore counts may disappear in summer, DNA analysis indicates that the bees may still be infected. This is something of a mystery, as the bee population turns over rapidly during the summer, suggesting that N. ceranae is somehow infecting new bees without spores being evident!
So the next question is, is an infection by N. ceranae more pathogenic than one by N. apis? Although some initial cage trials indicated extreme virulence for the new nosema, trials in which bees were allowed to feed upon natural pollen generally found that both species affect bee longevity about the same (Forsgren 2010, Porrini 2011, Huang pers comm) despite the fact that spore levels get much higher with N. ceranae.
Take home: We clearly still have lots to learn about N. ceranae! It does not appear to cause rapid death of well-fed bees. The inapparent summer infections are puzzling.
So what's the cause of the seasonality of nosema spore counts? With N. apis it is presumed to be due to the requisites of transmission via dysentery by infected bees in the hive during the winter and colony nutritional stress, and limited by its sensitivity to high temperature. Martin-Hernandez (2009, 2010) demonstrated that N. apis can only grow in a narrow range of temperature (about 33degC). N. ceranae, on the other hand, grows readily over a range from 25degC to 37degC. However, N. ceranae spores are surprisingly susceptible to chilling (Fries 2010), which may limit their infectivity at lower temperatures.
Studies from a number of countries coinfected with both of the nosema cousins suggest that N. apis will continue to be the historical problem during winter and spring, with typical fall and spring spikes, whereas ceranae will be more prevalent in warmer climes, present throughout much of the year, spiking in late spring (perhaps tracking pollen flows), and then again sporadically in fall through winter.
Take home: if Nosema apis was a problem in your area prior to the invasion of N. ceranae, it may still contribute to colony health issues during the fall and spring!
Sample Interpretation
It would sure be easier if there were a simple sampling protocol that everyone could follow, and if there were clear treatment (or worry) thresholds based upon nosema spore counts, as there are for varroa (Fig. 4), but alas, I'm sorry to say that there aren't.
Figure 4. Average varroa infestation rates from 2700 colonies in 13 states (many of which received mite treatments). Sampling for varroa infestation level is relatively straightforward and simple to interpret. Typical treatment thresholds are below 5 mites per 100 bees. Graph from Rennich, K, et al (2011) 2010-2011 National Honey Bee Pests and Diseases Survey Report.
Unlike sampling for varroa, which are easily seen with the naked eye, sampling for nosema requires either a microscope or laboratory apparatus that can perform PCR. However, a number of researchers (Meana 2010, Bourgeouis 2010, Traver 2010) have demonstrated that spore counts alone do not give an accurate picture of the actual degree of infection. Unfortunately, as far as assessment methods available to Joe Beekeeper, spore counts will have to suffice as a surrogate measure of the actual degree of infection (Fig 5).
Figure 5. Average nosema spore counts from the same 2700 hives. Note the typical huge spike in spore counts (predominantly from N. ceranae) in spring, and then again lesser spikes in fall and winter. Important note: these spore counts were from samples of bees from brood frames--counts from entrance bees would likely be several times higher (compare to Figure 2). Graph from Rennich, K, et al (2011) 2010-2011 National Honey Bee Pests and Diseases Survey Report.
That said, let's return to sampling for a bit. If you want to find spores, then sample older bees, such as foragers at the entrance (Meana 2010)--spore counts will typically be about 10 times higher in older bees, since it takes a while for the infection to build up in a bee (Smart 2011). He found that in infected colonies with a background spore count of 0.5-1M in bees from under the inner cover, almost no bees younger than 12 days old contained spores (at least detectable by microscopy).
This is not at all surprising, since El-Shemy (1989) found the same to be true for N. apis--spore counts were an order of magnitude higher in bees from the entrance. Indeed, he suggested that it was best to sample exiting bees at the entrance, since returning bees have likely defecated. The magnitude of the spore counts from an infected colony generally increases in samples (in order from lowest to highest), of bees from the broodnest, outer areas of the cluster, entrance bees, exiting foragers, returning foragers.
Both El-Shemy and Higes (2008) found that the best indicator of degree of infection was to squash bees from an entrance sample one at a time in order to determine the percentage of bees infected. My own sampling of sick colonies supports this recommendation. But in reality, few of us have time to squash dozens of bees one at a time for each sample--so I won't even suggest that you go there!
The next best method may be to do a spore count for a pooled sample of 50 bees from the entrance (but don't forget that even one or two highly-infected bees can greatly skew the count). In practice, however, it is often danged difficult and time consuming to collect 50 entrance bees, even if you use a special vacuum (Oliver 2008b), especially in cool weather or from sick colonies with few foragers.
For this reason, many researchers simply take standardized samples of bees from under the cover, or from an outside comb. There is support for this, as Gajda (2009) found that although spore counts were much higher in entrance bees, the relative proportion of infected bees was similar in samples taken from an outside comb.
Practical application: If you want to find out whether N. ceranae is present to any significant extent in your operation, sample bees from the entrance. If you want to know if the infection is serious, sample house bees from under the cover.
If you are curious as to whether you have gotten old or young bees in your sample, here is an easy general observation that I've made: since only nurse bees normally eat pollen, they are the only ones that will have it in their guts (duh). But my point is, that this is really easy to use that pollen as an indicator of bee age if you use the ziplock bag method for processing samples (see my previous article, and Fig. 6).
Figure 6. How to tell if your sample contains young or old bees. (Left photo) when you crush samples of nurse bees in a ziplock bag, and then mush them in water, the fluid will typically turn opaque yellow (since the guts of nurse bees are full of pollen). (Right photo) on the other hand, the fluid from the guts of entrance bees will typically be a tan/gray color (since foragers and guards don't eat pollen).
What If You're Dealing With N. Apis?
Oh, that it were only so simple as dealing with only one nosema, but the previously cited studies suggest that many of us actually may still have N. apis popping up in fall and early spring. To make things even harder, spore counts of N. apis, on a per bee, or per pooled sample basis, are generally only a fraction (about 1/10th, as best I can tell from previous studies) of what we see with N. ceranae. But it also appears that an infection by N. apis at that low level can be as serious as an infection by N. ceranae at a much higher spore count!
Important note: Martin-Hernandez (2011) easily found N. ceranae in samples of either foragers or house bees, whereas she only found N. apis in foragers and drones. So if N. apis is your concern, then you should take entrance samples! N. apis infection may be serious at a much lower spore level!
Seasonality
The other consideration is that you must put any spore count into the context of time of year, the climate that your bees are in, the nutritional status of the colonies, and especially the load of other pathogens. I will discuss these points in the next article.
In cold climates, nosema management may have other considerations. Hedtke (2011) performed a detailed 6-year study of 220 hives in Germany, and (surprisingly) found that "No statistical relation between N. ceranae detection in autumn and the following spring could be demonstrated, meaning that colonies found to be infected in autumn did not necessarily still carry a detectable infection in spring, and colonies which developed a detectable infection over winter had not been detectably infected in autumn." So much for careful sampling!
Recommendations
Heck, I'd be crazy to stick my neck out and give any recommendations! So let's look at what sort of nosema levels are involved in crashing colonies. The CCD colonies analyzed by Cox-Foster (2007) had mean spore counts in the range of tens to hundreds of millions from broodnest samples! Is it really any surprise that those colonies collapsed? The house bees in Higes' (2008) winter-collapsing colonies hit 20M before they went down (field bees hit 50M), but those that collapsed in summer only hit 3M.
But note that in the U.S. survey graph above, that 2M was the average spore count across the U.S. in April and May of this year, yet I'm not hearing of massive colony collapses, despite very poor conditions in many states.
In my own California foothill operation (we get snow during the winter, and move to almonds in February), it is not unusual to see entrance spore counts in May in the millions or tens of millions, but they generally drop during summer, provided that colonies are not stressed by other factors. Entrance counts during summer and fall are typically in the zero to 5M range (25 spores per field of view if you follow the protocol in my previous article--I'll call these FOV counts (Oliver 2008c)). I have not looked at near as many samples of house bees, but counts are generally zero to a fraction of a million, even in colonies running at 10M at the entrance.
I am by no means suggesting that you follow my lead, but I simply no longer worry about high spore counts in spring, as they generally spontaneously drop later in the season, and I haven't experienced winter losses associated with N. ceranae (unless I've intentionally inoculated the hives with viruses). However, I do keep my mite levels down, and feed pollen supplement to maintain good nutrition if necessary. And I monitor nosema levels throughout the year so that I don't get blindsided!
I've never treated for nosema (except in experiments), yet have not experienced colony collapses since 2006. But I'm not saying that you have no reason for concern--I will be writing about a trial in which I did compare survival of treated vs. untreated colonies that had virus issues, and fumagillin appeared to help.
I'd be concerned if counts for house bees got above 5 per FOV at any time, although I know several large commercial beekeepers who routinely ignore such counts with no dire consequences so far. I just checked a number of samples of house bees today (late October), and they ran from zero to 2 spores per FOV, despite there often being counts of 100-200 per FOV of entrance samples this spring.
In some operations where N. ceranae apparently got out of hand, treatment and comb sterilization seemed to help. However, in other operations with sky-high spore counts in spring, lack of treatment did not result in any noticeable problems. Due to these huge discrepancies, it is confoundingly difficult to come up with recommendations. However, the more beekeepers who start tracking spore counts, the more we will learn about appropriate treatment decisions.
If you are in an area with a long, cold winter which keeps the bees confined, you may be dealing with Nosema apis, for which the economic threshold of 1M (5 per FOV) for house bees has been well established.
Practical application: since spore counts for N. apis generally only reach levels about 1/10th of those for N. ceranae, you'd be wise to ask your local university determine which nosema species you're dealing with, since it follows that the economic threshold for treatment for N. apis may be far less than that for N. ceranae.
I will continue this review of N. ceranae in the next issue, including treatments, and its relationship to colony mortality and honey production.
Acknowledgements
Thanks to you, my readers! It just occurred to me that I've recently passed the 5 year mark in writing for ABJ, and it's been one wild ride! If I had any idea what I was getting into, I would probably have chickened out. But your feedback and appreciation keep me going--my motivation is simply the gratification that I get from sharing what I've learned with other beekeepers. Your donations also allow me to perform the sort of quick and dirty research necessary to answer burning questions. I am constantly on the learning curve, and greatly appreciate hearing information that is relevant to better bee management--feel free to contact me (no beginners questions please) randy@randyoliver.com.
As always, Peter Loring Borst has helped me greatly with research. I thank Dr. Mariano Higes for his patience in discussing his research. Dr. Steve Pernal and Ingemar Fries have been gracious with their time. I also thank all the other nosema researchers who have patiently answered my questions.
References
Botias, C, et al (2011) The growing prevalence of Nosema ceranae in honey bees in Spain, an emerging problem for the last decade. Research in Veterinary Science (in press).
Bourgeois, AL (2010) Genetic detection and quantification of Nosema apis and N. ceranae in the honey bee. Journal of Invertebrate Pathology 103: 53-58.
Cali, A and PM Takvorian (1999) Developmental morphology and life cycles of the microsporidia. P. 121. in Wittner, M and LM Weiss, eds. The Microsporidia and Microsporidiosis.,American Society for Microbiology.
Chen, Y.P., et al (2008). Nosema ceranae is a long-present and widespread microsporidian infection of the European honeybee (Apis mellifera) in the United States. J Invertebr Pathol 582 97: 186-188.
Chen, YP, et al (2009) Asymmetrical coexistence of Nosema ceranae and Nosema apis in honey bees. Journal of Invertebrate Pathology 101 (2009) 204-209.
Cox-Foster, DL, et al. (2007) A metagenomic survey of microbes in honey bee colony collapse disorder. Science 318(5848): 283-287.
El-Shemy, A.A.M. and RS Pickard (1989) Nosema apis Zander infection levels in honeybees of known age. J. Apic. Res. 28 (2), 101-106.
Forsgren, E, and I Fries (2010) Comparative virulence of Nosema ceranae and Nosema apis in individual European honey bees. Veterinary Parasitology 170: 212-217.
Fries, I (2010) Nosema ceranae in European honey bees (Apis mellifera). Journal of Invertebrate Pathology 103: S73-S79. https://bienenkunde.uni-hohenheim.de/uploads/media/Nosema_ceranae_in_European_honey_bees__Fries.PDF
Gajda, A (2009) The size of bee sample for investigation of Nosema sp. infection level in honey bee colony. http://www.coloss.org/publications/Nosema-Workshop-Proceedings.pdf
Gisder S, et al. (2010) Five-year cohort study of Nosema spp. in Germany: does climate shape virulence and assertiveness of Nosema ceranae? Appl Environ Microbiol 76: 3032-3038.
Hedtke, K, et al (2011) Evidence for emerging parasites and pathogens influencing outbreaks of stress-related diseases like chalkbrood. Journal of Invertebrate Pathology 108:167-173.
Higes, M (2010) Nosema ceranae in Europe: an emergent type C nosemosis. Apidologie 14(3): 375 - 392.
Higes, M., et al (2005) El sindrome de despoblamiento de las colmenas en Espana. Consideraciones sobre su origen. Vida Apicola 133: 15-21.
Higes M, et al (2006) Nosema ceranae, a new microsporidian parasite in honeybees in Europe, Invertebr Pathol. 92(2):93-5.
Higes, M, et al (2007) Experimental infection of Apis mellifera honeybees with Nosema ceranae (Microsporidia). J Invertebr Pathol. 94(3):211-7
Category: Nosema Summaries and Updates
Tags: N. ceranae, Nosema cereanae, Nosema Cousins, part 14, sick bees | Nosema Cousins Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/nosema-cousins/ |
Old Bees/ Cold bees/ No bees? Part 2
Old Bees/ Cold Bees/ No Bees? Part 2
©️ Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in July 2008
One day during his tenure as a professor, Albert Einstein was visited by a student. "The questions on this year's exam are the same as last year's!" the young man exclaimed.
"Yes," Einstein answered, "but this year all the answers are different."
Beekeepers today may feel that they are in a similar situation. Colony management that was previously successful may no long work! Here at Next Year We're Going to Make the Big Bucks Apiaries, unexpected losses of colonies have been eating up our profit margin. We've been making increase like crazy each spring, only see some fail to build, or crash during fall or winter.
However, being the optimist that I am, I think that I'm beginning to get a handle on the situation!
Last month, I was describing how a forager has limited longevity at best. Even that brief lifespan can be shortened further by disease or poor nutrition.
Protein levels
Protein intake of newly-emerged bees has recently been correlated with their subsequent behavior (Nelson, et al 2007). The authors found that bees with low vitellogenin levels begin foraging earlier in life, and tend to forage more for nectar than pollen. This is an insidious effect of lack of pollen in a colony--that the bees will begin to forage, and thus begin aging, sooner in life. (Research on this topic is ongoing, and sometimes contradictory--see Matilla and Otis 2006).
The "salary" that the hard-working foragers get from the colony is a daily allotment of protein-rich jelly. Schmickl & Crailsheim (2004) point out that although the older bees acting as foragers collect the pollen, most of it is eaten by the nurse bees. The nurse bees then process it into protein-rich jelly, which is then fed back to returning foragers to fulfill their protein requirements. Since the forager immune system and antioxidant system is dependent upon vitellogenin, their lifespan as seniors is partially limited by how well the younger bees feed them.
Predictably, the nurse bees prioritize first the hungry older larvae (since the colony has invested considerable resources in them). Foragers will feel the pinch during a protein shortage. Indeed, this appears to be part of a feedback loop that stimulates foragers to collect more pollen.
So imagine the situation during a drought--foragers work extra hard to locate pollen, yet there is not enough to spare to keep their own body protein levels up. Ditto when inclement weather during broodrearing keeps the foragers inside. The colony eats up all available pollen in a few days. The nurse bees cut back on the jelly fed to brood, may cannibalize eggs and younger larvae, and are ultimately forced to steal protein from their own bodies to continue feeding the oldest brood to maturity. No jelly will be left for the foragers. The bottom line is that when pollen resources get scarce, the foragers may suffer from lack of protein. This could again shorten their lifespan.
From a practical standpoint, it is important to remember that a low protein level in a colony will not only initiate premature aging of the bees, but will depress the immune system of the colony overall, thus making the colony as a whole more susceptible to any diseases.
As an aside, we beekeepers must be careful when feeding our bees protein supplements or sugar syrup. Poor quality ingredients-such as aged soy flour, or "off spec" HFCS can be quite toxic to bees. In addition, foragers can be poisoned by mycotoxins (fungal toxins) in fermented nectar or sugar syrup, leading to large losses (Manning 2008).
General infections
Sick bees are short-lived bees. Bees that had to fight infection (bacterial or viral) or parasitism (varroa) when they were in the larval or pupal stage may never reach their full potential as adults. Adult bees then have their own set of problems. A forager carrying a varroa mite, or infected with nosema has less chance of returning from each foray than an unparasitized bee. Or perhaps they don't return on purpose-- "This behavior can be interpreted as suicidal pathogen removal, serving as a disease defense mechanism which reduces the colony's load of parasites or pathogens" (Kralj, et al 2006). Nature has likely selected for a behavior in which dying foragers remove themselves from the hive, rather than forcing undertaker bees to carry them out.
When a bee is "challenged" by a pathogen or parasite, it activates its immune system. This process is metabolically expensive (Moret & Schmid-Hempel 2000). A bee (or colony) fighting a disease requires more food, and is not as productive. The extra metabolic effort required for cold-weather flight may prove to be more than it can summon. For an older bee with a low vitellogenin titer, similar to an elderly malnourished human, a normally minor disease may be fatal.
Parasites
As I mentioned earlier, colony collapse events have a recurrent history--which suggests that weather and/or the subtle effects of well-established pathogens are involved. However, in the last 25 years three new serious players have entered the picture: tracheal mites in 1984, varroa mites in 1988, and Nosema ceranae (apparently) sometime in the past decade. These parasites did not enter the scene quietly, but rather have each wreaked havoc. In the aftermath, they have added continual new stresses to our beleaguered bees, by weakening them, suppressing their immune systems, creating points of entry for pathogens, and adding entirely new vectors for viruses. Therefore, the current widespread collapses could be caused by the action of historical environmental stresses and pathogens, exacerbated by the additional parasite stresses.
The internal parasite, nosema, has long been called the "invisible killer" --since by shortening forager lifespan, it can devastate a colony without visible symptoms. Dr. Mariano Higes has detailed the pathology of N. ceranae that can lead to colony collapse. Nosema alone can be bad for a colony, but in concert with poor nutrition and/or viruses, it can be devastating. Indeed, some bee viruses are only found in conjunction with nosema infection.
Nosema can have an additional effect upon colony population. Some older research (Fisher 1964) suggested that nosema infection increases the level of juvenile hormone (JH) in the insect. In the case of honey bees, JH is antagonistic to vitellogenin, and higher levels of JH would cause premature aging.
I've corresponded with JH expert Dr. Zachary Huang, and vitellogenin expert Dr. Gro Amdam about this. Dr. Huang has unpublished data showing that nosema does not produce JH directly, but that infected bees can indeed have elevated JH titers, which cause bees to begin foraging earlier. (In some colonies, bees do not respond to the infection by showing earlier foraging, but he did not examine these colonies to see if the infected bees also had higher JH titers). The actual mechanism has not been determined, but likely involves vitellogenin, just as in healthy bees.
The colony-to-colony difference in response to nosema infection is notable, since it may explain why nosema is harder on some colonies than others. Anything that induces bees in a colony to begin foraging at an earlier age, will accelerate the aging of the workers, and restrain population growth.
Parasitic mites have also clearly demonstrated their impact upon bee longevity. Both varroa and tracheal mites can cause colony depopulation. The tracheal mite is especially rough on wintering bees, and the varroa mite on fall and winter bees. However, it is possible that neither mite kills the colony directly, but rather initiates a viral epidemic that polishes the bees off.
From a practical standpoint, it is moot whether the parasite actually kills a colony, or rather just sets it up for a fatal blow from one or more viruses. Control the parasite, and the bees can generally keep viral infections to a low level on their own.
Viruses
Bees are ubiquitously afflicted by continuously morphing RNA viruses, much as beekeepers are afflicted by the continuously morphing cold and flu RNA viruses. However, bee viruses tend to lie latent in the bees--only occasionally causing observable illness. In this manner they act more analogously to herpes viruses--virtually all humans carry them, but they only flare up when we are stressed, infected by another disease, or immune compromised.
Bee viruses were a relatively unimportant issue to beekeepers until the arrival of varroa. Then we quickly discovered that the combination of varroa and nearly any virus can be lethal. Dr. Norman Carreck (2008) writes:
"Infestation by Varroa and subsequent infection by ABPV and KBV can lead to many of the symptoms associated with CCD, namely the spectacular and rapid loss of strong colonies, leaving empty hives with just the queen and a few workers remaining."
So the obvious question is, can a normally latent virus, or one of its mutants, flare up periodically to cause an epidemic (or more properly, epizootic) in the bee population, perhaps due to an earlier nutritional stress event, and especially with the assistance of nosema? Such a virus could be newly identified, such as Israeli Acute Paralysis Virus (IAPV--still a suspect in my book), or an old timer like Sacbrood Virus (SBV).
Sacbrood is a good example of how the effect of a virus can be overlooked. We generally think of sacbrood as an uncommon virus of bee larvae in spring and summer, generally associated with poor weather or nutritional stress. In actuality, it has always been an extremely common virus, and can be found in adult bees on all continents at high frequency throughout the year (Tentcheva 2004, Koglberger 2005, Berenyi 2006, Nielson 2008). It can exist as an inapparent infection in pupae, which then emerge as infected adults (Dall 1985).
Not surprisingly, sacbrood is commonly found in collapsing colonies (Kulincevic 1984, Cox-Foster 2007, Bromenshenk 2008). However, one would expect such a common virus to be found in any survey--that doesn't necessarily mean that it is creating the problem.
But get this: in my own operation, I have historically rarely seen sacbrood. Yet the past two years, I've seen it commonly. Notably, I'm seeing it with regularity in colonies that are collapsing, or recovering from collapse. These observations certainly make me a bit suspicious!
SBV is only noticed when it kills last-instar larvae (which die stretched out on their backs, with their heads upturned--see Goodwin (2003) to download photos). It is normally spread as workers remove infected larvae, and get exposed to the highly-infected ecdysial fluid under the skin. Only young workers are easily infected by ingesting the virus--but these are the very workers that typically clean cells. Once infected, the nurse bees or foragers can spread the virus through their saliva, jelly, and stored pollen. Shen, et al (2005), additionally found that SBV can be transmitted by the queen to her eggs, and likely by the varroa mite. I will go into more detail about bee viruses later, but first let me quote from the legendary bee pathologist, Dr. Lesley Bailey (1972):
"sacbrood virus accumulates in the brains of infected bees...without causing symptoms [emphasis mine]. However, infected individuals fly earlier in life than healthy bees and infected foragers fail to collect pollen....The few infected bees that gather pollen contaminate their loads with much sacbrood virus. Infection...much shortens the...lives of workers that have eaten pollen."
Bailey found that the median number of days for foragers to failure to return to the colony went from 14 days for healthy bees, down to 5 days for SBV-infected foragers! This fact could have major implications on colony population (recall Figure 3), and there are no symptoms for infected adults other than that they just disappear. Now I am not suggesting that Sacbrood Virus is the cause of CCD, but merely pointing out how easy it is to overlook the potential contribution of an inapparent infection by a virus.
Yet another tidbit from the paper was especially striking to me: "Infected workers...are unable to maintain the usual metabolic rates of bees at temperatures below 35oC [brood nest temperature], or to resist chilling." Remember how colonies often dwindle during cold spells? This brings us to the subject of...
Hot-Blooded Ladies
The honey bee is a tropical insect that has adapted to temperate climates, much as humans have done--by living in heated shelters. Harvard zoologist Bernd Heinrich describes bee thermal strategies in two fascinating books: The Thermal Warriors and Bumblebee Economics. Unlike most insects, honey bees normally maintain body temperatures above ambient temperature, both individually, and as a colony. They do so in a clever way--they can "uncouple" their wings from the massive flight muscles in the thorax, and shiver--much as we shiver to warm up. However, bees have refined their shivering to such an extent, that they do it without visible shaking.
And shiver they do. They shiver to keep the brood nest at 94oF. Individual bees shiver to maintain a flight muscle temperature of at least 85oF, below which they are unable to fly. A bee readying itself to take off shivers to warm its flight motor up to about 100oF, and typically maintains it at about 95oF. Bees at the outside of a cluster hold their temperature to a minimum of 41oF, since below that temperature they are too cold to initiate shivering, and will die.
Although the bee's thorax is covered with an insulating pile, it will still chill quickly in cool air if it is not constantly generating heat. Due to the laws of thermodynamics, for every 20oF that the ambient temperature drops, the bee needs to work about twice as hard to stay warm. As I mentioned before, foraging in cool weather is very wearing on the bees!
When bees are returning from foraging during a cool day, one can see them occasionally stop to "rest." They are hardly resting! Rather, they have lost too much heat from their flight motor (thoracic muscles) due to the 15 mph "wind" passing over their bodies as they fly. They need to stop to warm back up. Indeed, an apparently resting bee may be working its flight muscles harder than it would while flying!
A bee stores about 15 minutes worth of fuel in its flight muscles, and about another 15 minutes worth in its blood (Southwick 1992). Once these sources are depleted, it is dependent upon whatever nectar it has in the honey sac--and can fly much faster if the sac contains high-sugar nectar. Should a forager run out of sugar fuel while it is flying or shivering, it will die in the field.
So how can you tell if a bee is really resting, or whether it is working hard to warm itself up? Simple: look at its abdomen. From the drawing in Figure 5, you can see that much of the bee's abdomen is taken up with air sacs. These sacs function as pumps to move fresh air efficiently through the bee (more efficiently than our own lungs). Insects obtain oxygen, and dump carbon dioxide by using branched tubes called trachea that open to the outside air at holes called spiracles on the sides of their bodies--three pairs on the thorax, and six on the abdomen.
In order to ventilate, the bee "pumps" its abdomen like an accordion, and opens and closes its spiracles so that it sucks air into the tracheal sacs in the thorax, and expels it from the abdominal spiracles (Stoffolano nd). The largest intake spiracle is the first thoracic, and it is screened by "hairs" to prevent the entry of dust and parasites (although the tracheal mite can enter this spiracle in newly-emerged bees of susceptible stocks).
The illustration above may mainly apply to a bee that has high respiratory needs, such as when flying or producing heat. Otherwise, the the breathing may occur mainly in the thorax (Bailey 1954), with air entering through the first thoracic spiracle, and exiting through the third thoracic spiracle (rather than out the abdominal spiracles).
So if an apparently "resting" bee is pumping its abdomen, you know that it is in actuality working as hard as it can to warm up--pumping oxygen to its flight muscles, and carbon dioxide out. This one-way flow-through system of ventilation is extremely efficient. Indeed, when not flying or shivering, the bee stops the pumping action in order to minimize its tissue exposure to harmful oxygen.
The bee has a clever countercurrent heat exchange system at its waist (the petiole) which prevents thoracic heat from being lost to the abdomen. The abdomen remains unheated. However, the bee instead uses its haemolymph (blood) to pump heat to the head! By placing its head or thorax against a cell wall or capping, the bee can transfer considerable heat to the brood (Figure 6).
Figure 6. At left is a top-view thermograph of three bees inside empty cells adjacent to brood. The upper bee is generating the most heat. Note how the heat transfers to the head. At right is a side view of two bees in cells. The upper is resting, the lower generating heat. The asterisks mark the walls of adjacent pupae. The white line is the comb midrib. From Marco Kleinhenz, Brigitte Bujok, Stefan Fuchs and Jurgen Tautz (2003) Hot bees in empty broodnest cells: heating from within ©️ 2003 The Company of Biologists Ltd, by permission.
The ability to transfer heat to the head allows honey bees to perform another neat trick--they can fly at temperatures that would kill most insects (up to 113oF). They do so by using their hot head as a radiator, and if necessary, exuding a droplet of nectar from their mouth to cool by evaporation! I am struck by what an amazing insect the bee is--it can maintain a constant body temperature similar to ours, cool itself when necessary, transfer heat to its offspring, and regulate the amount of oxygen that its tissues are exposed to!
OK, I've digressed, so let me return again to the question, What factor(s) could prevent the return of a bee that was initially healthy enough to fly away from the hive? Obviously, a pesticide kill, but those instances are generally pretty clear, and there are often piles of twitching bees in front of the hive. Instead, perhaps we should focus on the ability to fly. Sudden depopulation of a colony with no dead bees present, means that the bees must have flown away, and not flown back.
The non-returning bees were healthy enough rev up their flight motor and fly out, so were unlikely to have suddenly succumbed to mortality. More plausibly, they were simply unable to get their wing muscles back up to takeoff temperature once they cooled after leaving the warm colony. A bee can raise its thoracic temperature roughly 30oF above the ambient temperature while it is flying. That means that if it is flying in 55o weather, that once it leaves the warmth of the hive, it will barely be able to keep its wing muscles up to their minimum operating temperature (85oF)--hence bees don't fly much at temperatures below 55 degrees. And if they do, they often don't return.
So it appears that we should be looking for factors that affect ability of a bee to warm up its thoracic flight muscles. The most likely are age, poor nutrition, and/or disease--especially any disease that affects the flight musculature, the nerves that control it, or its energy conversion. The preliminary CCD report (van Englesdorp, et al 2007) describes some apparent pathologies of the flight muscles, including "white nodules" and "crystalline arrays." And remember Bailey's findings detailed earlier, that bees infected with sacbrood virus chilled more quickly, and were unable to maintain normal metabolic rates once cooled below broodnest temperature. I'm eager to hear of any research as to how any particular pathogen might accelerate the "aging" of the flight muscles.
Whatever the specific mechanism, the most likely reason that bees fly out, but don't return, is simply that once out of the hive, they couldn't generate flight muscle temperatures necessary for the return trip.
This brings up the additional question as to whether some factor is causing such flight-impaired bees to leave the colony at unfavorable temperatures. An intriguing hypothesis is based upon the observations that prior to some recent collapses, the colonies appeared "restless," bees may move away from the brood area toward the entrance(s), or that the combs may become repellent to bees. A pathogen or condition that changes the behavior of the bees to exit the hive at an early age, to initiate forays at inappropriate temperatures, or to abandon their hive and drift into others could certainly bring about a depopulation.
The Bottom Line
The dwindling of healthy-appearing colonies appears to be largely a function of the combined effects of the age of onset of foraging (or exit from the hive), and the number of days that the foragers then survive. Should the average age for forager "failure to return" drop to only a few days, the colony population dynamics go seriously into the red, and we observe that the colony "dwindles" as younger and younger bees are forced to shift from nursing responsibilities to foraging.
Several factors can promote early foraging, or accelerate the aging of foragers--especially poor nutrition or nosema, which also increase their vulnerability to disease and stress. In some collapses, something appears to cause a restlessness of the bees, or a repellency of the combs.
Some diseases, especially nosema, mites, and viruses, decrease the survivability of foragers without any apparent symptoms. The effect of any of these factors is greatest when foragers leave the warmth of the hive in cool weather, lose body heat, and are later unable to warm up for the return flight. Hence, spring and fall dwindling are often observed at the onset of cool weather events.
This is unfortunate for beekeepers preparing for almond pollination. A cold snap in fall or close to beginning of bloom can turn of profitable-looking yard of bees into a bunch of dinks seemingly overnight! We can only hope that further understanding of the causes leading up to such collapses, can help us to avert them in the future.
I have spoken with a number of beekeepers who were successful at taking strong colonies to almonds this season. There doesn't appear to be any single formula or magical potion for success, but rather, common sense husbandry may be the best approach:
* Be diligent with varroa! Don't let levels ever get high. Any number of methods will work to control the mite. But definitely get mite levels way down mid August at the latest. This will help keep viruses in check.
* Monitor nosema infestation, and treat in a timely manner if appropriate. Especially check colonies that fail to build normally.
* Don't baby colonies that aren't thriving, or have spotty brood. Kill or requeen them! (Some successful beekeepers requeen more than once a year!) Get sick colonies off to a hospital yard.
* Maintain good colony nutrition with regard to pollen, especially in late summer and fall. Move to better pasture, or feed your bees if necessary.
* It may be wise to maintain genetic diversity in your operation, since colonies vary in their resistance to different pathogens. Naturally resistant stocks go a long way toward success.
References
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Category: Aging and Thermoregulation | Old Bees/ Cold bees/ No bees? Part 2 - Scientific Beekeeping | https://scientificbeekeeping.com/old-bees-cold-bees-no-bees-part-2/ |
Pollen Supplement Formula
Update February 2023: Be sure to check out an updated Homebrew formula from my research in 2020 at https://scientificbeekeeping.com/a-comparative-trial-of-the-pollen-subs-part-5-revisiting-de-groot/
Update December 28, 2013
I am currently running a beekeeper-supported controlled trial of the major pollen supplements on the market, with a positive control of natural pollen, and a negative control of no protein feeding. 162 colonies total in the trial, 18 in each test group. I've recently completed the first grading for strength. The results were surprising, with two products outperforming natural pollen! As expected, the negative control is doing the worst. Both yeast-based formulations (including a variation of my homebrew formula below) are being poorly consumed. Final results will be in in February.
Interestingly, the Ontario Tech Team found that a yeast/egg homebrew formula similar to my original "homebrew" formula outperformed two off-the-shelf patties. I've copied it below. I am not promoting or recommending any formula. When my field trial is complete in February, I will post the results for you to interpret yourselves.
Update April 2012
There are new protein supplements on the market, most of which are very good. I am experimenting with several.
To most, I still add a corn/canola oil blend, food grade dried egg yolk, ground up multivitamin/minerals, some citric acid or lemon juice, and a splash of HBH or ProHealth as a feeding stimulant.
I see that the Kushlan mixer that I use is no longer on the market. Normal concrete mixers will not work-you need a mortar mixer or sausage mixer with rotating paddles. For mixing one sack at a time, it is surprising how quickly you can simply mix it with a garden hoe in a wheelbarrow!
UPDATES NOTE: If you don't see the changes, hit reload or clear your cashe.
added calc on Hackenberg formula
added Keith Jarret
Updated Feb 25, 2009 added comparison paragraph and table, corrected recipe % dry wt
Update 8/2/09 Jarret analysis
Update 8/25/09 Global patty link
Update 7/3/10 Protein sources
I've been asked again and again for the formula that I use. Well, I play with the formula often, and do not swear by any yet. The formula below was a composite of homebrews from various beekeepers, plus my own experimentation. It tested well against others, and I found it to be definitely better than brewers yeast/sugar alone. I will not comment on other proprietary products, since none have enough repeated data to support comparisons.
Testing by the USDA-ARS found that their product, licensed as MegaBee®️, performed better than the other products that they tested (www.megabeediet.com/). Commercial beekeepers report success with all the brands offered by the supply houses, Global, Norm Carey, Keith Jarret etc. See also http://www.honeybeeworld.com/misc/pollen/default.htm and http://globalpatties.com/pages/why.htm
Pollen supplement should be fed during pollen dearths. Appropriate times are prior to honey flows, in fall while the last rounds of brood are being raised, if bees are set in almonds prior to actual bloom, and immediately after almond bloom.
The most bang for the feeding buck is in late summer. California beekeepers should start feeding when natural pollen drops off in August, and by September at the latest. Continue as long as bees will take it, generally until about November 1st. Do not let colonies go long between feedings if they are actively rearing brood.
Field trials and practical experience have shown that colonies do well with about a pound a week of supplement, depending on protein content. Successful commercial migratory operations are feeding 10-20 lbs per colony per year, depending upon available natural pollen.
Please let me know of your successes and failures, so that we can figure out better formulas. Please do not post this formula to your web pages. Instead, send the link, or link back to this page, so that I can keep the formula updated.
Update: OK guys, there is a lot of confusion out there in comparing formulas. In general, when comparing livestock feeds, the number one thing that you pay for is protein. So if you want to see if you are getting the most bang for your buck, calculate out how much you are paying per pound of protein.
However, be aware of a few caveats!
1. This assumes that the proteins that you are comparing are equivalent nutritionally. For example, a protein that is either indigestible, or lacking in a single amino acid can't be compared to a digestible, complete protein.
2. Mann Lake's use of deGroot's amino acid ratio is not quite accurate. deGroot did not specify percentages of amino acids-he specified a "normalized" ratio of amino acid weights relative to the amount of tryptophan. deGroot never implied that a formula should be 1.00% trypotophan-rather, divide all other amino acid weights (or percentages) by the weight/percentage of tryptophan, to obtain their relative value. For example, brewers yeast runs about 0.62% tryptophan and 1.7% threonine. So you'd divide 1.7 by 0.62 to obtain a ratio of 2.74:1 threonine:tryptophan, which is close to deGroot's suggested ratio of 3:1.
The way you use these ratios is to see if any of the amino acids fall below the suggested ratio relative to tryptophan. Any that fall below would be called "limiting amino acids" since they would limit the amount of the total protein that can be utilized by the bees. To overcome that limitation, you would add a second protein source that was high in the limiting amino acid.
3. We are not sure what the optimum protein level is! Kleinschmidt found that the best pollens ran about 25% protein. The other 75% was fat, carbohydrates (some indigestible), minerals, sterols, and fiber. We don't really know how this works out in a pollen supplement that contains lots of sugar. We will probably find out by trial and error. Mann Lake, Dr. Gordon Wardell, and others selling supplements have done a great deal of research, but have clearly come to different conclusions as to what percent protein is best, or at least, most cost efficient (it's smart business practice to sell sugar at a dollar a pound).
4. When you are comparing formulas, make sure that you are comparing apples to apples! That is, you can't compare dry weight to wet weight, or with or without sugar. The only way to really compare them is in the finished, ready-to-feed patty.
There are two ways to determine the actual composition of a patty-by calculation, based upon the guaranteed analysis of the ingredients, or (most accurate) by actual lab analysis. Here are some actual comparisons of ready-to-feed patties. Those that were lab analyzed were guaranteed "fresh" from the distributors, and analyzed by an impartial agricultural lab in California.
Name Type analysis % Protein % Fat pH
MegaBee Lab 17.5 1.1 4.2
Bee-Pro Lab 10.3 5.3 4.8
Global 15% pollen Lab 14.8 2.4 5.5
Keith Jarrett Lab 17.6 7.5 4.9
"Kitchen Sink" Calc'd 19 6 low
Hackenberg Calc'd Can't compare, since amt water is not spec'd, but dry weight protein is ~15; I'm guessing it would take about 5 gal, which would put protein at 13%
The formula in the table below is experimental, but works well. It is likely that some of the ingredients can be deleted. I added the soy isolate in order to boost the protein level, and to balance the amino acids a bit, but need to test further to see if there is an added benefit. Compare the formula to David Hackenberg's formula following it.
Update 2022: The best formula that I've now tested is shown near the end of A Comparative Trial of the Pollen Subs: Part 5- Revisiting de Groot - Scientific Beekeeping
I mix all ingredients except the sugar and yeast into the water in a bucket with a motorized paint stirrer. I put the dry sugar into the mixer, then pour in the water solution from the bucket, and stir until mixed (put a bucket under the gate to catch any drip). Then I add the yeast on top, and stir until uniform (about 5 minutes). This procedure gives the best mixing in a Kushlan mixer. Water content is critical-too little gives a soupy mix, to much sets up too hard.
We pour the mix into oiled plastic storage tubs, and allow it to set up overnight. It will get firmer, so the poured mix must be soft. I sprinkle sugar over the top of it, so that you can pack it into the tub with your hands without it sticking.
In the field, we dump the tub out onto a sugared board, and cut it up with a spade or floor scraper into 2-3 lb slices, depending upon how much we want to feed. We place the slices between the brood boxes, after smoking the bees off the frames. If you make the formula soft, it will squeeze between the frames.
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Here is a formula developed, and successfully used, by Dave Hackenberg (by permission):
HACK'S SACK PROTEIN PATTIES
Protein Patty Recipe
1. 125 lbs. Sugar (Add water and keep wet. Should be a little thicker than pancake batter.)
2. Add either 3 cups citric acid or 4 quarts of lemon juice, (this is to put the ph at 4 1/2 to 5) 3. Add 1 cup Honey Bee Healthy (optional , but we prefer)
4. Add 1/2 bag Vitamins & Electrolytes (we use Russell's) (2 oz. worth)
5. Add 10 lbs. pollen (optional)
(keep the mix wet)
6. Mix in 25 lbs. of Inedible Dried eggs (available from Hackenberg Apiaries)
7. Add 3 1/2 cups Canola Oil
8. Mix in 24 lbs. (2 gallons) Honey
9. Finish by adding 50 lbs. Brewtech Brewers Yeast. Water until it has the consistency you desire. (available from Hackenberg Apiaries, Pat Heitkam or David Mendes)
David says that this formula tests out from 16-20% protei; however, by my math it would be about 15% before adding water.
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Note that his formula has much more sugar (plus honey). I tried inedible whole spray dried egg, but didn't like the consistency, and found that bees didn't much care for it at high percentage. The brand that I used also smelled like rotten eggs! I found that the dried egg yolks from Honeyville (human food grade) cost a bit more, but are of the highest quality (and smell good).
Sources of mixed supplement:
Keith Jarret ( cnhoney@att.netThis e-mail address is being protected from spam bots, you need JavaScript enabled to view it ) Ingredients not disclosed. Keith says that his product tests at "fat 9% & protein 16%, that is finished product just as the bees would eat. It comes in 200 lb tubs @ $1.05 lb."
Protein Sources
it is by far easiest in the U.S. to buy off-the-shelf pollen supplements, already tested and proven. There are several excellent ones on the market.
If you choose to mix your own, the most important item in any supplement is the protein source. A great review is in "Fat Bees, Skinny Bees"-a free download https://rirdc.infoservices.com.au/downloads/05-054.pdf Here is a list of some tried and true sources:
1. Natural pollen: the best, but problems with price, parasite spores, nutritional degradation, and pesticides.
2. Brewers Yeast: Brewtech brand works very well. Roller dried yeast may be better than spray dried. Debittered may be more palatable, but I'm not sure. Some brands (such as from corn ethanol production) dry rock hard if not eaten.
3. Torula yeast: good reviews
4. Soy flour: Expeller pressed best, not defatted. This process destroys the anti nutritional factors of soy. Problem with low B vitamins, and some complex sugars.
5. Soy protein isolate: expensive, but might have use as a protein booster and amino acid balancer.
6. Pea protein
7. Corn gluten
8. Barley flour
9. Quinoa flour
10. Dried egg or egg yolk
11. Milk products without lactose. Casein excellent, but too expensive.
Sources for ingredients:
(Broken Link!) http://store.honeyvillegrain.com/powdereddriedwholeeggsandeggwhites.aspx egg yolk, soy
Pat Heitkam, Orland, Calif. 530-865 -9562 Brewtech yeast, commercial orders
tackabery@aol.comThis e-mail address is being protected from spam bots, you need JavaScript enabled to view it commercial orders. soy isolate (tested to be free of melamine), yeast
This photo shows the desired consistency of the fresh mixture. I pour it into oiled tubs to set up. In the field, we dump the tub over onto a board sprinkled with sugar, and slice it up with a floor scraper.
Feedback:
Q: I have a question on the protein receipe. I see you have vitamins added to boost micro nutrients. Can I use kelp meal also? is this an exact receipe or can I add to it?
A: The recipe is a work in progress. It tested very well in a recent controlled trial by myself. I have no idea as to whether additions (or deletions) would help. Might I suggest making a batch in portions, tweaking one ingredient at a time. Then test side by side in colonies. Please let me know your results!
Category: Bee Nutrition | Pollen Supplement Formula - Scientific Beekeeping | https://scientificbeekeeping.com/pollen-supplement-formula/ |
Sick Bees - Part 14: An Update on the "Nosema Cousins"
Contents
Worldwide Status and Distribution
Ceranae vs. apis
Coinfection
Seasonality
Sample Interpretation
What if You're Dealing with N. apis?
Seasonality
Recommendations
Acknowledgements
References
Sick Bees 14:
An Update On The "Nosema Cousins"
First published in ABJ December 2011
Randy Oliver
ScientificBeekeeping.com
In my last article, I described how to quickly sample for nosema. So what do the spore counts actually mean as far as colony health is concerned? I wrote an article a little over two years ago with the tongue in cheek title "Nosema ceranae: Kiss of Death, or Much Ado about Nothing." Well, N. ceranae is still an enigma, but it appears that the answer lies somewhere in between.
Dr. Mariano Higes (2005, 2006) was the first to raise the flag to alert beekeepers worldwide that a new species of nosema had invaded Europe, and appeared to be the cause of the unusual colony collapses that plagued Spain (a major beekeeping country) in 2003 and 2004. Then in 2007, just as Colony Collapse Disorder was rampaging through our own bee operations, we found out that Nosema ceranae had somehow spread throughout the U.S. right under our eyes!
Drs. Diana Cox-Foster and Ian Lipkin (2007) then published a paper suggesting that a newly-described virus was involved in CCD, but later research indicated that IAPV wasn't the only culprit, leaving N. ceranae as a leading suspect.
Shortly afterward, Higes (2008) described in great detail the progression of N. ceranae infection (in his Spanish apiaries) through four stages: Asymptomatic, Replacement, False Recovery, and finally the dreaded Depopulation. The logic, the numbers, and the devastating final result were all clear and compelling. The specter of N. ceranae ravaging our hives resulted in unnerved beekeepers boosting the sales of fumagillin to the point that supplies ran short.
I had never previously worried about nosema, but I pulled out a microscope and found out that N. ceranae was indeed widespread in my operation. I ran trials, and found out that the danged parasite could flourish despite being drowned in fumagillin (Oliver 2008a), but more surprisingly, that colonies here at Comedy of Errors Apiaries thrived despite exhibiting spore counts in the millions. To try to reconcile the differences between the very different outcomes of N. ceranae infection in my operation with those reported for Spain, I began an ongoing correspondence with Dr. Higes, which continues to this day.
To be frank, some other Spanish researchers dispute Higes' conclusions (debate leads to better science), so I have often questioned and challenged him on details of methodology and interpretation, which he and his team of collaborators have generally clarified with additional research. In this series of articles I will be citing a number of the Higes team's papers, since they have clearly led the pack in N. ceranae research, meticulously investigating nearly every aspect of this pathogen's effects upon bees.
I've previously written at length about N. ceranae in my "Nosema Twins" series (all available at ScientificBeekeeping.com), but feel that there has been so much recent research completed that it would benefit the reader for me to write a digest of our current state of knowledge. I've scoured the literature for every relevant research paper (including a number still in press), and have discussed as well current findings with many of the world's nosema researchers. I wish that at this time I could say that I have the answers to all your questions about Nosema ceranae, but unfortunately, in many aspects this parasite still remains an enigma.
Worldwide Status And Distribution
Nosema ceranae has now spread into the European honey bee populations of most areas of the world, roughly concurrent with the spread of varroa (and its altering of virus dynamics), which greatly confuses analysis of the effect of these two novel parasites upon bee health. It is difficult to tell in which countries N. ceranae has already reached equilibrium, and in which it is still invading.
Since the first invasive wave of a novel parasite into naive hosts is generally that most damaging, it would be helpful to know when ceranae actually arrived in various countries. For example, we know from analysis of archived bee samples that N. ceranae has been present on the East Coast for at least two decades (Chen 2008). Unfortunately, any initial effects of its invasion may have been masked by our focus upon the massive impact of the arrival of varroa at about the same time.
Since no one was looking for N. ceranae in the U.S. until 2007, we obviously didn't start studying it until long after it was well established and likely homogenized throughout the bee population via migratory beekeeping practices. And it is also likely that by the time we started studying the impact of N. ceranae upon the health of colonies, natural selection may have already weeded out the bees least tolerant of the emergent pathogen.
In Europe, however, N. ceranae only recently invaded bee populations already suffering from varroa and viruses, miticide failure and comb contamination, extreme weather events, plus changes in agricultural practices and pesticide use--the combination of which likely factor into colony losses in that region.
In a fresh study (Botias 2011), the Higes team analyzed archived Spanish honey samples (frozen) and adult bee samples (in alcohol) dating back to 1998. They found that N. ceranae first appeared beginning in 2000 and increased in prevalence through 2009 (the latest samples analyzed), concurrent with a decrease in the prevalence of N. apis. It is noteworthy that Spain concurrently suffered from devastating drought during much of that period, which led to serious colony stress.
N. ceranae is still in the process of extending its range worldwide, and appears to be most successful in warmer climates. It is of interest that in varroa-free Australia, its invasion does not appear to be causing significant colony losses. Interestingly, although it is well-established in Canada, it is not yet common in some northern European countries, but this may be due to restrictions upon bee imports (Fries 2010).
N. ceranae is widely distributed throughout the U.S., but surprisingly, there were great differences in the percent of colonies infected in a recent state-by-state survey (Fig. 1).
Figure 1. Prevalence (percent of samples infected) of N. ceranae in various states as determined by PCR analysis (more sensitive than spore counts) of aggregate samples collected from 8 randomly selected colonies per apiary, 4 apiaries per state. Note that in some states over 70% of samples were infected! From Rennich, K, et al (2011) 2010-2011 National Honey Bee Pests and Diseases Survey Report.
Ceranae Vs. Apis
In a widely cited paper by Martin-Hernandez (2007), her arresting graph of nosema positive samples over time clearly shows a definite shift over the period from 1999 to 2005--there initially were only spikes in spring and fall (ostensibly from apis), transitioning to nearly 100% of samples being positive every month of the year (due to ceranae). Of note is that her data has an inherent bias, in that the samples were voluntarily sent to the lab by beekeepers for diagnosis of problems, suggesting that the data may reflect the change in nosema loads in sick hives. Also of note, is that despite this graph being widely cited, it is often misunderstood--it did not plot spore levels, but rather only the yes/no detection of nosema spores.
What the graph did strongly indicate was that N. ceranae rapidly and thoroughly invaded Spain over a period of only a few years! This initial finding has now been confirmed by Botias (2011). Likely, a similar phenomenon occurred in the U.S., since Chen (2008) found N. ceranae to already be widespread in archived U.S. bee samples dating back to 1995.
The general trend appears to be that N. ceranae now predominates in warmer countries, whereas N. apis is better adapted to colder areas. It has been often stated that N. ceranae has displaced N. apis, but more careful analysis suggests that that may not actually be the case!
When Dr. Robb Cramer asked me in 2007 to send him infected bees so that he could culture pure N. ceranae, he found that the samples often contained some N. apis as a "contaminant." In Dr. Diana Cox-Foster's (2007) analysis of CCD colonies, they also found both species of nosema. Later studies by Bourgeois (2010) and Runckel (2011) of commercial operations in the U.S. also found N. apis, but in far fewer hives than its cousin, only in spring and/or fall, and notably, at much lower spore levels than N. ceranae.
The differences between the detectability of the two nosema species (N. apis typically produces much lower spore counts and is generally only seen in spring and fall) may lead "to an increased chance of detecting N. ceranae over N. apis, which could have biased the impression that N. apis has been displaced" (Higes 2010).
So, has ceranae actually displaced apis, or have we merely been overlooking its cousin? In order to answer that question, Dr. Raquel Martin-Hernandez (2011) carefully analyzed over 2000 bee samples from all across Spain. She found ceranae and apis coexisting throughout country, with ceranae clearly predominant (in roughly 40% of hives), apis hanging in there (in up to 15%), and occasional mixed infections (below 7%). She also found that infection by ceranae was favored in hotter areas of the country, whereas apis succeeded better where winters are colder.
I'm seeing similar indications from other countries (e.g., Gisder 2010), which are appearing to confirm that apis is the more cold-adapted species. As far as seasonality, Martin-Hernandez found apis only in the spring and fall, whereas ceranae could be found all year, and notably, once ceranae infects a colony, it almost always persists (detectable with PCR, even if not obvious via spore counts).
Practical note: these studies indicate that N. ceranae remains present as an infection in a colony throughout the year, even if it is not detectable by microscopy. But we don't know whether these inapparent infections affect colony health.
I found one last study to be of special interest: Dr. Judy Chen (2009) looked at nosema invasion from the other direction--in a turn of the tables, N. apis appears to have been introduced from the Western honey bee (Apis mellifera) into the Eastern honey bee (Apis cerana) in Asia, and is now an emergent parasite in that species, which had historically been infected only by N. ceranae! She analyzed bee samples from China, Taiwan, and Japan. Her findings:
"N. apis was detected in 31% of examined bees and N. ceranae was detected in 71% of examined bees and that the copy number of N. ceranae was 100-fold higher than that of N. apis in co-infected bees, showing that N. ceranae is the more abundant of two Nosema species in the Eastern honey bees."
This study suggests that N. apis can not only hold its own against N. ceranae, but can actually invade into ceranae's turf! Interestingly, in the Eastern honey bee, despite its long coevolution with N. ceranae, ceranae still produces higher spore counts than its invading cousin.
Coinfection
This brings up the question of what happens when bees are infected simultaneously by both species of nosema? Dr. Zachary Huang (pers comm) found that in both cage trials and field observations that longevity was substantially shorter for coinfected bees as opposed to those infected by either species of nosema alone (unpublished data).
Note that in Cox-Foster's (2007) CCD study that they found "a trend for increased CCD risk in samples positive for N. apis" (100% of CCD colonies tested positive for ceranae and 90% for apis, but remember that apis is easy to miss when samples consist of house bees). As Jim Fischer noted in a post to Bee-L, "What was striking was that every hive showing CCD symptoms tested positive for BOTH Nosema apis and Nosema ceranae, and this correlation was better than the correlation between CCD and IAPV that was the focus of the paper."
These findings leave me very curious about the impact of coinfection by two nosema species upon colony health!
Seasonality
Spore counts of N. ceranae generally reach a peak in May, then drop spontaneously during summer, and may spike sporadically in fall and winter. But there is more to the picture than this. Dr. Ingemar Fries (2010), who has studied nosema for decades, explains thusly:
"The typical pattern for N. apis infections in temperate climates is low prevalence or hardly detectable levels during the summer with a small peak in the fall. During the winter there is a slight increased prevalence with a large peak in the spring before the winter bees are replaced by young bees... The pattern is similar both in the southern and northern hemisphere... Unfortunately, very few data exist for N. apis on the seasonal prevalence from tropical or subtropical conditions. The only published year round sampling under conditions where bees could fly all year round, revealed detectable levels of N. apis with no seasonal pattern of prevalence."
Along that line, Dr. Denis Anderson in Australia (pers comm) tells me that, "there are also many unseasonal occurrences of N. apis -- I get many samples sent in in the mid summer here that are loaded with N. apis." This could well be happening in the U.S., where, as far as I can tell, there have been few studies on N. apis in warmer areas, other than the fact that it was commonly found in package bees produced in the southern states.
Practical application: we need to learn more about the prevalence and seasonality of N. apis in the warmer parts of our country!
I've now seen data and presentations on N. ceranae seasonal prevalence from researchers from all over the world. Since a picture is worth a thousand words, I've summarized them in a crude graph below (Fig. 2).
Figure 2. A generic graph of typical N. ceranae spore counts over the course of the year in my operation. Important note: Counts of house bees would follow the same trend, but at much lower levels. The late-season spikes are often sporadic flare ups that spontaneously "go away."
Practical application: It is not unusual to see high nosema spore counts in April and May. Counts will typically drop in summer whether you treat or not. I'll cover treatments in a subsequent article.
But new technology is showing something surprising about nosema sampling--that spore counts do not necessarily reflect degree of actual nosema infection (Meana 2010)! Look at the following graph (Fig. 3), from a recent nationwide study of pathogens in U.S. bees--instead of measuring spore counts, the blue bars indicate the percentage of colonies infected by N. ceranae as determined by DNA analysis (PCR).
Figure 3. The blue bars indicate the percentage prevalence of N. ceranae in sampled colonies (e.g., 0.7 = present in 70% of hives). Note that even though spore counts suggest that N. ceranae disappears for much of the year (previous graph), a substantial proportion of colonies actually remain infected to some degree by the parasite. Also note how closely the coinfection with another intestinal parasite (the presumably opportunistic trypanosomes) tracks nosema infection. No one is sure whether there is a causal relationship, or whether the simple explanation is that both parasites flourish in stressed bees. Graph from Rennich, K, et al (2011) 2010-2011 National Honey Bee Pests and Diseases Survey Report.
As opposed to the above graph, Runckel (2011) also measured the amount of nosema DNA in samples, which presumably correlates with the intensity of the infection. They found high levels of N. ceranae transcripts in midsummer, at a time when spore counts are generally quite low (Fig. 5)! Their data indicated that N. apis was only present in spring and fall (which does correspond to spore counts). Go figure!
So what's up with high levels of N. ceranae DNA transcripts without correspondingly high spore counts? No one to my knowledge has answered that important question. What we do know is that N. ceranae can exist in the vegetative stage for a while before it produces spores (Martin-Hernandez 2009). But we're not clear on to what extent N. ceranae produces "autoinfective spores," as opposed to the "environmental" spores that are discharged into the gut contents (Cali 1999), and whether such autoinfective spores show up under microscopy. What is clear, however, is that N. ceranae appears to be able to reproduce within a bee without producing spores that are observable by microscopy.
Practical note: although N. ceranae spore counts may disappear in summer, DNA analysis indicates that the bees may still be infected. This is something of a mystery, as the bee population turns over rapidly during the summer, suggesting that N. ceranae is somehow infecting new bees without spores being evident!
So the next question is, is an infection by N. ceranae more pathogenic than one by N. apis? Although some initial cage trials indicated extreme virulence for the new nosema, trials in which bees were allowed to feed upon natural pollen generally found that both species affect bee longevity about the same (Forsgren 2010, Porrini 2011, Huang pers comm) despite the fact that spore levels get much higher with N. ceranae.
Take home: We clearly still have lots to learn about N. ceranae! It does not appear to cause rapid death of well-fed bees. The inapparent summer infections are puzzling.
So what's the cause of the seasonality of nosema spore counts? With N. apis it is presumed to be due to the requisites of transmission via dysentery by infected bees in the hive during the winter and colony nutritional stress, and limited by its sensitivity to high temperature. Martin-Hernandez (2009, 2010) demonstrated that N. apis can only grow in a narrow range of temperature (about 33degC). N. ceranae, on the other hand, grows readily over a range from 25degC to 37degC. However, N. ceranae spores are surprisingly susceptible to chilling (Fries 2010), which may limit their infectivity at lower temperatures.
Studies from a number of countries coinfected with both of the nosema cousins suggest that N. apis will continue to be the historical problem during winter and spring, with typical fall and spring spikes, whereas ceranae will be more prevalent in warmer climes, present throughout much of the year, spiking in late spring (perhaps tracking pollen flows), and then again sporadically in fall through winter.
Take home: if Nosema apis was a problem in your area prior to the invasion of N. ceranae, it may still contribute to colony health issues during the fall and spring!
Sample Interpretation
It would sure be easier if there were a simple sampling protocol that everyone could follow, and if there were clear treatment (or worry) thresholds based upon nosema spore counts, as there are for varroa (Fig. 4), but alas, I'm sorry to say that there aren't.
Figure 4. Average varroa infestation rates from 2700 colonies in 13 states (many of which received mite treatments). Sampling for varroa infestation level is relatively straightforward and simple to interpret. Typical treatment thresholds are below 5 mites per 100 bees. Graph from Rennich, K, et al (2011) 2010-2011 National Honey Bee Pests and Diseases Survey Report.
Unlike sampling for varroa, which are easily seen with the naked eye, sampling for nosema requires either a microscope or laboratory apparatus that can perform PCR. However, a number of researchers (Meana 2010, Bourgeouis 2010, Traver 2010) have demonstrated that spore counts alone do not give an accurate picture of the actual degree of infection. Unfortunately, as far as assessment methods available to Joe Beekeeper, spore counts will have to suffice as a surrogate measure of the actual degree of infection (Fig 5).
Figure 5. Average nosema spore counts from the same 2700 hives. Note the typical huge spike in spore counts (predominantly from N. ceranae) in spring, and then again lesser spikes in fall and winter. Important note: these spore counts were from samples of bees from brood frames--counts from entrance bees would likely be several times higher (compare to Figure 2). Graph from Rennich, K, et al (2011) 2010-2011 National Honey Bee Pests and Diseases Survey Report.
That said, let's return to sampling for a bit. If you want to find spores, then sample older bees, such as foragers at the entrance (Meana 2010)--spore counts will typically be about 10 times higher in older bees, since it takes a while for the infection to build up in a bee (Smart 2011). He found that in infected colonies with a background spore count of 0.5-1M in bees from under the inner cover, almost no bees younger than 12 days old contained spores (at least detectable by microscopy).
This is not at all surprising, since El-Shemy (1989) found the same to be true for N. apis--spore counts were an order of magnitude higher in bees from the entrance. Indeed, he suggested that it was best to sample exiting bees at the entrance, since returning bees have likely defecated. The magnitude of the spore counts from an infected colony generally increases in samples (in order from lowest to highest), of bees from the broodnest, outer areas of the cluster, entrance bees, exiting foragers, returning foragers.
Both El-Shemy and Higes (2008) found that the best indicator of degree of infection was to squash bees from an entrance sample one at a time in order to determine the percentage of bees infected. My own sampling of sick colonies supports this recommendation. But in reality, few of us have time to squash dozens of bees one at a time for each sample--so I won't even suggest that you go there!
The next best method may be to do a spore count for a pooled sample of 50 bees from the entrance (but don't forget that even one or two highly-infected bees can greatly skew the count). In practice, however, it is often danged difficult and time consuming to collect 50 entrance bees, even if you use a special vacuum (Oliver 2008b), especially in cool weather or from sick colonies with few foragers.
For this reason, many researchers simply take standardized samples of bees from under the cover, or from an outside comb. There is support for this, as Gajda (2009) found that although spore counts were much higher in entrance bees, the relative proportion of infected bees was similar in samples taken from an outside comb.
Practical application: If you want to find out whether N. ceranae is present to any significant extent in your operation, sample bees from the entrance. If you want to know if the infection is serious, sample house bees from under the cover.
If you are curious as to whether you have gotten old or young bees in your sample, here is an easy general observation that I've made: since only nurse bees normally eat pollen, they are the only ones that will have it in their guts (duh). But my point is, that this is really easy to use that pollen as an indicator of bee age if you use the ziplock bag method for processing samples (see my previous article, and Fig. 6).
Figure 6. How to tell if your sample contains young or old bees. (Left photo) when you crush samples of nurse bees in a ziplock bag, and then mush them in water, the fluid will typically turn opaque yellow (since the guts of nurse bees are full of pollen). (Right photo) on the other hand, the fluid from the guts of entrance bees will typically be a tan/gray color (since foragers and guards don't eat pollen).
What If You're Dealing With N. Apis?
Oh, that it were only so simple as dealing with only one nosema, but the previously cited studies suggest that many of us actually may still have N. apis popping up in fall and early spring. To make things even harder, spore counts of N. apis, on a per bee, or per pooled sample basis, are generally only a fraction (about 1/10th, as best I can tell from previous studies) of what we see with N. ceranae. But it also appears that an infection by N. apis at that low level can be as serious as an infection by N. ceranae at a much higher spore count!
Important note: Martin-Hernandez (2011) easily found N. ceranae in samples of either foragers or house bees, whereas she only found N. apis in foragers and drones. So if N. apis is your concern, then you should take entrance samples! N. apis infection may be serious at a much lower spore level!
Seasonality
The other consideration is that you must put any spore count into the context of time of year, the climate that your bees are in, the nutritional status of the colonies, and especially the load of other pathogens. I will discuss these points in the next article.
In cold climates, nosema management may have other considerations. Hedtke (2011) performed a detailed 6-year study of 220 hives in Germany, and (surprisingly) found that "No statistical relation between N. ceranae detection in autumn and the following spring could be demonstrated, meaning that colonies found to be infected in autumn did not necessarily still carry a detectable infection in spring, and colonies which developed a detectable infection over winter had not been detectably infected in autumn." So much for careful sampling!
Recommendations
Heck, I'd be crazy to stick my neck out and give any recommendations! So let's look at what sort of nosema levels are involved in crashing colonies. The CCD colonies analyzed by Cox-Foster (2007) had mean spore counts in the range of tens to hundreds of millions from broodnest samples! Is it really any surprise that those colonies collapsed? The house bees in Higes' (2008) winter-collapsing colonies hit 20M before they went down (field bees hit 50M), but those that collapsed in summer only hit 3M.
But note that in the U.S. survey graph above, that 2M was the average spore count across the U.S. in April and May of this year, yet I'm not hearing of massive colony collapses, despite very poor conditions in many states.
In my own California foothill operation (we get snow during the winter, and move to almonds in February), it is not unusual to see entrance spore counts in May in the millions or tens of millions, but they generally drop during summer, provided that colonies are not stressed by other factors. Entrance counts during summer and fall are typically in the zero to 5M range (25 spores per field of view if you follow the protocol in my previous article--I'll call these FOV counts (Oliver 2008c)). I have not looked at near as many samples of house bees, but counts are generally zero to a fraction of a million, even in colonies running at 10M at the entrance.
I am by no means suggesting that you follow my lead, but I simply no longer worry about high spore counts in spring, as they generally spontaneously drop later in the season, and I haven't experienced winter losses associated with N. ceranae (unless I've intentionally inoculated the hives with viruses). However, I do keep my mite levels down, and feed pollen supplement to maintain good nutrition if necessary. And I monitor nosema levels throughout the year so that I don't get blindsided!
I've never treated for nosema (except in experiments), yet have not experienced colony collapses since 2006. But I'm not saying that you have no reason for concern--I will be writing about a trial in which I did compare survival of treated vs. untreated colonies that had virus issues, and fumagillin appeared to help.
I'd be concerned if counts for house bees got above 5 per FOV at any time, although I know several large commercial beekeepers who routinely ignore such counts with no dire consequences so far. I just checked a number of samples of house bees today (late October), and they ran from zero to 2 spores per FOV, despite there often being counts of 100-200 per FOV of entrance samples this spring.
In some operations where N. ceranae apparently got out of hand, treatment and comb sterilization seemed to help. However, in other operations with sky-high spore counts in spring, lack of treatment did not result in any noticeable problems. Due to these huge discrepancies, it is confoundingly difficult to come up with recommendations. However, the more beekeepers who start tracking spore counts, the more we will learn about appropriate treatment decisions.
If you are in an area with a long, cold winter which keeps the bees confined, you may be dealing with Nosema apis, for which the economic threshold of 1M (5 per FOV) for house bees has been well established.
Practical application: since spore counts for N. apis generally only reach levels about 1/10th of those for N. ceranae, you'd be wise to ask your local university determine which nosema species you're dealing with, since it follows that the economic threshold for treatment for N. apis may be far less than that for N. ceranae.
I will continue this review of N. ceranae in the next issue, including treatments, and its relationship to colony mortality and honey production.
Acknowledgements
Thanks to you, my readers! It just occurred to me that I've recently passed the 5 year mark in writing for ABJ, and it's been one wild ride! If I had any idea what I was getting into, I would probably have chickened out. But your feedback and appreciation keep me going--my motivation is simply the gratification that I get from sharing what I've learned with other beekeepers. Your donations also allow me to perform the sort of quick and dirty research necessary to answer burning questions. I am constantly on the learning curve, and greatly appreciate hearing information that is relevant to better bee management--feel free to contact me (no beginners questions please) randy@randyoliver.com.
As always, Peter Loring Borst has helped me greatly with research. I thank Dr. Mariano Higes for his patience in discussing his research. Dr. Steve Pernal and Ingemar Fries have been gracious with their time. I also thank all the other nosema researchers who have patiently answered my questions.
References
Botias, C, et al (2011) The growing prevalence of Nosema ceranae in honey bees in Spain, an emerging problem for the last decade. Research in Veterinary Science (in press).
Bourgeois, AL (2010) Genetic detection and quantification of Nosema apis and N. ceranae in the honey bee. Journal of Invertebrate Pathology 103: 53-58.
Cali, A and PM Takvorian (1999) Developmental morphology and life cycles of the microsporidia. P. 121. in Wittner, M and LM Weiss, eds. The Microsporidia and Microsporidiosis.,American Society for Microbiology.
Chen, Y.P., et al (2008). Nosema ceranae is a long-present and widespread microsporidian infection of the European honeybee (Apis mellifera) in the United States. J Invertebr Pathol 582 97: 186-188.
Chen, YP, et al (2009) Asymmetrical coexistence of Nosema ceranae and Nosema apis in honey bees. Journal of Invertebrate Pathology 101 (2009) 204-209.
Cox-Foster, DL, et al. (2007) A metagenomic survey of microbes in honey bee colony collapse disorder. Science 318(5848): 283-287.
El-Shemy, A.A.M. and RS Pickard (1989) Nosema apis Zander infection levels in honeybees of known age. J. Apic. Res. 28 (2), 101-106.
Forsgren, E, and I Fries (2010) Comparative virulence of Nosema ceranae and Nosema apis in individual European honey bees. Veterinary Parasitology 170: 212-217.
Fries, I (2010) Nosema ceranae in European honey bees (Apis mellifera). Journal of Invertebrate Pathology 103: S73-S79. https://bienenkunde.uni-hohenheim.de/uploads/media/Nosema_ceranae_in_European_honey_bees__Fries.PDF
Gajda, A (2009) The size of bee sample for investigation of Nosema sp. infection level in honey bee colony. http://www.coloss.org/publications/Nosema-Workshop-Proceedings.pdf
Gisder S, et al. (2010) Five-year cohort study of Nosema spp. in Germany: does climate shape virulence and assertiveness of Nosema ceranae? Appl Environ Microbiol 76: 3032-3038.
Hedtke, K, et al (2011) Evidence for emerging parasites and pathogens influencing outbreaks of stress-related diseases like chalkbrood. Journal of Invertebrate Pathology 108:167-173.
Higes, M (2010) Nosema ceranae in Europe: an emergent type C nosemosis. Apidologie 14(3): 375 - 392.
Higes, M., et al (2005) El sindrome de despoblamiento de las colmenas en Espana. Consideraciones sobre su origen. Vida Apicola 133: 15-21.
Higes M, et al (2006) Nosema ceranae, a new microsporidian parasite in honeybees in Europe, Invertebr Pathol. 92(2):93-5.
Higes, M, et al (2007) Experimental infection of Apis mellifera honeybees with Nosema ceranae (Microsporidia). J Invertebr Pathol. 94(3):211-7
Category: Nosema Summaries and Updates
Tags: N. ceranae, Nosema cereanae, Nosema Cousins, part 14, sick bees | part 14 Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/part-14/ |
Sick Bees - Part 15: An Improved Method for Nosema Sampling
Author's Note
Samples from Within the Hive
Soundbite Science
Infection Rate
So How Did We Get on the Wrong Track?
How to Determine the Colony Infection Rate
So What if I Count the Number of Infected Bees out of 10?
An Assessment of Our Situation
One HUGE Assumption
Validation of the Method
Update
Sequential Sampling
A Neat Little Shortcut
Which Hives to Sample?
What Time of Year?
From Where Should You Take Samples?
Practical Application: Completely Subject to Revision
Adds
Follow Up on the Quick Squash Method
Infection Prevalence
From Where Should We Take Samples?
Next Month
Acknowledgements
References
Sick Bees 15:
An Improved Method For Nosema Sampling
Randy Oliver
ScientificBeekeeping.com
In the previous articles in this series I showed how to use a microscope to view nosema spores and discussed from what part of the hive to take bee samples, and how researchers are interpreting spore counts. But spore counts don't tell us what we really need to know!
Author's Note
I'm hoping that the reader is benefitting from my digestion and summarization of current (and past) nosema research. There is a tremendous amount of information out there (much of it conflicting or confusing), but I'm trying my best to condense and simplify it into terms meaningful to Joe Beekeeper. The frustrating thing, though, is that it is clearly apparent that we still have a great deal more to learn about these parasites before anyone can make definitive recommendations as far as best management practices!
So my apologies in advance for the length and depth of this article. But I'm going someplace different, and feel that it would benefit the reader to follow the history and thought process that led to the conclusions that I reach at the end.
Samples From Within The Hive
Most researchers take bee samples for nosema testing from under the lid, or from an outside comb, since such samples are generally easier to take and presumably more consistent as far as bee age structure. The expectation also is that such a sample would be most representative of the colony infection as a whole, as opposed to samples from the entrance, in which spore counts are often sky high, or samples of nurse bees, in which counts are generally minimal. The assumption, of course, is that a "peripheral" sample would contain mostly mid-aged and older bees.
In early November, I had the pleasure of being visited by Dr. Dewey Caron, so I used the opportunity to put the above hypothesis to the test. We had experienced rainy weather and cold nights the two previous days, so the bees had not foraged nor broken cluster during that time. We went out to the bee yard and took samples of bees from the outermost portion of the cluster, from honey frames in the upper hive body (the bees were in fairly tight cluster, so I doubt that there had been much bee movement in the past two days).
As I illustrated in Figure 6 of my previous article, it is a normally a relatively simple matter to determine the "age" of the bees in a sample by seeing how much pollen is in their guts--it is generally assumed that only young bees (nurses) consume pollen. So we froze the bees and then spread them on a grid and crushed them to squash out their gut contents. As you can see in Figure 1, to our great surprise, the vast majority of bees in the samples from the three hives that we tested had guts full of pollen!
Figure 1. A sample of crushed bees from the periphery of the cluster (on an upper honey comb) after two days of confinement by cold weather in early November. Note that every single bee's gut was full of pollen (the orange stains), indicating that they were likely nurse bees, rather than older bees, and thus would be less likely to be infected by nosema.
We confirmed by microscopy that the orange coloration of the gut contents was indeed due to pollen grains. I have done similar squashes during summer, and again found substantial proportions of bees throughout the hive to have pollen in their guts, as opposed to bees in entrance samples, which rarely contain appreciable pollen. In the sample illustrated above, the extremely high proportion (100%) of bees containing pollen could possibly be due to the population turnover in November, when the forager bees fly off to die, leaving only young bees in the hive to winter (Mattila and Otis 2007). I have not yet confirmed this.
Practical application: So I'm not clear at this point whether these pollen-filled bees are chronologically old bees or not!
Another interesting finding that we made was that in a 50-bee subsample of one of the above samples, the spore count (which appeared to be N. ceranae), was about 100 spores in a field of view, indicating an infection level of about 20M. This high count in ostensibly young bees caught my attention, so I squashed individual bees one at a time--in the first six, only one of them contained an appreciable number of spores. Apparently, in the 50-bee sample, a few highly-infected bees skewed the spore count to that alarming level (Fig. 2). My point is that you should not allow any individual spore count to scare you!
Figure 2. One highly-infected bee can really skew a spore count! This photo, taken at 400x, shows thousands of nosema spores packed into the Malpighian tubules (bee "kidneys"), which are running at an angle crossways. The treelike structure is a tracheal (breathing) tube. A bee infected to this degree could contain 500 million nosema spores!
Practical application: I would normally have been alarmed by a mean spore count of 20M in a sample of fifty young bees, but upon closer inspection, most of the bees in the subsample of 6 bees were not infected to any degree.
I have written extensively about varroa. Varroa is easy to monitor, and if one makes an effort to understand its well-documented biology and population dynamics, then it is a relatively straightforward matter to make wise and effective management decisions for controlling its degree of damage to bee colonies. Unfortunately, we are nowhere near that state of confidence with N. ceranae. Worldwide data from actual field studies are so conflicting that no one can really make meaningful recommendations as to what level of infection, based upon simple spore counts, is economically tolerable. Add to that, there are potential down sides to treatment--first, fumagillin's expensive, it may have negative side effects upon bee health, may contaminate honey (and is not approved in many countries), and many beekeepers simply are adverse to adding one more danged treatment to their hives (Figure 3). I will discuss the above concerns, as well as the potential consequences (or lack thereof) of untreated nosema infection in later articles.
Practical application: I seriously question whether spore counts can be translated into meaningful treatment thresholds!
Figure 3. Let me warn you, that if you actually start sampling for nosema, it will give you much more to worry about! When we find high spore counts here at WishWeKnewWhatWeWereDoing Apiaries, my sons (Eric, on left, and Ian) and I worry about filling our almond pollination contracts.
Until recently, I pretty much blew off Nosema ceranae as not being much of an issue in my operation, despite finding spore counts in the millions or tens of millions, especially in spring. Our colonies have generally fared well, and I haven't noticed any strong correlation between colony strength and nosema counts. However, I'm a bit uneasy since spore counts have seemed to climb each year, and are higher this season than ever.
What most troubles me, though, is recent evidence that nosema is more of a problem in colony health and mortality than I have previously suspected--I will be covering this in subsequent articles in this series (I often am forced to choose which subject to cover first). So I'm in the same boat with the rest of you who are wondering how best to diagnose the degree of nosema infection in your operations, and whether treatment would be worthwhile.
Soundbite Science
We currently live in an age of information overload, largely due to the internet, with snippets of knowledge thrown at us faster then we can put them all together. This is a mixed blessing with scientific research, as sometimes quality is sacrificed in the race to be first to report some finding. Due to competition for limited funding, we are seeing a lot of "soundbite science" being published by grad students and post docs fighting to make a name for themselves, or faculty needing to "publish or perish."
But back in the day, the government subsidized the kind of painstaking, grinding, and detailed agricultural research seldom seen today. To see an example, download Dr. G.F. White's 1919 exhaustive 9-year study on nosema (Google Books "bulletin 780 nosema") undertaken after he discovered its presence in the U.S. --these guys with a government mandate were thorough! In this age of budget cutting and taxpayer support for giant agribusiness (less than 2% of USDA spending goes toward research these days), there is a strong case to be made for we beekeepers to encourage government funding of bee research.
Dr. White concluded:
"As a rule, colonies which in the spring of the year show less than 10 per cent of Nosema-infected bees gain in strength and the losses are not detected. This is often true also in cases where the infection is somewhat greater than 10 per cent. When the number of infected bees approaches 50 per cent the colonies become noticeably weakened and in many instances death takes place. When more than 50 per cent are infected they become weakened and usually die as a result of the infection. Generally speaking, therefore, it may be said that when a colony contains less than 10 per cent of Nosema-infected bees the prognosis is excellent; that when it contains more than 10 and less than 50 per cent the prognosis is unfavorable; and that when the number of Nosema-infected bees present approaches 100 per cent the prognosis is especially grave."
Pay attention: This prognosis is remarkably similar to that of Higes (2008)--that the tip point for colony health appears to occur when more than about 40% of the bees in the hive become infected (a 40% infection rate). The practical application is that spore counts may not be the best way to assess the impact of nosema infection upon colony health--it may be more important to determine the relative proportion of infected bees to healthy bees.
I will continue to return to Dr. White's findings in this series, as well as those by Dr. Mariano Higes and his collaborators in Spain, in which, by the way, there are about the same number of hives as in the entire contiguous U.S., in approximately 1/15th of the land area! What strikes me is the similarity in their conclusions, nearly a century apart, when they discovered, and then thoroughly investigated, nosema epidemiology and pathology in their respective countries!
Infection Rate
The proportion of infected bees in a hive is called the infection rate, and expressed as a percentage--if a quarter of the bees are infected, that would be a 25% infection rate. Remember, a colony of bees is a superorganism, with each individual bee somewhat akin to a single cell of your own body (of which millions die every day). A colony can easily handle the loss of a certain percentage of sick bees every day, especially if those bees are aged, and nosema infection is generally worse in the oldest bees (since aging allows more cycles of parasite reproduction within the bee).
Dr. White suggested that an average of about 10-15% infected bees in a hive is "normal." The rate in sick hives could go up to 100%! He found that the infection rate would often go to 70% in experimentally-inoculated hives.
So let's digest this. If only, say, 5 percent of the bees in a hive were actually infected (and only seriously infected during their last days of foraging life), the overall nosema infection would have little impact upon the colony, as they would be quickly replaced by the 1500-2000 new bees emerging each day. However, if 50 percent of the bees were infected, then that is entirely another matter! During the spring and summer, their shortened lifespan could seriously affect the population dynamics of the hive, reining back its normal population growth and ability to forage. And during the winter, when bees must live to a ripe old age in order for the cluster to survive until spring, a high nosema infection rate could lead to colony collapse. I will return to the details of this subject in an upcoming article.
Practical application: Nosema can be a serious problem during either winter or spring, should a high proportion of bees in the hive become infected. The infection rate is a more accurate measure of the seriousness of the infection than is a mean spore count, since a high spore count may merely reflect that one or a few highly-infected bees happened to be in the sample.
So why have we been focusing on spore counts, rather than infection rate? I just got off the phone with a large commercial queen producer who has closely tracked N. ceranae levels (and spent a large amount of money on treatments). He has nearly given up on looking at spore counts, since they simply did not appear to correlate to any significant degree with colony health and production. Ditto for my operation, and for much of the worldwide research. I feel that it is time for us to move beyond spore counts!
I'm not the only one who feels this way. Dr. Higes team's recently entreated: "There is an urgent need ... to decide on the reliability of standard methods to establish the levels of infection, a measure that will be necessary to standardize procedures to accurately, reliably and meaningfully quantify the degree of Nosema infection in honey bees" (Meana 2010). It's time for a paradigm shift of moving away from sample means, and to go back to looking at the actual percentage of infected individual bees.
So How Did We Get On The Wrong Track?
Good question! I've always wondered how the 10-bee sample size figure ever got engraved in stone. It appears that it evolved from a statement by Dr. White himself, who wrote that "Ten bees from a colony constitute a satisfactory sample as a rule."
So 10 bees became the typical sample size from the early 1900's until we found out that we had N. ceranae. At that point, I was misled by "discovery sampling" statistics (Oliver 2008), since I thought that I needed to "discover" whether I had nosema in my operation, and thus recommended taking samples of at least 50 bees. This number (or even 100) is commonly used by researchers these days, since it also helps to minimize the influence of any single highly-infected bee upon the mean spore count.
Unfortunately, many of us became seduced by the attractiveness of thinking that the number of spores counted in a hemacytometer actually reflected the seriousness of an N. ceranae infection in a hive. Fifty-bee samples are good for discovery, but in truth, once you've discovered that you have N. ceranae in your operation, they actually can be misleading. Here's the funny thing: Dr. White's 10-bee samples are actually a better assessment of the seriousness of a nosema infection! But when he recommended 10-bee samples, he wasn't talking about counting spores! What he actually recommended was:
"When a diagnosis of the disease is being made in practical apiculture, therefore, considerable caution should be observed. A colony showing only a small percentage of Nosema-infected bees and not other evidence of the disease is practically healthy. In reporting the presence of infection it would seem well to indicate in some way the amount of infection present. The percentage of infected bees among those examined might be given."
This is a major point! Nosema infection at the colony level is not about spore counts--rather, it is about the percentage of the bees that are infected!
So why the heck did most everyone go from determining the infection rate to counting spores? Well, several researchers found that, at least with Nosema apis, spore counts of a 10-bee sample roughly correlated with infection rate. Then some Canadian scientists (Fingler 1982) found that a 25-bee sample was an even more "reliable method of assessing the degree to which colonies are infected by nosema." But again, those researchers clearly understood that spore counts were merely crude proxies for the actual rate of infection. I doubt that beekeepers (or even many subsequent researchers) ever fully grasped that message.
So is a 10-bee sample enough? Look at it this way: since a single nosema-infected bee typically contains more than 10M spores (Forsgren 2010; Smart 2011), then having even one single infected bee in a 10-bee sample (indicating > than a 10% infection rate) would put the mean spore count above 1M--the typical rule of thumb for treatment. So what's the chance of hitting at least one infected bee in a 10-bee sample.
In order to answer this question, we need to use probability theory, which was ironically, initially developed to help gamblers make better decisions in games of chance. As an aside, doesn't it seem funny that the ABF national convention is going to be in Las Vegas? I mean, commercial beekeepers already live their lives gambling their life savings on the weather, the price of honey, varroa treatments, and honey flows, and are going to be in Las Vegas just before the big roulette wheel stops spinning and tells them whether they'll hit the jackpot in the almonds the next month!
But I digress. Probability theory can be used to predict, for example, the chance of being dealt two aces in a hand of five cards (4/52 x 3/51 = 1/221, or less than half of one percent probability). Bee samples can be looked in a similar manner, since when you are squashing bee guts, nosema infections generally show as either positive (tons of spores) or negative (zero to a very few spores)--sort of a sick/not sick litmus test. So I did some homework with probability tables, and was able to answer my question about hitting 1 infected bee out of 10 (Figure 4).
Figure 4. In this graph the bottom scale is the actual infection rate of the colony. The blue line plots the chance of hitting at least one infected bee in a sample of 10 bees. The red line indicates "negatives," in which you would not find a single infected bee. You can see that it's almost impossible to miss getting at least one infected bee in a 10-bee sample if the colony infection rate is over 30%.
So the 1M spore rule of thumb is very conservative, meaning that you certainly wouldn't miss a nosema infection, but also means that you'd often wind up feeding fumagillin to apiaries that in actuality were dealing just fine with relatively "safe" infection rates. In the case of N. ceranae, in which individual bee spore counts may exceed 100M, having even a single infected bee would result in a mean spore count of 10M, which might scare the pants off you, despite the substantial likelihood that the colony was only infected at a minimal rate!
A recent study by Traver and Fell (2011a) supports the above interpretation--they found that colonies that tested low for nosema DNA exhibited zero spores in 10-bee samples about a third of the time, whereas samples from colonies with "high-level" infections seldom were free of spores. So it appears to me that the good old 10-bee spore count works fairly well as a crude but conservative proxy for the actual infection rate, with spore counts stepping up sharply with each additional infected bee in the sample. However, it should not be interpreted as any sort of linear measure of the degree of infection. It worked, but it likely led to too many unnecessary treatments.
The problem with spore counts: spore counts from a pooled homogenate of many bees are more or less a measure of the reproductive success of nosema in a relatively few bees. The infection rate (percentage of bees actually infected) is a much better measure of the actual impact of nosema upon colony health.
How To Determine The Colony Infection Rate
OK, I hope that I've convinced you now that it's time to move away from counting spores--but that certainly doesn't mean that you should throw away that shiny new microscope that I earlier convinced you to buy!
You may have wondered why, when I was squashing bees in my kitchen with Dr. Caron, that I stopped after crushing only six bees. Well, in truth, squashing individual bees is time consuming, and my gut feeling was that I would have hit more than one infected bee in the sample should the actual infection rate have been high.
Of course, my readers should know that I'm not about publishing "gut feelings." So, being the curious sort of guy, I bit the bullet and plowed into an investigation to see whether I could come up with some sort of shortcut for determining a colony's infection rate without having to individually squash a whole bunch of bees. I spent some serious time working out the math (much to my long-suffering wife's dismay, such as when she groggily walked into the kitchen first thing in the morning, and was immediately barraged by me excitedly showing her the results of some probability calculations that I've been working on since before dawn).
My personal issues aside, what I found was that the problem with extrapolating from samples is that you want to avoid false negatives (missing a serious infection; easy to do with samples of only a few bees), while at the same time not misdiagnosing false positives (erroneously concluding that a healthy hive is seriously infected--which is a problem with the mean (average) spore count from of a pooled bee sample).
Scientists just love hard, accurate figures out to the third decimal place, with 99% confidence levels. But in reality, there is rarely that kind of certainty when you're dealing with any data derived from bee samples! And there's a lot of elbow room when making management decisions. So first, let's perform a reality check. Suppose that you have a colony that is infected at the 40% rate, and that the infected bees are evenly distributed in the hive. And then suppose that you take a sample of 100 bees from that colony.
You'd expect that the sample would contain 40 infected bees (40 per 100 = 40%). And the average sample would indeed contain 40 bees. But no single sample is an average! Any single sample has only an 8% chance of containing exactly 40 infected bees!
That's fine, you say--all that I really care about is whether that sample contains at least 40 bees. The chance of that happening with a single sample of 100 bees is still only 54%! You would still get 46% false negatives. A 46% chance at losing a bet isn't bad if you're betting five bucks in Las Vegas. But it's pretty poor odds if you're risking your bee operation on it!
Motivational message: For the arithmetically-challenged among you whose eyes are starting to glaze over because I'm using three-syllable words and talking about math, please hang in there!
So What If I Count The Number Of Infected Bees Out Of 10?
You'd sure think that this would make sense! After all, Dr. White recommended this method. But surprisingly, it's not that accurate. Let's look at the probabilities. Suppose that a colony is actually infected at the 40% rate, and that you took a perfectly representative sample of 10 bees. You'd still have only a 25% chance of finding exactly 4 infected bees (but a 67% chance of hitting between 3 and 5 bees). So counting the number of infected bees in a 10-bee sample will give you only a very rough assessment of the actual infection rate.
But here's a big surprise-counter intuitively, as the sample size goes down, your chances of missing that infection actually go down too! For that same 40% infected colony, here are the probabilities of underestimating the infection rate (Table 1):
Sample Size Probability of getting fewer than 40% infected bees in the sample
100 46% (46 times out of 100)
10 38%
5 34%
Table 1. Probabilities of underestimating the infection rate of a colony in which 40 out of 100 bees were actually infected, by sample size (number of bees in the sample), assuming a perfectly representative sample.
I'm hoping that you're catching my drift here--that we may be able to streamline the process of estimating the degree to which a colony is infected, by utilizing 5-bee samples.
An Assessment Of Our Situation
So let's review where we stand with regard to nosema sampling methods and interpretation:
We want to avoid dangerous false negatives, since they might lead you to not treat a truly sick apiary.
However, you (and your bees) could live with false positives, since the worst that you'd do is to give unnecessary treatments.
But you're still a penny pinching beekeeper who doesn't want to waste money (or you don't want to use treatments for other reasons).
Sending a sample of 10 bees to the lab for a spore count has an unacceptably high rate of false positives--at least two-thirds of the time.
Spore counts of even 25-bee samples of either house or forager bees are still unreliable predictors of colony health (Meana 2010).
And even individually squashing 10 bees one at a time will underestimate a serious 40% infection rate over a third of the time!
So what to do? I'm not telling you all this merely to frustrate you--I and my sons live off the income from our bees, so I've got a vested interest in finding a way out of this quandary! Researchers worldwide are coming to the conclusion that simple spore counts generally have little correlation with observed colony health status. What you really need to know is one of two things--are your bees in the "safe" zone (under 20% infected) or in the danger zone (over 40% infected). And what you don't want to do is to spend all day squashing bees one at a time and viewing their guts under a scope. Are we all agreed on the above?
So I got out the probability tables, a pocket calculator, found a handy online binomial distribution calculator (http://stattrek.com/Tables/Binomial.aspx), and started playing with the numbers. I found that for our purposes of differentiating between a benign nosema prevalence and serious infection,that the sweet spot for sample sizes lies in the range of 5-10 bees (sort of a Goldilocks "not too many, but not too few"). See for yourself (Fig. 5):
Figure 5. This graph is for 5-bee samples. Compare identical colored markers between the left column and the right column--the greater the vertical spread, the better the discrimination between infection rates. Note that at "benign" infection rates (green and blue dots) you'd nearly always hit either zero or 1 infected bee, but rarely 2 or more. At dangerous infection rates (red markers) the reverse holds true--you'd rarely hit zero infected bees (not shown), and seldom even 1, but nearly always at least 2 positive bees if the colony infection rate exceeded 60%. I will post this article to ScientificBeekeeping.com for handy reference.
One HUGE Assumption
All of these probabilities are contingent upon your taking a representative sample that reflects the overall infection rate of the hive. Would this be the case in real life? Would 5-bee samples give consistent results? I didn't know, so l decided to put it to the test the day before I sent this article off to press!
Validation Of The Method
The "boys" and I were treating colonies with an oxalic acid dribble in November (bees were still flying most days), so I took samples of bees from the weakest hives in each yard, and later processed subsamples of 5 bees at a time. Here are the results (Table 2):
Colony number
Number of nosema-positive bees per 5-bee sample, and (below) per 10-bee sample (by subsequent pairs)
Overall infection rate of sampled bees
Notes
1
0/5, 0/5
0/10
0/10 =
0%
Appeared to be free of nosema.
2
0/5, 0/5
0/10
0/10 =
0%
Appeared to be free of nosema.
3
2/5, 1/5, 2/5, 1/5, 2/5, 4/5, 0/5
3/10, 3/10, 3/10, 3/10, 6/10, 4/10
12/35 =
34%
Only 1 zero in the 5-bee samples. Note the consistency of the 10-bee samples.
4
0/5, 0/5
0/10
0/10 =
0%
Appeared to be free of nosema.
5
3/5, 2/5, 1/5, 3/5, 1/5, 1/5
5/10, 3/10, 4/10, 4/10, 2/10
11/30 =
37%
No zeroes. Only the last pair of 1/5's would have missed the infection.
6
4/5, 0/5, 3/5, 5/5, 2/5
4/10, 3/10,8/10,7/10
14/25 =
56%
The 10-bee samples certainly picked up the infection! This colony had the most intensely infected bees, plus a serious amoeba infection.
7
0/5, 0/5
0/10
0/10 =
0%
Appeared to be free of nosema.
8
0/5, 1/5, 0/5, 0/5, 1/5
1/10, 1/10/ 0/10, 1/10
2/25 =
<1%
Very consistent results
9
3/5, 0/5, 3/5, 1/5, 0/5
3/10, 3/10, 4/10, 1/10
7/25 =
28%
2 bees were only slightly infected. One 10-bee sample underestimated.
10
2/5, 2/5, 3/5, 0/5, 2/5
4/10, 5/10, 3/10, 2/10
9/25 =
36%
2 bees were only slightly infected. The last 2/10 missed, but the 2/5 would have flagged the infection.
Table 2. Results of bee samples from 10 weak colonies in the fall. I sub sampled each sample, 5 bees at a time, with each bee being individually squashed (total of 205 bees), and rated each bee as to whether it was positive for nosema spores or not. I stopped counting after two groups of 5 if I hadn't yet detected any nosema. Out of 31 pairs of 5-bee samples (the lower figures in column 2), in only 2 cases out of 31 would I have underestimated the actual colony infection rate (by not hitting either 2 positive bees in 5, or 3 in 10). Note how consistently the paired 10-bee samples reflected the overall infection rate!
Practical application: I found the above reality check instructive, to say the least! In fact, I could say that I learned more about the degree of nosema infection in my operation in three hours of bee squashing than I'd learned in the last four years of counting spores! I doubt that I will ever do another spore count.
I love this method! For one, I learned that nosema was only associated with half of my weakest hives, so I can now sleep a bit better. On the other hand, half of those weak hives did have high nosema levels, so I need to address this (spot treatment?). I'm now eager to go sample some strong colonies. What is also apparent is that the method worked remarkably well! It's not perfect, but it appears that I'd rarely miss an infection if I processed two samples of 5 bees for each tested hive. And the method readily picked out the really sick hive! Clearly, this is only a preliminary test of the procedure, and needs to be repeated with a lot more hives, but the apparent accuracy of the method is very encouraging to me.
The only remaining problem is that most beekeepers will choke at the thought of how much time it would take them to squash and microscopically view 10 bees out of each sampled hive. And that leads us to:
Sequential Sampling
Think of this Quick Squash method as similar to doing an alcohol wash of 300 bees. If I only see 1 mite, no worries for a while, as mite populations take about a month to double. If I see more than 6 mites, I treat. In between, I make a note to check back soon. It's a similar case for nosema sampling (although it may take less time for the infection rate to double).
I'm immensely grateful to Dr. Jose Villa of the Baton Rouge Bee Lab for bringing to my attention that I was reinventing the wheel--this sort of decision making process based upon small sample sizes already has a fancy name: it's called "sequential sampling," and was develped for quality control inspections during World War II. Furthermore, Dr. Villa dug into the library and forwarded me existing "Decision Tables" for tracheal mite sampling produced by Tomasko (1993) and Frazier (2000). They exactly fit the bill for what I was crudely trying to work out!
Sequential sampling is all about the tradeoff between tedium (the number of bees that you need to squash and view) and confidence (the error rate which you are willing to accept). And it appears that for our purposes I estimated the minimum number of bees to sample right on the nose!
So here's the gist (backed by some complex math) for the following parameters. Given that you want to decide whether about 10% or fewer of the bees in the population are infected (the "tolerable" level), or if the rate is above the 30-40% range ("intolerable"), and are willing to allow an error rate of 20% for overestimating ("false positives"), but only a 10% limit for underestimating a serious infection (I'm intentionally avoiding most of the associated mathematical jargon). The cutoffs are:
Practical application: it appears that in order to make a decision whether to treat or not, that a couple of 5-bee samples should be adequate, interpreted as follows:
0 positive bees out of 5, or no more than 1 positive out of 10 indicates < 10% infection
3 positive bees out of 5, or at least 4 positives out of 10 indicates > 30% infection
Any number of positive bees lying between these cutoffs (e.g., 2 bees out of 5, or 3 out of 10) suggest an infection level that lies in the gray zone, but I doubt that going beyond a 10-bee sample is worth the effort--I'd just move on to the next sample.
So I've got us down to 10-bee samples. But even so, I must advise you that nosema infection appears to exist in "pockets" of bees in the hive, so any single small sample is inadequate for making an apiary-level decision (Botias 2011). It's obvious that what is needed is a quick method for processing samples of 10 bees at a time!
Acknowledgements
I wish to thank my wife Stephanie for her patience, and helpful comments on my manuscripts. As always Peter Borst helped with the research for this article. Thanks to Dr. Jerry Bromenshenk for his helpful suggestions. And a big thanks to Drs. Mariano Higes, Aranzazu Meana, and Raquel Martin-Hernandez for their diligent work on nosema! For financial support toward this research, I've very appreciative of Joe Traynor, Heitkam's Honey Bees, Jester Bee Company, the Virginia State Beekeepers Assoc, and individual beekeepers Paul Limbach, Chris Moore, and Keith Jarret.
References
Botias, C, et al (2011) Critical aspects of the Nosema spp. diagnostic sampling in honey bee (Apis mellifera L.) colonies. Parasitology Research (in press).
Fingler BG, WT Nash, and TI Szabo (1982) A comparison of two techniques for the measurement of nosema disease in honey bee colonies wintered in Alberta, Canada. ABJ 122(5):369-371.
Forsgren, E, and I Fries (2010) Comparative virulence of Nosema ceranae and Nosema apis in individual European honey bees. Veterinary Parasitology 170: 212-217.
Frazier, MT, et al (2000) A sequential sampling scheme for detecting infestation levels of tracheal mites (Heterostigmata: Tarsonemidae) in honey bee (Hymenoptera: Apidae) colonies. Journal of Economic Entomology 93(3):551-558.
Higes, M, et al (2008) How natural infection by Nosema ceranae causes honeybee colony collapse. Environ Microbiol 10: 2659-2669.
Mattila HR, and GW Otis (2007) Dwindling pollen resources trigger the transition to broodless populations of long-lived honeybees each autumn. Ecol Entomol 32:496-505.
Meana, A, et al (2010) The reliability of spore counts to diagnose Nosema ceranae infections in honey bees. Journal of Apicultural Research and Bee World 49(2): 212-214.
Oliver, R (2008) The Nosema Twins Part 3: Sampling. ABJ 148(2): 149-154. https://scientificbeekeeping.com/the-nosema-twins-part-3-sampling/
Porrini, MP, et al (2011) Nosema ceranae development in Apis mellifera: influence of diet and infective inoculum. Journal of Apicultural Research 50(1): 35-41
Smart, MD and WS Sheppard (2011, in press) Nosema ceranae in age cohorts of the western honey bee (Apis mellifera). J. Invertebr. Pathol. doi:10.1016/j.jip.2011.09.009
Tomasko, M. Finley, J. Harkness, W. Rajotte, E. 1993. A sequential sampling scheme for detecting the presence of tracheal mite (Acarapis woodi) infestations in honey bee (Apis mellifera L.) colonies. Penn. State College of Agricultural Sciences, Agricultural Experiment Station Bulletin 871.
Traver, B., and RD Fell (2011a) Prevalence and infection intensity of Nosema in honey bee (Apis mellifera L.) colonies in Virginia. J Invertebr Pathol 107 (1):43-49.
Traver, BE MR Williams, and RD Fell (2011b; in press) Comparison of within hive sampling and seasonal activity of Nosema ceranae in honey bee colonies. Journal of Invertebrate Pathology.
White, GF (1919) Nosema-Disease. USDA Bulletin No. 780.
Category: Nosema Summaries and Updates, Sampling
Tags: N. ceranae, Nosema cereanae, sampling | sampling Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/sampling-2/ |
A Comparative Trial of the Pollen Subs: Part 4-Why did some Subs Outperform Others
A COMPARATIVE TRIAL OF THE POLLEN SUBS Part 4: Why did some Subs Outperform Others? Beekeeper-Funded Research Randy Oliver ScientificBeekeeping.com Contents Back to my 2020 california trial Have we been focusing on the wrong suspects? Protein in Animal feed formulations Mixing of protein sources Crude Protein and Amino Acids EAAs as percent of crude [...]
Read More | Topics Archives - Page 2 of 4 - Scientific Beekeeping | https://scientificbeekeeping.com/topics/page/2/ |
The Suck-a-Bee
The Suck-a-Bee Randy Oliver ScientificBeekeeping.com First Published in ABJ in Aug. 2008 This sleek sucker makes nosema sampling a breeze! And you can build it yourself for about $40. Randy Oliver [ ** Suck-a-Bee update: Dirt Devil makes a nearly identical, but more expensive, vac that operates with a 15v battery and has greater [...]
Read More | Nosema ceranae Archives - Page 3 of 3 - Scientific Beekeeping | https://scientificbeekeeping.com/nosema-ceranae/page/3/ |
Sick Bees - Part 16: The "Quick Squash" Method for Determining Nosema Prevalence in a Colony
Infection Prevalence
Sequential Sampling
A Neat Little Shortcut
Validation
Summary (completely subject to revision)
More Details
Next Month
Acknowledgements
References
2019 Quick Nosema Prevalence Assessment Method
First published in ABJ February 2012
Updated March 13, 2019
Randy Oliver
Since the discovery of Nosema ceranae, I and many other beekeepers and researchers have been frustrated by the tedium and apparent futility of counting nosema spores, since many of us haven't seen any meaningful relationship between spore counts and colony health or production. I strongly suspect that the issue is not that N. ceranae does not cause problems, but rather that our methodology for assessing the degree of infection has been flawed.
The quickest way that I've found to determine the degree of nosema infection in a hive is to do a 2-step sampling.
Step 1: open the hive and take a sample of about 50 workers from an outer frame, or from under the hive cover. These bees can be salvaged from an alcohol wash for varroa. Set at least 15 bees aside for the time being, and use the rest for the next step.
I now typically use only 10 bees. This is based upon the thorough research on Nosema apis by GF White in the early 1900s. What he found was that individually sampling 10 bees in order to determine the prevalence of nosema infection in the house bees gave the best indication of its biological relevance-a finding later suggested by Cameron Jack in Colony Level Prevalence and Intensity of Nosema ceranae in Honey Bees (Apis mellifera L.).
Be sure to read https://scientificbeekeeping.com/the-seasonality-of-nosema-ceranae/
Step 2: place at least 25 of the bees in a ziplock sandwich bag, and roll a round jar over them to crush their guts thoroughly. Then add about 3 mL of water for every 10 bees in the sample, and massage the bag in your fingers until you've homogenized all the gut contents into the water, creating a semi-opaque suspension (not too clear, not too thick). For details on this step, see https://scientificbeekeeping.com/sick-bees-part-13-simple-microscopy-of-nosema/
Step 3: immediately place a drop of the suspension on a slide, drop on a cover slip, and view under the scope. Scan a few fields of view for nosema spores. If you don't see any (or only one or two), that indicates that the infection prevalence of that sample of bees was zero-end of assessment.
On the other hand, if you see spores in the sample, then perform 10 individual bee gut squashes from the remaining bees in the original sample in order to determine the biological relevance of the infection prevalence in the colony-details below.
Infection Prevalence
The current "standard" method for monitoring nosema "level" in hives is to determine the mean spore count per bee in an aggregate sample (of typically 10-100 bees). The method is relatively quick and gives the sort of quantifiable numbers that scientists love. Unfortunately, as noted by Meana (2010), "the spore count is not directly related to the parasite burden and health status of whole colonies naturally infected by N. ceranae under field conditions."
Spore counts certainly have their uses, such as quantifying the progress of nosema infection in individual bees in cage trials by researchers. They are also appropriate as a method for "discovery sampling." For example, one can "discover" whether nosema is present to any extent in an apiary by taking an aggregate sample of say ten bees from the entrance of every hive and determining the mean spore count. If the count is less than 1M (1 million spores per bee), then nosema is likely not a problem in the sampled hives.
The point that I'm trying to make about sampling for nosema is that we are well beyond the "discovery" phase. Rennich (2011) found N. ceranae in at least half of all random bee samples taken in the U.S. during winter and spring.
So instead of "discovery" sampling, what we need to do is to shift to the most meaningful way to measure the potential impact of nosema upon colony health--the proportion of infected bees. Of the various terms used to describe this measure--"proportion of infected bees in a sample," "percent infected," or "infection rate"- I prefer the term used by epidemiologists: "prevalence."
Practical application: I henceforth plan to use the term "prevalence" as the measure of the proportion of bees infected by nosema. For example, if 2 bees out of 10 were infected, that would be a prevalence of 20%.
There is a strong case to be made for shifting our assessment of nosema infection from "intensity" (as measured by spore counts) to "prevalence" (the percent of bees actually infected). The only problem with determining prevalence is that most of us choke at the thought of having to inspect jillions of bees one at a time. Luckily, there are practical shortcuts:
Sequential Sampling
In my last article, I proposed that even a small sample of bees might be adequate for making management decisions. I'm immensely grateful to Dr. Jose Villa of the Baton Rouge Bee Lab for bringing to my attention that I was reinventing the wheel--this sort of decision making process, based upon small sample sizes, already has a fancy name: it's called "sequential sampling," and was develped as a time-saving method for quality control inspections during World War II. Furthermore, Dr. Villa dug into the library and forwarded me existing "Decision Tables" for tracheal mite sampling produced by Tomasko (1993).
Dr. Maryann Frazier (2000), following up on Tomasko's work, discussed the situation regarding the assement of tracheal mite prevalence as opposed to "parasite load" (analagous to spore counts). It is remarkable in that it almost exactly mirrors today's situation with nosema! And in her paper she validated the accuracy of sequential sampling.
Sequential sampling is all about the tradeoff between tedium (the number of bees that you need to squash and view) and confidence (the error rate which you are willing to accept). And it appears that for our purposes, I estimated the minimum number of bees to sample right on the nose!
So let's set some arbitrary parameters for our decision making:
An infection prevalence of 10% is "tolerable."
A prevalence of 30-40% is "intolerable."
We'll accept a 20% error rate for overestimating the prevalence.
But we won't accept an error rate above 10% for underestimating the prevalence.
We'll use the above parameters to set our treatment thresholds--below 10% prevalence, don't treat; above 30%, treat. The math gets complex, but here's the gist of the outcome:
Practical application: it appears that in order to make a decision whether to treat or not, that a couple of 5-bee samples should be adequate, interpreted as follows:
0 positive bees out of 5, or no more than 1 positive out of 10 indicates < 10% infection
3 positive bees out of 5, or at least 4 positives out of 10 indicates > 30% infection
Any number of positive bees lying between these cutoffs (e.g., 2 bees out of 5, or 3 out of 10) is not enough to make a firm decision, but suggests an infection level that lies in the gray zone. But I doubt that going beyond a 10-bee sample is worth the effort--I'd just move on to the next sample.
With true sequential sampling, you'd keep sampling until you hit a critical number of positive or negative bees in order to make a treatment decision. However, my limited experience suggests that we hit a point of diminishing returns after viewing 10 bees.
Update July 5, 2012 Beekeeper Ruary Rudd (ruaryrudd@iol.ie) has developed a great Excel spreadsheet for sequential sampling. You can write him for a copy-thanks Ruary!
So I've got us down to sampling a maximum of 10-bees. But even so, I must advise you that nosema infection appears to exist in "pockets" of bees in the hive, so any single small sample is inadequate for making an apiary-level decision (Botias 2011). Therefore, it's necessary to process a number of samples. What's been holding us back from determining actual nosema prevalence is the lack of a quick method for processing a number of samples of 10 bees!
Nosema apis becomes a serious problem if about a third of the bees in a hive become infected. It appears that Nosema ceranae may be a problem at even a lower prevalence.
A Neat Little Shortcut
Since I really wanted to find a quicker way to prepare and view the 200 bees for the validation table in the previous article, I racked my brain trying to figure out a technique for speeding things up, and finally hit upon a relatively simple procedure (Figures 1,2, and 3). I've now got over 400 individual gut squashes under my belt, and am pretty excited about the method! This solution allows me to process bees at an overall turnaround rate of less than five minutes per sample of 10 bees!
Figure 1. This photo shows the necessary equipment for a Quick Squash--5 bees, a plain microscope slide, 5 custom-made thin plastic cover slips, a table knife, and a paper towel.
The size of the cover slips is critical--they must be narrow enough not to touch at the edges, in order to keep the individual gut slurries from mixing. The easiest solution is to cut off-the-shelf plastic microscopy cover slips in half with scissors. You can then just discard them after use (cost about 20C//10-bee sample), or wash and reuse (use your mite shaker jar).
Update Feb 2019: I prefer to recycle rather than discard. But when I looked at costs, getting a large order of #1 thickness glass cover slips works out to only about a penny a slip. At Amazon: Karter Scientific 211Z2 Standard Microscope Cover Slip, #1 Thick, 22x22mm, 200pk (Case of 2000).
Be sure to order #1 thickness cover slips, since thicker cover slips won't allow you to focus upon the spores.
The other thing is that you don't need to make custom cover slips at all. Three standard glass cover slips will fit across a slide, and can be discarded after use if you don't want to wash them (although they wash easily in warm water with a tiny bit of dishwashing detergent).
But if you don't have plastic cover slips at hand, don't despair! You can make cover slips out of clear plastic scrap around the home--but only some plastics will work; I've experimented with several. Clear plastic transparency sheets unfortunately refract light in such a way that they make nosema spores look like little rectangles, so they don't fit the bill.
The heavy blister packs from the hardware store are too thick to focus through--a cover slip for 400x viewing needs to be thin. But then I found just the thing--the clear lid from a tub of the Colonel's Kentucky mashed potatoes (get the gravy too, so you get an extra lid). Cut it into 11mm x 22mm rectangles--they work perfectly! You can wash them in soapy water, rinse, blot, and reuse until they get scratchy.
Practical tip: Cut a whole bunch of cover slips and keep them in a custard dish for easy pick up--this greatly expedites the slide prep time. Look for thin clear plastic with the #1 recycling symbol for polyethylene terephthalate:
Beekeeper Health Breakthrough: Wracked as I was by images of beekeepers stuffing themselves with mashed potatoes in order to be able to monitor nosema levels, I forayed to the grocery to see if I could recommend a more healthful suggestion. To my great relief, I found that the rectangular containers for the nutritious "Baby Mixed Greens" are also made from PETE, and make excellent cover slips!
Figure 2. Hold a bee by the head/thorax, then use the table knife to "milk" the gut contents (or the gut itself) out of its abdomen directly onto the slide. Use the knife tip to mash the material in a droplet of water in order to distribute any spores into the macerate. Then remove any excess bee tissue, leaving a thin slurry (note the stinger and rectum on the slide, and on the towel to the right). Finally, place a cover slip over the drop of slurry. In this photo, I've completed two preps at the top (neither contained much pollen). I'm working on the third, which will make a more opaque slurry.
The technique of "milking" the bee's abdomen by rocking a flat blade from front to rear will quickly cause the discharge of the gut contents, or with increased pressure, the gut itself. It is critical to thoroughly crush and mash these in a little water--I wet the tip of the knife blade in a stream of water if necessary--until you create a cloudy, but not opaque, macerate. Tip: it's critical to be able to press the knife tip down flat against the slide, so work with the slide near the edge of a raised cutting board, so that your knuckles can drop below the work surface level. Be careful to keep the macerate on the portion of the slide that will be under each cover slip. Then be sure to flip off any thick chunks of excess tissue, especially the sting or any dark pieces of exoskeleton, or they will space the cover slip up too high. Clean the knife tip under running water, and wipe it on the dry towel between each bee. With practice, this entire process takes only a few seconds!
Repeat the process down the slide, exercising caution to wipe the blade thoroughly between bees, and not allowing any liquid to run from sample to sample. The separate cover slips keep the samples from mixing. After you've crushed and covered 5 gut samples, then fold the towel over the slide and press down firmly and evenly to set all the cover slips down flat, and to absorb any liquid that might otherwise get onto the microscope lens.
Figure 3. Presto--you now have a 5-bee gut sample ready to view under a scope. It's then a simple matter to glance at each of the samples in turn to check for nosema spores. This technique works for either freshly-killed or preserved bees.
At this point is really helps to have a scope with an adjustable stage (having turnable knobs to move the slide around). Then you can easily move from one cover slip to the next, and quickly scan up and down each slip if necessary. It's also very easy to see whether you've gotten nurse bees or foragers, since each gut squash clearly shows any contained pollen (Figs. 4 and 5).
Figure 4. Close up of the differences between squashes containing pollen (center) and those from without. This sample was taken from the entrance on a cold November morning with minimal flight. See the following photos for how the two left-hand squashes looked under the scope. Two out of 5 of these bees were infected.
Squashed bee guts, especially the midgut, are typically either free of nosema, or strongly infected, as above.
Figure 5. This is a view of the orange-colored center squash shown above. This bee is only moderately infected with Nosema ceranae, and the gut also contains some orange-centered rust fungus spores-which are unhealthy for bees to consume.
Figure 6. A close up from a gut packed full of "fried eggs." It took me a while, but I finally identified these spores as being from rust fungus.
It took me quite a while, but I eventually identified the "fried eggs" in the bees' guts as being spores from a blackberry rust fungus. In the photo above, you can see the fluorescent-orange spores packed as beebread-this is not pollen! The fungus tricks the bees into gathering its spores. Note the dying larvae next to this abundant beebread-although this colony appears to have abundant beebread, in fact, the fungal spores are unhealthy to the hive. In my area, hives full of such spores go downhill, unless we feed them all the pollen sub that they will eat. See "Fried Eggs" Identified!
Back to nosema sampling, one of the major beauties of the Quick Squash method is how quick it is, since you don't need to count spores at all (Fig. 7)!
Practical application: After a bit of practice, my turnaround time for the entire process of preparing, viewing, and recording results for 10 bees (two 5-bee slides) is just over four minutes if I don't fumble something along the way. Tip: have plenty of precut cover slips at hand in a small bowl.
Figure 7. This is a view of the far left-hand squash from an older bee, whose gut does not contain pollen. Even though the preparation looked nearly clear to the naked eye, it is easy to see the degree of nosema infection.
Viewing individual bees gives you a much better idea of just how greatly the gut contents of bees vary from bee to bee within the same hive! Sometimes each of the 5 gut contents look completely different. All that I can say is that bees have a lot of different things going on in their guts, and numerous infections, most of which I can't identify (Fig. 8).
Figure 8. This poor bee is suffering from both Nosema ceranae and what appears to be a Malpighamoeba mellificae infection (the larger oval cysts). Amoeba infection is not something that most beekeepers even consider, but I find it commonly in failing hives.
Malpighamoeba mellificae in the Malphigian tubules of bees ©️ Institut fur Saat - und Pflanzgut, Pflanzenschutzdienst und Bienen Abteilung Bienenkunde und Bienenschutz -
I'm not a microbiologist, and have trouble differentiating yeast cells in the gut from amoeba cysts. Here's a photo of beebread to which I added a weak sucrose solution, and allowed to ferment. I'm guessing that the cells between the pollen grains are yeasts. If anyone can help me, please let me know!
This method takes less time than a standard hemacytometer count, yet provides you far more useful information.
Economic analysis: A scope (which will last the rest of your life) costs less than the rental rate for two hives in almonds. You can easily run a dozen of these samples in an hour, which would give you a good idea of the infection rate for the weaker hives a 50-hive apiary. This method can quickly let you know if you have a serious nosema problem. On the other hand, bottle of fumagillin to unnecessarily treat those 50 hives would set you back $140, plus syrup and labor.
Update: time and again I've had beekeepers tell me that they've been trying to control dysentery by feeding fumagillin. When I ask them to send me bee samples, I often find that there is no nosema present, suggesting that they've been blaming the wrong suspect! As far as I can tell, nosema does not cause dysentery-this is a common misconception. Dysentery can spread nosema in the hive, but it doesn't appear to be an indicator of nosema.
There is nothing new about knowing that measuring the infection rate is a better assessment of nosema infection than that of taking spore counts--Dr. White made that clear back in 1919, and it has been confirmed again and again. The problem has always been that it is simply too tedious to individually squash hundreds of bees (Dr. White individually squashed and microscopically viewed over 3000 bees). What has always been lacking is a time-efficient way to determine the infection rate, and that is what I tried to develop with this "Quick Squash" method. Shy of an automated device, this method may be the best practical assessment of colony infection rate, and appears to have a reasonable degree of accuracy.
Validation
OK, so this past week I took samples from the strongest hives and from dinks in some of my yards, and have so far processed a total of 40 samples (I still have a backlog at press time, and favored the samples from weak hives). I've graphed the results below (Fig. 9):
Figure 9. Distribution of nosema prevalence in the weakest and strongest hives in my apiaries in early December, based upon 10-bee samples taken from under the lid or outside combs. In none of the strong hives were more than 1 bee out of 10 infected; whereas the majority of the weak hives scored at least 1 or more infected bees out of 10, and 40% scored 2 or more positives.
The preliminary data above strongly suggest that Nosema ceranae infection is associated with colony weakness in my own operation, which is not surprising, based upon the vast body of previous research on the negative effects of nosema! At this point in time, I am rather disillusioned with any field research findings based upon spore counts, and hope that other researchers follow the lead of Dr. Mariano Higes and include the percentage of infected bees.
Practical application: The point of the above graph is that up 'til this point, I have never been able to correlate N. ceranae infection intensity, based upon spore counts, with either colony health or production. But when I switched to a different assessment method--quantifying nosema prevalence based upon the number of infected bees in a sample of 10--the relationship jumps right out!
Summary (Completely Subject To Revision):
Early spring and early fall are likely the most appropriate times to sample, or during winter if you're going to almonds. No need to look for nosema in July or August, as it normally "disappears" during that time.
Take samples any time of year from any colonies or yards that appear to not be performing well--lagging, poor weight gain, lack of foragers or bees over the brood. I'm not sure whether it's worthwhile to routinely bother with taking nosema samples, provided that your colonies are not under stress, and so long as they are kicking butt.
Brush a dozen bees from under the lid or an outside comb into a ziplock bag, and add a glug of rubbing alcohol (for long-term storage use bottles and additional alcohol, or freeze). If you wish to label the sample, make sure the marker is alcohol resistant, or write with a pencil and put the label inside the bag.
(Alternate assessment) Process about 50 bees by the ziplock method (see Sick Bees Part 12). If you see fewer than about 5 spores in a field of view (about 1M equivalent), then you've got nothing to worry about. If more, go to the next step.
From each sample, prepare two slides of 5 bees each per the "Quick Squash" method in this article.
Interpret the entire 10-bee sample as follows:
0-1/10 positive for spores-likely safe
3/10-likely moderate infection
4/10-likely serious infection
>4/10- very likely serious
Be concerned any time that you hit 2 or more positive bees out of 5.
The odds of hitting 3 or more bees out of 10 climbs rapidly with infection rate--to a definitive 95% chance once half the bees in the hive are infected!
6. I feel that it is likely not worth the effort to sample more than 10 bees from any single hive-10 bees should give you a fairly close estimate of infection prevalence in that hive. Better to spend the time sampling more hives!
7. Important: don't base any management decisions upon only a single sample! Keep sampling until you are comfortable with the consistency of the results.
I realize that I just threw a lot of numbers at you, but in practice the method is really intuitive. It's very much like playing poker--your brain easily grasps the probabilities of getting either one ace or four in a hand. Chances are that you'll get more positive hits from colonies with a serious nosema infection, and few or no hits from healthy colonies.
Processing bee samples by this "Quick Squash" method offers an easy way for beekeepers to monitor whether nosema is actually a problem in their operations. It takes me less time to process a 10-bee sample than it does to do a single hemacytometer count, but the results of this method are much more meaningful from a practical standpoint. The "old school" researchers found this method to be a reliable assessment of the seriousness of nosema infection for N. apis; I suspect (subject to verification) that it may also prove to be the best for N. ceranae.
It sometimes seems that beekeepers need to reinvent the wheel. Anyway, I just came up with this quick method and really like it! My sons mastered the technique in a couple of tries. My favorite part is that I no longer need to count spores--a quick glance gives you a yes/no for infection. I'd be a happy guy if I never had to count another varroa mite or nosema spore--I'd much rather be counting all the money I'll be making from my healthy hives!
I feel that it is time for a paradigm shift in the way that we assess the impact of nosema infection upon colonies--moving from spore counting back to determining the proportion of infected bees! To that end, this method is practical and surprisingly quick, and gives you a much better idea of what's actually happening in the hive. I'd really appreciate hearing your results or suggestions for improvement if you try it (randy@randyoliver.com).
More Details--Web Version
I'm not looking to belabor the point of the reliability, or lack thereof, of spore counts, but I feel that this is an important enough issue to the beekeeping industry, in light of potential reduced honey production, increased colony mortality, and the cost of treatment, that interested beekeepers have a thorough understanding of the strong and weak points of various sampling methods.
The key question then is whether researchers, testing labs, and beekeepers can all agree upon a "standardized" method of testing, so that we can all compare results and recommendations. The current problem is that spore counts, even from the same colony, are frustratingly variable, depending upon the time of day at which the bee samples are taken (Fig. 1), the weather conditions, the place in the hive from which they are taken, the number of bees in the sample, how they are processed (mortar and pestle, filtration, squashing, etc.), how they are viewed (simple microscopy or hemacytometer), and even then counts are largely based upon the pure chance of whether or not one gets one or more highly-infected old bees in the sample!
Figure 1. Spore counts of four 25-bee samples taken each day from the same hive--from the entrance or the inside, and at either 9:30am or 12:30 pm. Note that counts on the same day varied from nearly zero to 10M spores--testament to the inherent variability of spore counts! It is also unlikely that the infection level varied as greatly from week to week as the data suggest. This finding really makes me question the comparability of spore counts unless they are taken at exactly the same time of day, under similar weather conditions, and from the same place in the hive each time! Data reworked from Meana (2010).
The colony sampled in Figure 1 was presumably moderately-infected, but in apparent good health. The researchers concluded, "This strong variation in the spore count was not associated with signs of illness and indeed, the colony was apparently as healthy (asymptomatic) as any other. It would thus appear that the spore count is not useful to measure the state of a colony's health [emphasis mine]." I echo this conclusion (as do a number of other studies), since while monitoring nosema counts in my own operation over the past four years, I have been unable to detect any correlation between spore counts and colony health, productivity, nor survival.
The above authors conclude that "the mean proportion of infected bees may be a more reliable method to establish colony health." This suggestion goes right back to Dr. White's findings at the beginning of the last century, and has withstood the test of time. I guarantee that looking at the individual gut contents of a sample of 10 bees gives one a much better feeling as to the severity of nosema infection in that hive!
From Where Should We Take Samples?
Figure 2. Spore counts vs. percent infection for house and field bees, n = 30 for each sample; all samples taken at 12:30pm. Data reworked from Higes (2008). Note that spore counts roughly reflect the percent infection rate for either group, but that spore counts of house bees may not be a particularly good indicator of the infection rate of field bees, which is likely the best assessment of the impact of nosema upon colony health. On the other hand, in this data set, the infection rates of both house and field bees roughly tracked each other. This data set suggests that spore counts of field bees is the most sensitive measure of the degree of nosema infection in a hive.
Experts' Opinions
Smart and Sheppard (2011) concluded that: "Based on these findings, we speculate that bees collected from the inner hive cover represent a mixture of age classes of bees and, depending on the goals of the sampler, may provide a better estimate of the whole colony mean infection level than sampling just foragers.
So I asked Dr. Brian Johnson, who had considerable experience with tracking bees in observation hives. He told me:
"The bees just under the lid tend to be older middle age bees, while the bees on the outside combs are mostly middle age bees with smaller numbers of nurses and foragers. In general, the foragers are near the entrance, the nurses are in the brood zone, and the middle age bees are everywhere, but with a slight bias for the honey zone."
I also asked the preeminent bee behavioralist, Dr. Tom Seeley. His response:
"Interesting question. The only information that I have regarding the age distribution of bees who are spending time just under the lid or on one of the outer combs (i.e., ones without brood) comes from a study that I did back in 1982. In it, I mapped out the locations (in a large observation hive) of various activities and at the same time I took data on the age distributions of the bees performing these tasks. These results make it clear that the middle-aged bees are mainly working in the peripheral (outside the brood nest) regions of the nest. So if bees are collected from these areas during the day, then they will be mainly middle-age and forager-age bees. At night, the percentage of forager-age bees will be higher. You've probably seen in observation hives how the foragers literally hang out in the edge areas of a hive at night."
Finally, there is one more piece of supportive evidence for taking samples from under the lid: Moeller (1956) found that "nosema-infected bees congregate in and above warm brood areas."
Conclusions
Hey, I'll leave the conclusions up to you. Today, I did some spore counts of 20-bee samples of piles dead bees from the front of three hives in one yard. They had little nosema--about 5 spores per field of view, so approx. 1M/bee. So not enough spores to indicate that a 10-bee squash would be useful. Since the bees were dead, it would have entailed rehydration in order to do gut squashes.
I also did some Quick Squashes of bees from under the lid for other hives. Each method has its advantages and limitations. The smart beekeeper understands them!
Next Month
Nosema: The Smoldering Epidemic
Acknowledgements
I wish to thank my wife Stephanie for her patience, and helpful comments on my manuscripts (she chokes on math and graphs, and is immensely helpful to me for making my charts more user friendly). As always Peter Borst helped with the research for this article. A special thanks to Dr. Jose Villa, as mentioned previously. Thanks to Dr. Jerry Bromenshenk for his helpful suggestions. And a big thanks to Drs. Mariano Higes, Aranzazu Meana, and Raquel Martin-Hernandez for their diligent work on nosema! For financial support toward this research, I've very appreciative of Joe Traynor, Heitkam's Honey Bees, Jester Bee Company, the Virginia State Beekeepers Assoc, and individual beekeepers Paul Limbach, Chris Moore, and Keith Jarret.
References
Botias, C, et al (2011) Critical aspects of the Nosema spp. diagnostic sampling in honey bee (Apis mellifera L.) colonies. Parasitology Research (in press).
Fingler BG, WT Nash, and TI Szabo (1982) A comparison of two techniques for the measurement of nosema disease in honey bee colonies wintered in Alberta, Canada. ABJ 122(5):369-371.
Forsgren, E, and I Fries (2010) Comparative virulence of Nosema ceranae and Nosema apis in individual European honey bees. Veterinary Parasitology 170: 212-217.
Frazier, MT, et al (2000) A sequential sampling scheme for detecting infestation levels of tracheal mites (Heterostigmata: Tarsonemidae) in honey bee (Hymenoptera: Apidae) colonies. Journal of Economic Entomology 93(3):551-558.
Higes, M, et al (2008) How natural infection by Nosema ceranae causes honeybee colony collapse. Environ Microbiol 10: 2659-2669.
Mattila HR, and GW Otis (2007) Dwindling pollen resources trigger the transition to broodless populations of long-lived honeybees each autumn. Ecol Entomol 32:496-505.
Meana, A, et al (2010) The reliability of spore counts to diagnose Nosema ceranae infections in honey bees. Journal of Apicultural Research and Bee World 49(2): 212-214.
Moeller, F.E., 1956. The behavior of nosema infected bees affecting their position in the winter cluster. J. Econ. Entomol. 49 (6), 743-745.
Oliver, R (2008) The Nosema Twins Part 3: Sampling. ABJ 148(2): 149-154. https://scientificbeekeeping.com/the-nosema-twins-part-3-sampling/
Porrini, MP, et al (2011) Nosema ceranae development in Apis mellifera: influence of diet and infective inoculum. Journal of Apicultural Research 50(1): 35-41
Smart, MD and WS Sheppard (2011, in press) Nosema ceranae in age cohorts of the western honey bee (Apis mellifera). J. Invertebr. Pathol. doi:10.1016/j.jip.2011.09.009
Tomasko, M. Finley, J. Harkness, W. Rajotte, E. 1993. A sequential sampling scheme for detecting the presence of tracheal mite (Acarapis woodi) infestations in honey bee (Apis mellifera L.) colonies. Penn. State College of Agricultural Sciences, Agricultural Experiment Station Bulletin 871.
Traver, B., and RD Fell (2011a) Prevalence and infection intensity of Nosema in honey bee (Apis mellifera L.) colonies in Virginia. J Invertebr Pathol 107 (1):43-49.
Traver, BE MR Williams, and RD Fell (2011b; in press) Comparison of within hive sampling and seasonal activity of Nosema ceranae in honey bee colonies. Journal of Invertebrate Pathology.
White, GF (1919) Nosema-Disease. USDA Bulletin No. 780.
Category: Nosema Summaries and Updates, Sampling
Tags: infection, n. apis, N. ceranae, nosema apis, Nosema cereanae, squash | squash Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/squash/ |
Concepts in varroa management 2023
2023 Concepts in varroa management
Category: Topics | Concepts in varroa management 2023 - Scientific Beekeeping | https://scientificbeekeeping.com/concepts-in-varroa-management-2023/ |
Refining the Mite Wash: Part 1 - Treatment Threshold and Solutions to Use
Refining the Mite Wash Part 1 Treatment Threshold and Solutions to Use Randy Oliver ScientificBeekeeping.com First published in ABJ July 2020 Once you've shaken a sample of bees, you then need to separate the mites from them. There are various recommendations for using alcohol, detergent water, powdered sugar, ether, or CO2. I've been using inexpensive [...]
Read More | Varroa Management Archives - Page 3 of 8 - Scientific Beekeeping | https://scientificbeekeeping.com/varroa-management/page/3/ |
The Learning Curve - Part 5: The Future
The Learning Curve: The Future Randy Oliver ScientificBeekeeping.com First Published in ABJ in Nov. 2009 "I look to the future because that's where I'm going to spend the rest of my life." - George Burns Miticides in Development There are a number of new varroacides currently in development by various parties--some fairly close to release. [...]
Read More | Treatments For Varroa Archives - Page 3 of 3 - Scientific Beekeeping | https://scientificbeekeeping.com/varroa-management/treatments-for-varroa/page/3/ |
The Primer Pheromones and Managing the Labor Pool - Part 2
First published in: American Bee Journal May 2010
The Primer Pheromones and Managing the Labor Pool Part 2 Randy Oliver ScientificBeekeeping.com First published in American Bee Journal May 2010 In the first part of this article, I explained how the allotment of the hive labor pool was largely controlled through communication via the process of sharing protein-rich jelly via trophallaxis, plus non-feeding interchange [...]
Read More | Bee Behavior and Biology Archives - Page 3 of 3 - Scientific Beekeeping | https://scientificbeekeeping.com/bee-behavior-biology/page/3/ |
Sick Bees - Part 16: The "Quick Squash" Method for Determining Nosema Prevalence in a Colony
Infection Prevalence
Sequential Sampling
A Neat Little Shortcut
Validation
Summary (completely subject to revision)
More Details
Next Month
Acknowledgements
References
2019 Quick Nosema Prevalence Assessment Method
First published in ABJ February 2012
Updated March 13, 2019
Randy Oliver
Since the discovery of Nosema ceranae, I and many other beekeepers and researchers have been frustrated by the tedium and apparent futility of counting nosema spores, since many of us haven't seen any meaningful relationship between spore counts and colony health or production. I strongly suspect that the issue is not that N. ceranae does not cause problems, but rather that our methodology for assessing the degree of infection has been flawed.
The quickest way that I've found to determine the degree of nosema infection in a hive is to do a 2-step sampling.
Step 1: open the hive and take a sample of about 50 workers from an outer frame, or from under the hive cover. These bees can be salvaged from an alcohol wash for varroa. Set at least 15 bees aside for the time being, and use the rest for the next step.
I now typically use only 10 bees. This is based upon the thorough research on Nosema apis by GF White in the early 1900s. What he found was that individually sampling 10 bees in order to determine the prevalence of nosema infection in the house bees gave the best indication of its biological relevance-a finding later suggested by Cameron Jack in Colony Level Prevalence and Intensity of Nosema ceranae in Honey Bees (Apis mellifera L.).
Be sure to read https://scientificbeekeeping.com/the-seasonality-of-nosema-ceranae/
Step 2: place at least 25 of the bees in a ziplock sandwich bag, and roll a round jar over them to crush their guts thoroughly. Then add about 3 mL of water for every 10 bees in the sample, and massage the bag in your fingers until you've homogenized all the gut contents into the water, creating a semi-opaque suspension (not too clear, not too thick). For details on this step, see https://scientificbeekeeping.com/sick-bees-part-13-simple-microscopy-of-nosema/
Step 3: immediately place a drop of the suspension on a slide, drop on a cover slip, and view under the scope. Scan a few fields of view for nosema spores. If you don't see any (or only one or two), that indicates that the infection prevalence of that sample of bees was zero-end of assessment.
On the other hand, if you see spores in the sample, then perform 10 individual bee gut squashes from the remaining bees in the original sample in order to determine the biological relevance of the infection prevalence in the colony-details below.
Infection Prevalence
The current "standard" method for monitoring nosema "level" in hives is to determine the mean spore count per bee in an aggregate sample (of typically 10-100 bees). The method is relatively quick and gives the sort of quantifiable numbers that scientists love. Unfortunately, as noted by Meana (2010), "the spore count is not directly related to the parasite burden and health status of whole colonies naturally infected by N. ceranae under field conditions."
Spore counts certainly have their uses, such as quantifying the progress of nosema infection in individual bees in cage trials by researchers. They are also appropriate as a method for "discovery sampling." For example, one can "discover" whether nosema is present to any extent in an apiary by taking an aggregate sample of say ten bees from the entrance of every hive and determining the mean spore count. If the count is less than 1M (1 million spores per bee), then nosema is likely not a problem in the sampled hives.
The point that I'm trying to make about sampling for nosema is that we are well beyond the "discovery" phase. Rennich (2011) found N. ceranae in at least half of all random bee samples taken in the U.S. during winter and spring.
So instead of "discovery" sampling, what we need to do is to shift to the most meaningful way to measure the potential impact of nosema upon colony health--the proportion of infected bees. Of the various terms used to describe this measure--"proportion of infected bees in a sample," "percent infected," or "infection rate"- I prefer the term used by epidemiologists: "prevalence."
Practical application: I henceforth plan to use the term "prevalence" as the measure of the proportion of bees infected by nosema. For example, if 2 bees out of 10 were infected, that would be a prevalence of 20%.
There is a strong case to be made for shifting our assessment of nosema infection from "intensity" (as measured by spore counts) to "prevalence" (the percent of bees actually infected). The only problem with determining prevalence is that most of us choke at the thought of having to inspect jillions of bees one at a time. Luckily, there are practical shortcuts:
Sequential Sampling
In my last article, I proposed that even a small sample of bees might be adequate for making management decisions. I'm immensely grateful to Dr. Jose Villa of the Baton Rouge Bee Lab for bringing to my attention that I was reinventing the wheel--this sort of decision making process, based upon small sample sizes, already has a fancy name: it's called "sequential sampling," and was develped as a time-saving method for quality control inspections during World War II. Furthermore, Dr. Villa dug into the library and forwarded me existing "Decision Tables" for tracheal mite sampling produced by Tomasko (1993).
Dr. Maryann Frazier (2000), following up on Tomasko's work, discussed the situation regarding the assement of tracheal mite prevalence as opposed to "parasite load" (analagous to spore counts). It is remarkable in that it almost exactly mirrors today's situation with nosema! And in her paper she validated the accuracy of sequential sampling.
Sequential sampling is all about the tradeoff between tedium (the number of bees that you need to squash and view) and confidence (the error rate which you are willing to accept). And it appears that for our purposes, I estimated the minimum number of bees to sample right on the nose!
So let's set some arbitrary parameters for our decision making:
An infection prevalence of 10% is "tolerable."
A prevalence of 30-40% is "intolerable."
We'll accept a 20% error rate for overestimating the prevalence.
But we won't accept an error rate above 10% for underestimating the prevalence.
We'll use the above parameters to set our treatment thresholds--below 10% prevalence, don't treat; above 30%, treat. The math gets complex, but here's the gist of the outcome:
Practical application: it appears that in order to make a decision whether to treat or not, that a couple of 5-bee samples should be adequate, interpreted as follows:
0 positive bees out of 5, or no more than 1 positive out of 10 indicates < 10% infection
3 positive bees out of 5, or at least 4 positives out of 10 indicates > 30% infection
Any number of positive bees lying between these cutoffs (e.g., 2 bees out of 5, or 3 out of 10) is not enough to make a firm decision, but suggests an infection level that lies in the gray zone. But I doubt that going beyond a 10-bee sample is worth the effort--I'd just move on to the next sample.
With true sequential sampling, you'd keep sampling until you hit a critical number of positive or negative bees in order to make a treatment decision. However, my limited experience suggests that we hit a point of diminishing returns after viewing 10 bees.
Update July 5, 2012 Beekeeper Ruary Rudd (ruaryrudd@iol.ie) has developed a great Excel spreadsheet for sequential sampling. You can write him for a copy-thanks Ruary!
So I've got us down to sampling a maximum of 10-bees. But even so, I must advise you that nosema infection appears to exist in "pockets" of bees in the hive, so any single small sample is inadequate for making an apiary-level decision (Botias 2011). Therefore, it's necessary to process a number of samples. What's been holding us back from determining actual nosema prevalence is the lack of a quick method for processing a number of samples of 10 bees!
Nosema apis becomes a serious problem if about a third of the bees in a hive become infected. It appears that Nosema ceranae may be a problem at even a lower prevalence.
A Neat Little Shortcut
Since I really wanted to find a quicker way to prepare and view the 200 bees for the validation table in the previous article, I racked my brain trying to figure out a technique for speeding things up, and finally hit upon a relatively simple procedure (Figures 1,2, and 3). I've now got over 400 individual gut squashes under my belt, and am pretty excited about the method! This solution allows me to process bees at an overall turnaround rate of less than five minutes per sample of 10 bees!
Figure 1. This photo shows the necessary equipment for a Quick Squash--5 bees, a plain microscope slide, 5 custom-made thin plastic cover slips, a table knife, and a paper towel.
The size of the cover slips is critical--they must be narrow enough not to touch at the edges, in order to keep the individual gut slurries from mixing. The easiest solution is to cut off-the-shelf plastic microscopy cover slips in half with scissors. You can then just discard them after use (cost about 20C//10-bee sample), or wash and reuse (use your mite shaker jar).
Update Feb 2019: I prefer to recycle rather than discard. But when I looked at costs, getting a large order of #1 thickness glass cover slips works out to only about a penny a slip. At Amazon: Karter Scientific 211Z2 Standard Microscope Cover Slip, #1 Thick, 22x22mm, 200pk (Case of 2000).
Be sure to order #1 thickness cover slips, since thicker cover slips won't allow you to focus upon the spores.
The other thing is that you don't need to make custom cover slips at all. Three standard glass cover slips will fit across a slide, and can be discarded after use if you don't want to wash them (although they wash easily in warm water with a tiny bit of dishwashing detergent).
But if you don't have plastic cover slips at hand, don't despair! You can make cover slips out of clear plastic scrap around the home--but only some plastics will work; I've experimented with several. Clear plastic transparency sheets unfortunately refract light in such a way that they make nosema spores look like little rectangles, so they don't fit the bill.
The heavy blister packs from the hardware store are too thick to focus through--a cover slip for 400x viewing needs to be thin. But then I found just the thing--the clear lid from a tub of the Colonel's Kentucky mashed potatoes (get the gravy too, so you get an extra lid). Cut it into 11mm x 22mm rectangles--they work perfectly! You can wash them in soapy water, rinse, blot, and reuse until they get scratchy.
Practical tip: Cut a whole bunch of cover slips and keep them in a custard dish for easy pick up--this greatly expedites the slide prep time. Look for thin clear plastic with the #1 recycling symbol for polyethylene terephthalate:
Beekeeper Health Breakthrough: Wracked as I was by images of beekeepers stuffing themselves with mashed potatoes in order to be able to monitor nosema levels, I forayed to the grocery to see if I could recommend a more healthful suggestion. To my great relief, I found that the rectangular containers for the nutritious "Baby Mixed Greens" are also made from PETE, and make excellent cover slips!
Figure 2. Hold a bee by the head/thorax, then use the table knife to "milk" the gut contents (or the gut itself) out of its abdomen directly onto the slide. Use the knife tip to mash the material in a droplet of water in order to distribute any spores into the macerate. Then remove any excess bee tissue, leaving a thin slurry (note the stinger and rectum on the slide, and on the towel to the right). Finally, place a cover slip over the drop of slurry. In this photo, I've completed two preps at the top (neither contained much pollen). I'm working on the third, which will make a more opaque slurry.
The technique of "milking" the bee's abdomen by rocking a flat blade from front to rear will quickly cause the discharge of the gut contents, or with increased pressure, the gut itself. It is critical to thoroughly crush and mash these in a little water--I wet the tip of the knife blade in a stream of water if necessary--until you create a cloudy, but not opaque, macerate. Tip: it's critical to be able to press the knife tip down flat against the slide, so work with the slide near the edge of a raised cutting board, so that your knuckles can drop below the work surface level. Be careful to keep the macerate on the portion of the slide that will be under each cover slip. Then be sure to flip off any thick chunks of excess tissue, especially the sting or any dark pieces of exoskeleton, or they will space the cover slip up too high. Clean the knife tip under running water, and wipe it on the dry towel between each bee. With practice, this entire process takes only a few seconds!
Repeat the process down the slide, exercising caution to wipe the blade thoroughly between bees, and not allowing any liquid to run from sample to sample. The separate cover slips keep the samples from mixing. After you've crushed and covered 5 gut samples, then fold the towel over the slide and press down firmly and evenly to set all the cover slips down flat, and to absorb any liquid that might otherwise get onto the microscope lens.
Figure 3. Presto--you now have a 5-bee gut sample ready to view under a scope. It's then a simple matter to glance at each of the samples in turn to check for nosema spores. This technique works for either freshly-killed or preserved bees.
At this point is really helps to have a scope with an adjustable stage (having turnable knobs to move the slide around). Then you can easily move from one cover slip to the next, and quickly scan up and down each slip if necessary. It's also very easy to see whether you've gotten nurse bees or foragers, since each gut squash clearly shows any contained pollen (Figs. 4 and 5).
Figure 4. Close up of the differences between squashes containing pollen (center) and those from without. This sample was taken from the entrance on a cold November morning with minimal flight. See the following photos for how the two left-hand squashes looked under the scope. Two out of 5 of these bees were infected.
Squashed bee guts, especially the midgut, are typically either free of nosema, or strongly infected, as above.
Figure 5. This is a view of the orange-colored center squash shown above. This bee is only moderately infected with Nosema ceranae, and the gut also contains some orange-centered rust fungus spores-which are unhealthy for bees to consume.
Figure 6. A close up from a gut packed full of "fried eggs." It took me a while, but I finally identified these spores as being from rust fungus.
It took me quite a while, but I eventually identified the "fried eggs" in the bees' guts as being spores from a blackberry rust fungus. In the photo above, you can see the fluorescent-orange spores packed as beebread-this is not pollen! The fungus tricks the bees into gathering its spores. Note the dying larvae next to this abundant beebread-although this colony appears to have abundant beebread, in fact, the fungal spores are unhealthy to the hive. In my area, hives full of such spores go downhill, unless we feed them all the pollen sub that they will eat. See "Fried Eggs" Identified!
Back to nosema sampling, one of the major beauties of the Quick Squash method is how quick it is, since you don't need to count spores at all (Fig. 7)!
Practical application: After a bit of practice, my turnaround time for the entire process of preparing, viewing, and recording results for 10 bees (two 5-bee slides) is just over four minutes if I don't fumble something along the way. Tip: have plenty of precut cover slips at hand in a small bowl.
Figure 7. This is a view of the far left-hand squash from an older bee, whose gut does not contain pollen. Even though the preparation looked nearly clear to the naked eye, it is easy to see the degree of nosema infection.
Viewing individual bees gives you a much better idea of just how greatly the gut contents of bees vary from bee to bee within the same hive! Sometimes each of the 5 gut contents look completely different. All that I can say is that bees have a lot of different things going on in their guts, and numerous infections, most of which I can't identify (Fig. 8).
Figure 8. This poor bee is suffering from both Nosema ceranae and what appears to be a Malpighamoeba mellificae infection (the larger oval cysts). Amoeba infection is not something that most beekeepers even consider, but I find it commonly in failing hives.
Malpighamoeba mellificae in the Malphigian tubules of bees ©️ Institut fur Saat - und Pflanzgut, Pflanzenschutzdienst und Bienen Abteilung Bienenkunde und Bienenschutz -
I'm not a microbiologist, and have trouble differentiating yeast cells in the gut from amoeba cysts. Here's a photo of beebread to which I added a weak sucrose solution, and allowed to ferment. I'm guessing that the cells between the pollen grains are yeasts. If anyone can help me, please let me know!
This method takes less time than a standard hemacytometer count, yet provides you far more useful information.
Economic analysis: A scope (which will last the rest of your life) costs less than the rental rate for two hives in almonds. You can easily run a dozen of these samples in an hour, which would give you a good idea of the infection rate for the weaker hives a 50-hive apiary. This method can quickly let you know if you have a serious nosema problem. On the other hand, bottle of fumagillin to unnecessarily treat those 50 hives would set you back $140, plus syrup and labor.
Update: time and again I've had beekeepers tell me that they've been trying to control dysentery by feeding fumagillin. When I ask them to send me bee samples, I often find that there is no nosema present, suggesting that they've been blaming the wrong suspect! As far as I can tell, nosema does not cause dysentery-this is a common misconception. Dysentery can spread nosema in the hive, but it doesn't appear to be an indicator of nosema.
There is nothing new about knowing that measuring the infection rate is a better assessment of nosema infection than that of taking spore counts--Dr. White made that clear back in 1919, and it has been confirmed again and again. The problem has always been that it is simply too tedious to individually squash hundreds of bees (Dr. White individually squashed and microscopically viewed over 3000 bees). What has always been lacking is a time-efficient way to determine the infection rate, and that is what I tried to develop with this "Quick Squash" method. Shy of an automated device, this method may be the best practical assessment of colony infection rate, and appears to have a reasonable degree of accuracy.
Validation
OK, so this past week I took samples from the strongest hives and from dinks in some of my yards, and have so far processed a total of 40 samples (I still have a backlog at press time, and favored the samples from weak hives). I've graphed the results below (Fig. 9):
Figure 9. Distribution of nosema prevalence in the weakest and strongest hives in my apiaries in early December, based upon 10-bee samples taken from under the lid or outside combs. In none of the strong hives were more than 1 bee out of 10 infected; whereas the majority of the weak hives scored at least 1 or more infected bees out of 10, and 40% scored 2 or more positives.
The preliminary data above strongly suggest that Nosema ceranae infection is associated with colony weakness in my own operation, which is not surprising, based upon the vast body of previous research on the negative effects of nosema! At this point in time, I am rather disillusioned with any field research findings based upon spore counts, and hope that other researchers follow the lead of Dr. Mariano Higes and include the percentage of infected bees.
Practical application: The point of the above graph is that up 'til this point, I have never been able to correlate N. ceranae infection intensity, based upon spore counts, with either colony health or production. But when I switched to a different assessment method--quantifying nosema prevalence based upon the number of infected bees in a sample of 10--the relationship jumps right out!
Summary (Completely Subject To Revision):
Early spring and early fall are likely the most appropriate times to sample, or during winter if you're going to almonds. No need to look for nosema in July or August, as it normally "disappears" during that time.
Take samples any time of year from any colonies or yards that appear to not be performing well--lagging, poor weight gain, lack of foragers or bees over the brood. I'm not sure whether it's worthwhile to routinely bother with taking nosema samples, provided that your colonies are not under stress, and so long as they are kicking butt.
Brush a dozen bees from under the lid or an outside comb into a ziplock bag, and add a glug of rubbing alcohol (for long-term storage use bottles and additional alcohol, or freeze). If you wish to label the sample, make sure the marker is alcohol resistant, or write with a pencil and put the label inside the bag.
(Alternate assessment) Process about 50 bees by the ziplock method (see Sick Bees Part 12). If you see fewer than about 5 spores in a field of view (about 1M equivalent), then you've got nothing to worry about. If more, go to the next step.
From each sample, prepare two slides of 5 bees each per the "Quick Squash" method in this article.
Interpret the entire 10-bee sample as follows:
0-1/10 positive for spores-likely safe
3/10-likely moderate infection
4/10-likely serious infection
>4/10- very likely serious
Be concerned any time that you hit 2 or more positive bees out of 5.
The odds of hitting 3 or more bees out of 10 climbs rapidly with infection rate--to a definitive 95% chance once half the bees in the hive are infected!
6. I feel that it is likely not worth the effort to sample more than 10 bees from any single hive-10 bees should give you a fairly close estimate of infection prevalence in that hive. Better to spend the time sampling more hives!
7. Important: don't base any management decisions upon only a single sample! Keep sampling until you are comfortable with the consistency of the results.
I realize that I just threw a lot of numbers at you, but in practice the method is really intuitive. It's very much like playing poker--your brain easily grasps the probabilities of getting either one ace or four in a hand. Chances are that you'll get more positive hits from colonies with a serious nosema infection, and few or no hits from healthy colonies.
Processing bee samples by this "Quick Squash" method offers an easy way for beekeepers to monitor whether nosema is actually a problem in their operations. It takes me less time to process a 10-bee sample than it does to do a single hemacytometer count, but the results of this method are much more meaningful from a practical standpoint. The "old school" researchers found this method to be a reliable assessment of the seriousness of nosema infection for N. apis; I suspect (subject to verification) that it may also prove to be the best for N. ceranae.
It sometimes seems that beekeepers need to reinvent the wheel. Anyway, I just came up with this quick method and really like it! My sons mastered the technique in a couple of tries. My favorite part is that I no longer need to count spores--a quick glance gives you a yes/no for infection. I'd be a happy guy if I never had to count another varroa mite or nosema spore--I'd much rather be counting all the money I'll be making from my healthy hives!
I feel that it is time for a paradigm shift in the way that we assess the impact of nosema infection upon colonies--moving from spore counting back to determining the proportion of infected bees! To that end, this method is practical and surprisingly quick, and gives you a much better idea of what's actually happening in the hive. I'd really appreciate hearing your results or suggestions for improvement if you try it (randy@randyoliver.com).
More Details--Web Version
I'm not looking to belabor the point of the reliability, or lack thereof, of spore counts, but I feel that this is an important enough issue to the beekeeping industry, in light of potential reduced honey production, increased colony mortality, and the cost of treatment, that interested beekeepers have a thorough understanding of the strong and weak points of various sampling methods.
The key question then is whether researchers, testing labs, and beekeepers can all agree upon a "standardized" method of testing, so that we can all compare results and recommendations. The current problem is that spore counts, even from the same colony, are frustratingly variable, depending upon the time of day at which the bee samples are taken (Fig. 1), the weather conditions, the place in the hive from which they are taken, the number of bees in the sample, how they are processed (mortar and pestle, filtration, squashing, etc.), how they are viewed (simple microscopy or hemacytometer), and even then counts are largely based upon the pure chance of whether or not one gets one or more highly-infected old bees in the sample!
Figure 1. Spore counts of four 25-bee samples taken each day from the same hive--from the entrance or the inside, and at either 9:30am or 12:30 pm. Note that counts on the same day varied from nearly zero to 10M spores--testament to the inherent variability of spore counts! It is also unlikely that the infection level varied as greatly from week to week as the data suggest. This finding really makes me question the comparability of spore counts unless they are taken at exactly the same time of day, under similar weather conditions, and from the same place in the hive each time! Data reworked from Meana (2010).
The colony sampled in Figure 1 was presumably moderately-infected, but in apparent good health. The researchers concluded, "This strong variation in the spore count was not associated with signs of illness and indeed, the colony was apparently as healthy (asymptomatic) as any other. It would thus appear that the spore count is not useful to measure the state of a colony's health [emphasis mine]." I echo this conclusion (as do a number of other studies), since while monitoring nosema counts in my own operation over the past four years, I have been unable to detect any correlation between spore counts and colony health, productivity, nor survival.
The above authors conclude that "the mean proportion of infected bees may be a more reliable method to establish colony health." This suggestion goes right back to Dr. White's findings at the beginning of the last century, and has withstood the test of time. I guarantee that looking at the individual gut contents of a sample of 10 bees gives one a much better feeling as to the severity of nosema infection in that hive!
From Where Should We Take Samples?
Figure 2. Spore counts vs. percent infection for house and field bees, n = 30 for each sample; all samples taken at 12:30pm. Data reworked from Higes (2008). Note that spore counts roughly reflect the percent infection rate for either group, but that spore counts of house bees may not be a particularly good indicator of the infection rate of field bees, which is likely the best assessment of the impact of nosema upon colony health. On the other hand, in this data set, the infection rates of both house and field bees roughly tracked each other. This data set suggests that spore counts of field bees is the most sensitive measure of the degree of nosema infection in a hive.
Experts' Opinions
Smart and Sheppard (2011) concluded that: "Based on these findings, we speculate that bees collected from the inner hive cover represent a mixture of age classes of bees and, depending on the goals of the sampler, may provide a better estimate of the whole colony mean infection level than sampling just foragers.
So I asked Dr. Brian Johnson, who had considerable experience with tracking bees in observation hives. He told me:
"The bees just under the lid tend to be older middle age bees, while the bees on the outside combs are mostly middle age bees with smaller numbers of nurses and foragers. In general, the foragers are near the entrance, the nurses are in the brood zone, and the middle age bees are everywhere, but with a slight bias for the honey zone."
I also asked the preeminent bee behavioralist, Dr. Tom Seeley. His response:
"Interesting question. The only information that I have regarding the age distribution of bees who are spending time just under the lid or on one of the outer combs (i.e., ones without brood) comes from a study that I did back in 1982. In it, I mapped out the locations (in a large observation hive) of various activities and at the same time I took data on the age distributions of the bees performing these tasks. These results make it clear that the middle-aged bees are mainly working in the peripheral (outside the brood nest) regions of the nest. So if bees are collected from these areas during the day, then they will be mainly middle-age and forager-age bees. At night, the percentage of forager-age bees will be higher. You've probably seen in observation hives how the foragers literally hang out in the edge areas of a hive at night."
Finally, there is one more piece of supportive evidence for taking samples from under the lid: Moeller (1956) found that "nosema-infected bees congregate in and above warm brood areas."
Conclusions
Hey, I'll leave the conclusions up to you. Today, I did some spore counts of 20-bee samples of piles dead bees from the front of three hives in one yard. They had little nosema--about 5 spores per field of view, so approx. 1M/bee. So not enough spores to indicate that a 10-bee squash would be useful. Since the bees were dead, it would have entailed rehydration in order to do gut squashes.
I also did some Quick Squashes of bees from under the lid for other hives. Each method has its advantages and limitations. The smart beekeeper understands them!
Next Month
Nosema: The Smoldering Epidemic
Acknowledgements
I wish to thank my wife Stephanie for her patience, and helpful comments on my manuscripts (she chokes on math and graphs, and is immensely helpful to me for making my charts more user friendly). As always Peter Borst helped with the research for this article. A special thanks to Dr. Jose Villa, as mentioned previously. Thanks to Dr. Jerry Bromenshenk for his helpful suggestions. And a big thanks to Drs. Mariano Higes, Aranzazu Meana, and Raquel Martin-Hernandez for their diligent work on nosema! For financial support toward this research, I've very appreciative of Joe Traynor, Heitkam's Honey Bees, Jester Bee Company, the Virginia State Beekeepers Assoc, and individual beekeepers Paul Limbach, Chris Moore, and Keith Jarret.
References
Botias, C, et al (2011) Critical aspects of the Nosema spp. diagnostic sampling in honey bee (Apis mellifera L.) colonies. Parasitology Research (in press).
Fingler BG, WT Nash, and TI Szabo (1982) A comparison of two techniques for the measurement of nosema disease in honey bee colonies wintered in Alberta, Canada. ABJ 122(5):369-371.
Forsgren, E, and I Fries (2010) Comparative virulence of Nosema ceranae and Nosema apis in individual European honey bees. Veterinary Parasitology 170: 212-217.
Frazier, MT, et al (2000) A sequential sampling scheme for detecting infestation levels of tracheal mites (Heterostigmata: Tarsonemidae) in honey bee (Hymenoptera: Apidae) colonies. Journal of Economic Entomology 93(3):551-558.
Higes, M, et al (2008) How natural infection by Nosema ceranae causes honeybee colony collapse. Environ Microbiol 10: 2659-2669.
Mattila HR, and GW Otis (2007) Dwindling pollen resources trigger the transition to broodless populations of long-lived honeybees each autumn. Ecol Entomol 32:496-505.
Meana, A, et al (2010) The reliability of spore counts to diagnose Nosema ceranae infections in honey bees. Journal of Apicultural Research and Bee World 49(2): 212-214.
Moeller, F.E., 1956. The behavior of nosema infected bees affecting their position in the winter cluster. J. Econ. Entomol. 49 (6), 743-745.
Oliver, R (2008) The Nosema Twins Part 3: Sampling. ABJ 148(2): 149-154. https://scientificbeekeeping.com/the-nosema-twins-part-3-sampling/
Porrini, MP, et al (2011) Nosema ceranae development in Apis mellifera: influence of diet and infective inoculum. Journal of Apicultural Research 50(1): 35-41
Smart, MD and WS Sheppard (2011, in press) Nosema ceranae in age cohorts of the western honey bee (Apis mellifera). J. Invertebr. Pathol. doi:10.1016/j.jip.2011.09.009
Tomasko, M. Finley, J. Harkness, W. Rajotte, E. 1993. A sequential sampling scheme for detecting the presence of tracheal mite (Acarapis woodi) infestations in honey bee (Apis mellifera L.) colonies. Penn. State College of Agricultural Sciences, Agricultural Experiment Station Bulletin 871.
Traver, B., and RD Fell (2011a) Prevalence and infection intensity of Nosema in honey bee (Apis mellifera L.) colonies in Virginia. J Invertebr Pathol 107 (1):43-49.
Traver, BE MR Williams, and RD Fell (2011b; in press) Comparison of within hive sampling and seasonal activity of Nosema ceranae in honey bee colonies. Journal of Invertebrate Pathology.
White, GF (1919) Nosema-Disease. USDA Bulletin No. 780.
Category: Nosema Summaries and Updates, Sampling
Tags: infection, n. apis, N. ceranae, nosema apis, Nosema cereanae, squash | N. ceranae Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/n-ceranae/ |
Sick Bees - Part 16: The "Quick Squash" Method for Determining Nosema Prevalence in a Colony
Infection Prevalence
Sequential Sampling
A Neat Little Shortcut
Validation
Summary (completely subject to revision)
More Details
Next Month
Acknowledgements
References
2019 Quick Nosema Prevalence Assessment Method
First published in ABJ February 2012
Updated March 13, 2019
Randy Oliver
Since the discovery of Nosema ceranae, I and many other beekeepers and researchers have been frustrated by the tedium and apparent futility of counting nosema spores, since many of us haven't seen any meaningful relationship between spore counts and colony health or production. I strongly suspect that the issue is not that N. ceranae does not cause problems, but rather that our methodology for assessing the degree of infection has been flawed.
The quickest way that I've found to determine the degree of nosema infection in a hive is to do a 2-step sampling.
Step 1: open the hive and take a sample of about 50 workers from an outer frame, or from under the hive cover. These bees can be salvaged from an alcohol wash for varroa. Set at least 15 bees aside for the time being, and use the rest for the next step.
I now typically use only 10 bees. This is based upon the thorough research on Nosema apis by GF White in the early 1900s. What he found was that individually sampling 10 bees in order to determine the prevalence of nosema infection in the house bees gave the best indication of its biological relevance-a finding later suggested by Cameron Jack in Colony Level Prevalence and Intensity of Nosema ceranae in Honey Bees (Apis mellifera L.).
Be sure to read https://scientificbeekeeping.com/the-seasonality-of-nosema-ceranae/
Step 2: place at least 25 of the bees in a ziplock sandwich bag, and roll a round jar over them to crush their guts thoroughly. Then add about 3 mL of water for every 10 bees in the sample, and massage the bag in your fingers until you've homogenized all the gut contents into the water, creating a semi-opaque suspension (not too clear, not too thick). For details on this step, see https://scientificbeekeeping.com/sick-bees-part-13-simple-microscopy-of-nosema/
Step 3: immediately place a drop of the suspension on a slide, drop on a cover slip, and view under the scope. Scan a few fields of view for nosema spores. If you don't see any (or only one or two), that indicates that the infection prevalence of that sample of bees was zero-end of assessment.
On the other hand, if you see spores in the sample, then perform 10 individual bee gut squashes from the remaining bees in the original sample in order to determine the biological relevance of the infection prevalence in the colony-details below.
Infection Prevalence
The current "standard" method for monitoring nosema "level" in hives is to determine the mean spore count per bee in an aggregate sample (of typically 10-100 bees). The method is relatively quick and gives the sort of quantifiable numbers that scientists love. Unfortunately, as noted by Meana (2010), "the spore count is not directly related to the parasite burden and health status of whole colonies naturally infected by N. ceranae under field conditions."
Spore counts certainly have their uses, such as quantifying the progress of nosema infection in individual bees in cage trials by researchers. They are also appropriate as a method for "discovery sampling." For example, one can "discover" whether nosema is present to any extent in an apiary by taking an aggregate sample of say ten bees from the entrance of every hive and determining the mean spore count. If the count is less than 1M (1 million spores per bee), then nosema is likely not a problem in the sampled hives.
The point that I'm trying to make about sampling for nosema is that we are well beyond the "discovery" phase. Rennich (2011) found N. ceranae in at least half of all random bee samples taken in the U.S. during winter and spring.
So instead of "discovery" sampling, what we need to do is to shift to the most meaningful way to measure the potential impact of nosema upon colony health--the proportion of infected bees. Of the various terms used to describe this measure--"proportion of infected bees in a sample," "percent infected," or "infection rate"- I prefer the term used by epidemiologists: "prevalence."
Practical application: I henceforth plan to use the term "prevalence" as the measure of the proportion of bees infected by nosema. For example, if 2 bees out of 10 were infected, that would be a prevalence of 20%.
There is a strong case to be made for shifting our assessment of nosema infection from "intensity" (as measured by spore counts) to "prevalence" (the percent of bees actually infected). The only problem with determining prevalence is that most of us choke at the thought of having to inspect jillions of bees one at a time. Luckily, there are practical shortcuts:
Sequential Sampling
In my last article, I proposed that even a small sample of bees might be adequate for making management decisions. I'm immensely grateful to Dr. Jose Villa of the Baton Rouge Bee Lab for bringing to my attention that I was reinventing the wheel--this sort of decision making process, based upon small sample sizes, already has a fancy name: it's called "sequential sampling," and was develped as a time-saving method for quality control inspections during World War II. Furthermore, Dr. Villa dug into the library and forwarded me existing "Decision Tables" for tracheal mite sampling produced by Tomasko (1993).
Dr. Maryann Frazier (2000), following up on Tomasko's work, discussed the situation regarding the assement of tracheal mite prevalence as opposed to "parasite load" (analagous to spore counts). It is remarkable in that it almost exactly mirrors today's situation with nosema! And in her paper she validated the accuracy of sequential sampling.
Sequential sampling is all about the tradeoff between tedium (the number of bees that you need to squash and view) and confidence (the error rate which you are willing to accept). And it appears that for our purposes, I estimated the minimum number of bees to sample right on the nose!
So let's set some arbitrary parameters for our decision making:
An infection prevalence of 10% is "tolerable."
A prevalence of 30-40% is "intolerable."
We'll accept a 20% error rate for overestimating the prevalence.
But we won't accept an error rate above 10% for underestimating the prevalence.
We'll use the above parameters to set our treatment thresholds--below 10% prevalence, don't treat; above 30%, treat. The math gets complex, but here's the gist of the outcome:
Practical application: it appears that in order to make a decision whether to treat or not, that a couple of 5-bee samples should be adequate, interpreted as follows:
0 positive bees out of 5, or no more than 1 positive out of 10 indicates < 10% infection
3 positive bees out of 5, or at least 4 positives out of 10 indicates > 30% infection
Any number of positive bees lying between these cutoffs (e.g., 2 bees out of 5, or 3 out of 10) is not enough to make a firm decision, but suggests an infection level that lies in the gray zone. But I doubt that going beyond a 10-bee sample is worth the effort--I'd just move on to the next sample.
With true sequential sampling, you'd keep sampling until you hit a critical number of positive or negative bees in order to make a treatment decision. However, my limited experience suggests that we hit a point of diminishing returns after viewing 10 bees.
Update July 5, 2012 Beekeeper Ruary Rudd (ruaryrudd@iol.ie) has developed a great Excel spreadsheet for sequential sampling. You can write him for a copy-thanks Ruary!
So I've got us down to sampling a maximum of 10-bees. But even so, I must advise you that nosema infection appears to exist in "pockets" of bees in the hive, so any single small sample is inadequate for making an apiary-level decision (Botias 2011). Therefore, it's necessary to process a number of samples. What's been holding us back from determining actual nosema prevalence is the lack of a quick method for processing a number of samples of 10 bees!
Nosema apis becomes a serious problem if about a third of the bees in a hive become infected. It appears that Nosema ceranae may be a problem at even a lower prevalence.
A Neat Little Shortcut
Since I really wanted to find a quicker way to prepare and view the 200 bees for the validation table in the previous article, I racked my brain trying to figure out a technique for speeding things up, and finally hit upon a relatively simple procedure (Figures 1,2, and 3). I've now got over 400 individual gut squashes under my belt, and am pretty excited about the method! This solution allows me to process bees at an overall turnaround rate of less than five minutes per sample of 10 bees!
Figure 1. This photo shows the necessary equipment for a Quick Squash--5 bees, a plain microscope slide, 5 custom-made thin plastic cover slips, a table knife, and a paper towel.
The size of the cover slips is critical--they must be narrow enough not to touch at the edges, in order to keep the individual gut slurries from mixing. The easiest solution is to cut off-the-shelf plastic microscopy cover slips in half with scissors. You can then just discard them after use (cost about 20C//10-bee sample), or wash and reuse (use your mite shaker jar).
Update Feb 2019: I prefer to recycle rather than discard. But when I looked at costs, getting a large order of #1 thickness glass cover slips works out to only about a penny a slip. At Amazon: Karter Scientific 211Z2 Standard Microscope Cover Slip, #1 Thick, 22x22mm, 200pk (Case of 2000).
Be sure to order #1 thickness cover slips, since thicker cover slips won't allow you to focus upon the spores.
The other thing is that you don't need to make custom cover slips at all. Three standard glass cover slips will fit across a slide, and can be discarded after use if you don't want to wash them (although they wash easily in warm water with a tiny bit of dishwashing detergent).
But if you don't have plastic cover slips at hand, don't despair! You can make cover slips out of clear plastic scrap around the home--but only some plastics will work; I've experimented with several. Clear plastic transparency sheets unfortunately refract light in such a way that they make nosema spores look like little rectangles, so they don't fit the bill.
The heavy blister packs from the hardware store are too thick to focus through--a cover slip for 400x viewing needs to be thin. But then I found just the thing--the clear lid from a tub of the Colonel's Kentucky mashed potatoes (get the gravy too, so you get an extra lid). Cut it into 11mm x 22mm rectangles--they work perfectly! You can wash them in soapy water, rinse, blot, and reuse until they get scratchy.
Practical tip: Cut a whole bunch of cover slips and keep them in a custard dish for easy pick up--this greatly expedites the slide prep time. Look for thin clear plastic with the #1 recycling symbol for polyethylene terephthalate:
Beekeeper Health Breakthrough: Wracked as I was by images of beekeepers stuffing themselves with mashed potatoes in order to be able to monitor nosema levels, I forayed to the grocery to see if I could recommend a more healthful suggestion. To my great relief, I found that the rectangular containers for the nutritious "Baby Mixed Greens" are also made from PETE, and make excellent cover slips!
Figure 2. Hold a bee by the head/thorax, then use the table knife to "milk" the gut contents (or the gut itself) out of its abdomen directly onto the slide. Use the knife tip to mash the material in a droplet of water in order to distribute any spores into the macerate. Then remove any excess bee tissue, leaving a thin slurry (note the stinger and rectum on the slide, and on the towel to the right). Finally, place a cover slip over the drop of slurry. In this photo, I've completed two preps at the top (neither contained much pollen). I'm working on the third, which will make a more opaque slurry.
The technique of "milking" the bee's abdomen by rocking a flat blade from front to rear will quickly cause the discharge of the gut contents, or with increased pressure, the gut itself. It is critical to thoroughly crush and mash these in a little water--I wet the tip of the knife blade in a stream of water if necessary--until you create a cloudy, but not opaque, macerate. Tip: it's critical to be able to press the knife tip down flat against the slide, so work with the slide near the edge of a raised cutting board, so that your knuckles can drop below the work surface level. Be careful to keep the macerate on the portion of the slide that will be under each cover slip. Then be sure to flip off any thick chunks of excess tissue, especially the sting or any dark pieces of exoskeleton, or they will space the cover slip up too high. Clean the knife tip under running water, and wipe it on the dry towel between each bee. With practice, this entire process takes only a few seconds!
Repeat the process down the slide, exercising caution to wipe the blade thoroughly between bees, and not allowing any liquid to run from sample to sample. The separate cover slips keep the samples from mixing. After you've crushed and covered 5 gut samples, then fold the towel over the slide and press down firmly and evenly to set all the cover slips down flat, and to absorb any liquid that might otherwise get onto the microscope lens.
Figure 3. Presto--you now have a 5-bee gut sample ready to view under a scope. It's then a simple matter to glance at each of the samples in turn to check for nosema spores. This technique works for either freshly-killed or preserved bees.
At this point is really helps to have a scope with an adjustable stage (having turnable knobs to move the slide around). Then you can easily move from one cover slip to the next, and quickly scan up and down each slip if necessary. It's also very easy to see whether you've gotten nurse bees or foragers, since each gut squash clearly shows any contained pollen (Figs. 4 and 5).
Figure 4. Close up of the differences between squashes containing pollen (center) and those from without. This sample was taken from the entrance on a cold November morning with minimal flight. See the following photos for how the two left-hand squashes looked under the scope. Two out of 5 of these bees were infected.
Squashed bee guts, especially the midgut, are typically either free of nosema, or strongly infected, as above.
Figure 5. This is a view of the orange-colored center squash shown above. This bee is only moderately infected with Nosema ceranae, and the gut also contains some orange-centered rust fungus spores-which are unhealthy for bees to consume.
Figure 6. A close up from a gut packed full of "fried eggs." It took me a while, but I finally identified these spores as being from rust fungus.
It took me quite a while, but I eventually identified the "fried eggs" in the bees' guts as being spores from a blackberry rust fungus. In the photo above, you can see the fluorescent-orange spores packed as beebread-this is not pollen! The fungus tricks the bees into gathering its spores. Note the dying larvae next to this abundant beebread-although this colony appears to have abundant beebread, in fact, the fungal spores are unhealthy to the hive. In my area, hives full of such spores go downhill, unless we feed them all the pollen sub that they will eat. See "Fried Eggs" Identified!
Back to nosema sampling, one of the major beauties of the Quick Squash method is how quick it is, since you don't need to count spores at all (Fig. 7)!
Practical application: After a bit of practice, my turnaround time for the entire process of preparing, viewing, and recording results for 10 bees (two 5-bee slides) is just over four minutes if I don't fumble something along the way. Tip: have plenty of precut cover slips at hand in a small bowl.
Figure 7. This is a view of the far left-hand squash from an older bee, whose gut does not contain pollen. Even though the preparation looked nearly clear to the naked eye, it is easy to see the degree of nosema infection.
Viewing individual bees gives you a much better idea of just how greatly the gut contents of bees vary from bee to bee within the same hive! Sometimes each of the 5 gut contents look completely different. All that I can say is that bees have a lot of different things going on in their guts, and numerous infections, most of which I can't identify (Fig. 8).
Figure 8. This poor bee is suffering from both Nosema ceranae and what appears to be a Malpighamoeba mellificae infection (the larger oval cysts). Amoeba infection is not something that most beekeepers even consider, but I find it commonly in failing hives.
Malpighamoeba mellificae in the Malphigian tubules of bees ©️ Institut fur Saat - und Pflanzgut, Pflanzenschutzdienst und Bienen Abteilung Bienenkunde und Bienenschutz -
I'm not a microbiologist, and have trouble differentiating yeast cells in the gut from amoeba cysts. Here's a photo of beebread to which I added a weak sucrose solution, and allowed to ferment. I'm guessing that the cells between the pollen grains are yeasts. If anyone can help me, please let me know!
This method takes less time than a standard hemacytometer count, yet provides you far more useful information.
Economic analysis: A scope (which will last the rest of your life) costs less than the rental rate for two hives in almonds. You can easily run a dozen of these samples in an hour, which would give you a good idea of the infection rate for the weaker hives a 50-hive apiary. This method can quickly let you know if you have a serious nosema problem. On the other hand, bottle of fumagillin to unnecessarily treat those 50 hives would set you back $140, plus syrup and labor.
Update: time and again I've had beekeepers tell me that they've been trying to control dysentery by feeding fumagillin. When I ask them to send me bee samples, I often find that there is no nosema present, suggesting that they've been blaming the wrong suspect! As far as I can tell, nosema does not cause dysentery-this is a common misconception. Dysentery can spread nosema in the hive, but it doesn't appear to be an indicator of nosema.
There is nothing new about knowing that measuring the infection rate is a better assessment of nosema infection than that of taking spore counts--Dr. White made that clear back in 1919, and it has been confirmed again and again. The problem has always been that it is simply too tedious to individually squash hundreds of bees (Dr. White individually squashed and microscopically viewed over 3000 bees). What has always been lacking is a time-efficient way to determine the infection rate, and that is what I tried to develop with this "Quick Squash" method. Shy of an automated device, this method may be the best practical assessment of colony infection rate, and appears to have a reasonable degree of accuracy.
Validation
OK, so this past week I took samples from the strongest hives and from dinks in some of my yards, and have so far processed a total of 40 samples (I still have a backlog at press time, and favored the samples from weak hives). I've graphed the results below (Fig. 9):
Figure 9. Distribution of nosema prevalence in the weakest and strongest hives in my apiaries in early December, based upon 10-bee samples taken from under the lid or outside combs. In none of the strong hives were more than 1 bee out of 10 infected; whereas the majority of the weak hives scored at least 1 or more infected bees out of 10, and 40% scored 2 or more positives.
The preliminary data above strongly suggest that Nosema ceranae infection is associated with colony weakness in my own operation, which is not surprising, based upon the vast body of previous research on the negative effects of nosema! At this point in time, I am rather disillusioned with any field research findings based upon spore counts, and hope that other researchers follow the lead of Dr. Mariano Higes and include the percentage of infected bees.
Practical application: The point of the above graph is that up 'til this point, I have never been able to correlate N. ceranae infection intensity, based upon spore counts, with either colony health or production. But when I switched to a different assessment method--quantifying nosema prevalence based upon the number of infected bees in a sample of 10--the relationship jumps right out!
Summary (Completely Subject To Revision):
Early spring and early fall are likely the most appropriate times to sample, or during winter if you're going to almonds. No need to look for nosema in July or August, as it normally "disappears" during that time.
Take samples any time of year from any colonies or yards that appear to not be performing well--lagging, poor weight gain, lack of foragers or bees over the brood. I'm not sure whether it's worthwhile to routinely bother with taking nosema samples, provided that your colonies are not under stress, and so long as they are kicking butt.
Brush a dozen bees from under the lid or an outside comb into a ziplock bag, and add a glug of rubbing alcohol (for long-term storage use bottles and additional alcohol, or freeze). If you wish to label the sample, make sure the marker is alcohol resistant, or write with a pencil and put the label inside the bag.
(Alternate assessment) Process about 50 bees by the ziplock method (see Sick Bees Part 12). If you see fewer than about 5 spores in a field of view (about 1M equivalent), then you've got nothing to worry about. If more, go to the next step.
From each sample, prepare two slides of 5 bees each per the "Quick Squash" method in this article.
Interpret the entire 10-bee sample as follows:
0-1/10 positive for spores-likely safe
3/10-likely moderate infection
4/10-likely serious infection
>4/10- very likely serious
Be concerned any time that you hit 2 or more positive bees out of 5.
The odds of hitting 3 or more bees out of 10 climbs rapidly with infection rate--to a definitive 95% chance once half the bees in the hive are infected!
6. I feel that it is likely not worth the effort to sample more than 10 bees from any single hive-10 bees should give you a fairly close estimate of infection prevalence in that hive. Better to spend the time sampling more hives!
7. Important: don't base any management decisions upon only a single sample! Keep sampling until you are comfortable with the consistency of the results.
I realize that I just threw a lot of numbers at you, but in practice the method is really intuitive. It's very much like playing poker--your brain easily grasps the probabilities of getting either one ace or four in a hand. Chances are that you'll get more positive hits from colonies with a serious nosema infection, and few or no hits from healthy colonies.
Processing bee samples by this "Quick Squash" method offers an easy way for beekeepers to monitor whether nosema is actually a problem in their operations. It takes me less time to process a 10-bee sample than it does to do a single hemacytometer count, but the results of this method are much more meaningful from a practical standpoint. The "old school" researchers found this method to be a reliable assessment of the seriousness of nosema infection for N. apis; I suspect (subject to verification) that it may also prove to be the best for N. ceranae.
It sometimes seems that beekeepers need to reinvent the wheel. Anyway, I just came up with this quick method and really like it! My sons mastered the technique in a couple of tries. My favorite part is that I no longer need to count spores--a quick glance gives you a yes/no for infection. I'd be a happy guy if I never had to count another varroa mite or nosema spore--I'd much rather be counting all the money I'll be making from my healthy hives!
I feel that it is time for a paradigm shift in the way that we assess the impact of nosema infection upon colonies--moving from spore counting back to determining the proportion of infected bees! To that end, this method is practical and surprisingly quick, and gives you a much better idea of what's actually happening in the hive. I'd really appreciate hearing your results or suggestions for improvement if you try it (randy@randyoliver.com).
More Details--Web Version
I'm not looking to belabor the point of the reliability, or lack thereof, of spore counts, but I feel that this is an important enough issue to the beekeeping industry, in light of potential reduced honey production, increased colony mortality, and the cost of treatment, that interested beekeepers have a thorough understanding of the strong and weak points of various sampling methods.
The key question then is whether researchers, testing labs, and beekeepers can all agree upon a "standardized" method of testing, so that we can all compare results and recommendations. The current problem is that spore counts, even from the same colony, are frustratingly variable, depending upon the time of day at which the bee samples are taken (Fig. 1), the weather conditions, the place in the hive from which they are taken, the number of bees in the sample, how they are processed (mortar and pestle, filtration, squashing, etc.), how they are viewed (simple microscopy or hemacytometer), and even then counts are largely based upon the pure chance of whether or not one gets one or more highly-infected old bees in the sample!
Figure 1. Spore counts of four 25-bee samples taken each day from the same hive--from the entrance or the inside, and at either 9:30am or 12:30 pm. Note that counts on the same day varied from nearly zero to 10M spores--testament to the inherent variability of spore counts! It is also unlikely that the infection level varied as greatly from week to week as the data suggest. This finding really makes me question the comparability of spore counts unless they are taken at exactly the same time of day, under similar weather conditions, and from the same place in the hive each time! Data reworked from Meana (2010).
The colony sampled in Figure 1 was presumably moderately-infected, but in apparent good health. The researchers concluded, "This strong variation in the spore count was not associated with signs of illness and indeed, the colony was apparently as healthy (asymptomatic) as any other. It would thus appear that the spore count is not useful to measure the state of a colony's health [emphasis mine]." I echo this conclusion (as do a number of other studies), since while monitoring nosema counts in my own operation over the past four years, I have been unable to detect any correlation between spore counts and colony health, productivity, nor survival.
The above authors conclude that "the mean proportion of infected bees may be a more reliable method to establish colony health." This suggestion goes right back to Dr. White's findings at the beginning of the last century, and has withstood the test of time. I guarantee that looking at the individual gut contents of a sample of 10 bees gives one a much better feeling as to the severity of nosema infection in that hive!
From Where Should We Take Samples?
Figure 2. Spore counts vs. percent infection for house and field bees, n = 30 for each sample; all samples taken at 12:30pm. Data reworked from Higes (2008). Note that spore counts roughly reflect the percent infection rate for either group, but that spore counts of house bees may not be a particularly good indicator of the infection rate of field bees, which is likely the best assessment of the impact of nosema upon colony health. On the other hand, in this data set, the infection rates of both house and field bees roughly tracked each other. This data set suggests that spore counts of field bees is the most sensitive measure of the degree of nosema infection in a hive.
Experts' Opinions
Smart and Sheppard (2011) concluded that: "Based on these findings, we speculate that bees collected from the inner hive cover represent a mixture of age classes of bees and, depending on the goals of the sampler, may provide a better estimate of the whole colony mean infection level than sampling just foragers.
So I asked Dr. Brian Johnson, who had considerable experience with tracking bees in observation hives. He told me:
"The bees just under the lid tend to be older middle age bees, while the bees on the outside combs are mostly middle age bees with smaller numbers of nurses and foragers. In general, the foragers are near the entrance, the nurses are in the brood zone, and the middle age bees are everywhere, but with a slight bias for the honey zone."
I also asked the preeminent bee behavioralist, Dr. Tom Seeley. His response:
"Interesting question. The only information that I have regarding the age distribution of bees who are spending time just under the lid or on one of the outer combs (i.e., ones without brood) comes from a study that I did back in 1982. In it, I mapped out the locations (in a large observation hive) of various activities and at the same time I took data on the age distributions of the bees performing these tasks. These results make it clear that the middle-aged bees are mainly working in the peripheral (outside the brood nest) regions of the nest. So if bees are collected from these areas during the day, then they will be mainly middle-age and forager-age bees. At night, the percentage of forager-age bees will be higher. You've probably seen in observation hives how the foragers literally hang out in the edge areas of a hive at night."
Finally, there is one more piece of supportive evidence for taking samples from under the lid: Moeller (1956) found that "nosema-infected bees congregate in and above warm brood areas."
Conclusions
Hey, I'll leave the conclusions up to you. Today, I did some spore counts of 20-bee samples of piles dead bees from the front of three hives in one yard. They had little nosema--about 5 spores per field of view, so approx. 1M/bee. So not enough spores to indicate that a 10-bee squash would be useful. Since the bees were dead, it would have entailed rehydration in order to do gut squashes.
I also did some Quick Squashes of bees from under the lid for other hives. Each method has its advantages and limitations. The smart beekeeper understands them!
Next Month
Nosema: The Smoldering Epidemic
Acknowledgements
I wish to thank my wife Stephanie for her patience, and helpful comments on my manuscripts (she chokes on math and graphs, and is immensely helpful to me for making my charts more user friendly). As always Peter Borst helped with the research for this article. A special thanks to Dr. Jose Villa, as mentioned previously. Thanks to Dr. Jerry Bromenshenk for his helpful suggestions. And a big thanks to Drs. Mariano Higes, Aranzazu Meana, and Raquel Martin-Hernandez for their diligent work on nosema! For financial support toward this research, I've very appreciative of Joe Traynor, Heitkam's Honey Bees, Jester Bee Company, the Virginia State Beekeepers Assoc, and individual beekeepers Paul Limbach, Chris Moore, and Keith Jarret.
References
Botias, C, et al (2011) Critical aspects of the Nosema spp. diagnostic sampling in honey bee (Apis mellifera L.) colonies. Parasitology Research (in press).
Fingler BG, WT Nash, and TI Szabo (1982) A comparison of two techniques for the measurement of nosema disease in honey bee colonies wintered in Alberta, Canada. ABJ 122(5):369-371.
Forsgren, E, and I Fries (2010) Comparative virulence of Nosema ceranae and Nosema apis in individual European honey bees. Veterinary Parasitology 170: 212-217.
Frazier, MT, et al (2000) A sequential sampling scheme for detecting infestation levels of tracheal mites (Heterostigmata: Tarsonemidae) in honey bee (Hymenoptera: Apidae) colonies. Journal of Economic Entomology 93(3):551-558.
Higes, M, et al (2008) How natural infection by Nosema ceranae causes honeybee colony collapse. Environ Microbiol 10: 2659-2669.
Mattila HR, and GW Otis (2007) Dwindling pollen resources trigger the transition to broodless populations of long-lived honeybees each autumn. Ecol Entomol 32:496-505.
Meana, A, et al (2010) The reliability of spore counts to diagnose Nosema ceranae infections in honey bees. Journal of Apicultural Research and Bee World 49(2): 212-214.
Moeller, F.E., 1956. The behavior of nosema infected bees affecting their position in the winter cluster. J. Econ. Entomol. 49 (6), 743-745.
Oliver, R (2008) The Nosema Twins Part 3: Sampling. ABJ 148(2): 149-154. https://scientificbeekeeping.com/the-nosema-twins-part-3-sampling/
Porrini, MP, et al (2011) Nosema ceranae development in Apis mellifera: influence of diet and infective inoculum. Journal of Apicultural Research 50(1): 35-41
Smart, MD and WS Sheppard (2011, in press) Nosema ceranae in age cohorts of the western honey bee (Apis mellifera). J. Invertebr. Pathol. doi:10.1016/j.jip.2011.09.009
Tomasko, M. Finley, J. Harkness, W. Rajotte, E. 1993. A sequential sampling scheme for detecting the presence of tracheal mite (Acarapis woodi) infestations in honey bee (Apis mellifera L.) colonies. Penn. State College of Agricultural Sciences, Agricultural Experiment Station Bulletin 871.
Traver, B., and RD Fell (2011a) Prevalence and infection intensity of Nosema in honey bee (Apis mellifera L.) colonies in Virginia. J Invertebr Pathol 107 (1):43-49.
Traver, BE MR Williams, and RD Fell (2011b; in press) Comparison of within hive sampling and seasonal activity of Nosema ceranae in honey bee colonies. Journal of Invertebrate Pathology.
White, GF (1919) Nosema-Disease. USDA Bulletin No. 780.
Category: Nosema Summaries and Updates, Sampling
Tags: infection, n. apis, N. ceranae, nosema apis, Nosema cereanae, squash | n. apis Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/n-apis/ |
Sick Bees - Part 16: The "Quick Squash" Method for Determining Nosema Prevalence in a Colony
Infection Prevalence
Sequential Sampling
A Neat Little Shortcut
Validation
Summary (completely subject to revision)
More Details
Next Month
Acknowledgements
References
2019 Quick Nosema Prevalence Assessment Method
First published in ABJ February 2012
Updated March 13, 2019
Randy Oliver
Since the discovery of Nosema ceranae, I and many other beekeepers and researchers have been frustrated by the tedium and apparent futility of counting nosema spores, since many of us haven't seen any meaningful relationship between spore counts and colony health or production. I strongly suspect that the issue is not that N. ceranae does not cause problems, but rather that our methodology for assessing the degree of infection has been flawed.
The quickest way that I've found to determine the degree of nosema infection in a hive is to do a 2-step sampling.
Step 1: open the hive and take a sample of about 50 workers from an outer frame, or from under the hive cover. These bees can be salvaged from an alcohol wash for varroa. Set at least 15 bees aside for the time being, and use the rest for the next step.
I now typically use only 10 bees. This is based upon the thorough research on Nosema apis by GF White in the early 1900s. What he found was that individually sampling 10 bees in order to determine the prevalence of nosema infection in the house bees gave the best indication of its biological relevance-a finding later suggested by Cameron Jack in Colony Level Prevalence and Intensity of Nosema ceranae in Honey Bees (Apis mellifera L.).
Be sure to read https://scientificbeekeeping.com/the-seasonality-of-nosema-ceranae/
Step 2: place at least 25 of the bees in a ziplock sandwich bag, and roll a round jar over them to crush their guts thoroughly. Then add about 3 mL of water for every 10 bees in the sample, and massage the bag in your fingers until you've homogenized all the gut contents into the water, creating a semi-opaque suspension (not too clear, not too thick). For details on this step, see https://scientificbeekeeping.com/sick-bees-part-13-simple-microscopy-of-nosema/
Step 3: immediately place a drop of the suspension on a slide, drop on a cover slip, and view under the scope. Scan a few fields of view for nosema spores. If you don't see any (or only one or two), that indicates that the infection prevalence of that sample of bees was zero-end of assessment.
On the other hand, if you see spores in the sample, then perform 10 individual bee gut squashes from the remaining bees in the original sample in order to determine the biological relevance of the infection prevalence in the colony-details below.
Infection Prevalence
The current "standard" method for monitoring nosema "level" in hives is to determine the mean spore count per bee in an aggregate sample (of typically 10-100 bees). The method is relatively quick and gives the sort of quantifiable numbers that scientists love. Unfortunately, as noted by Meana (2010), "the spore count is not directly related to the parasite burden and health status of whole colonies naturally infected by N. ceranae under field conditions."
Spore counts certainly have their uses, such as quantifying the progress of nosema infection in individual bees in cage trials by researchers. They are also appropriate as a method for "discovery sampling." For example, one can "discover" whether nosema is present to any extent in an apiary by taking an aggregate sample of say ten bees from the entrance of every hive and determining the mean spore count. If the count is less than 1M (1 million spores per bee), then nosema is likely not a problem in the sampled hives.
The point that I'm trying to make about sampling for nosema is that we are well beyond the "discovery" phase. Rennich (2011) found N. ceranae in at least half of all random bee samples taken in the U.S. during winter and spring.
So instead of "discovery" sampling, what we need to do is to shift to the most meaningful way to measure the potential impact of nosema upon colony health--the proportion of infected bees. Of the various terms used to describe this measure--"proportion of infected bees in a sample," "percent infected," or "infection rate"- I prefer the term used by epidemiologists: "prevalence."
Practical application: I henceforth plan to use the term "prevalence" as the measure of the proportion of bees infected by nosema. For example, if 2 bees out of 10 were infected, that would be a prevalence of 20%.
There is a strong case to be made for shifting our assessment of nosema infection from "intensity" (as measured by spore counts) to "prevalence" (the percent of bees actually infected). The only problem with determining prevalence is that most of us choke at the thought of having to inspect jillions of bees one at a time. Luckily, there are practical shortcuts:
Sequential Sampling
In my last article, I proposed that even a small sample of bees might be adequate for making management decisions. I'm immensely grateful to Dr. Jose Villa of the Baton Rouge Bee Lab for bringing to my attention that I was reinventing the wheel--this sort of decision making process, based upon small sample sizes, already has a fancy name: it's called "sequential sampling," and was develped as a time-saving method for quality control inspections during World War II. Furthermore, Dr. Villa dug into the library and forwarded me existing "Decision Tables" for tracheal mite sampling produced by Tomasko (1993).
Dr. Maryann Frazier (2000), following up on Tomasko's work, discussed the situation regarding the assement of tracheal mite prevalence as opposed to "parasite load" (analagous to spore counts). It is remarkable in that it almost exactly mirrors today's situation with nosema! And in her paper she validated the accuracy of sequential sampling.
Sequential sampling is all about the tradeoff between tedium (the number of bees that you need to squash and view) and confidence (the error rate which you are willing to accept). And it appears that for our purposes, I estimated the minimum number of bees to sample right on the nose!
So let's set some arbitrary parameters for our decision making:
An infection prevalence of 10% is "tolerable."
A prevalence of 30-40% is "intolerable."
We'll accept a 20% error rate for overestimating the prevalence.
But we won't accept an error rate above 10% for underestimating the prevalence.
We'll use the above parameters to set our treatment thresholds--below 10% prevalence, don't treat; above 30%, treat. The math gets complex, but here's the gist of the outcome:
Practical application: it appears that in order to make a decision whether to treat or not, that a couple of 5-bee samples should be adequate, interpreted as follows:
0 positive bees out of 5, or no more than 1 positive out of 10 indicates < 10% infection
3 positive bees out of 5, or at least 4 positives out of 10 indicates > 30% infection
Any number of positive bees lying between these cutoffs (e.g., 2 bees out of 5, or 3 out of 10) is not enough to make a firm decision, but suggests an infection level that lies in the gray zone. But I doubt that going beyond a 10-bee sample is worth the effort--I'd just move on to the next sample.
With true sequential sampling, you'd keep sampling until you hit a critical number of positive or negative bees in order to make a treatment decision. However, my limited experience suggests that we hit a point of diminishing returns after viewing 10 bees.
Update July 5, 2012 Beekeeper Ruary Rudd (ruaryrudd@iol.ie) has developed a great Excel spreadsheet for sequential sampling. You can write him for a copy-thanks Ruary!
So I've got us down to sampling a maximum of 10-bees. But even so, I must advise you that nosema infection appears to exist in "pockets" of bees in the hive, so any single small sample is inadequate for making an apiary-level decision (Botias 2011). Therefore, it's necessary to process a number of samples. What's been holding us back from determining actual nosema prevalence is the lack of a quick method for processing a number of samples of 10 bees!
Nosema apis becomes a serious problem if about a third of the bees in a hive become infected. It appears that Nosema ceranae may be a problem at even a lower prevalence.
A Neat Little Shortcut
Since I really wanted to find a quicker way to prepare and view the 200 bees for the validation table in the previous article, I racked my brain trying to figure out a technique for speeding things up, and finally hit upon a relatively simple procedure (Figures 1,2, and 3). I've now got over 400 individual gut squashes under my belt, and am pretty excited about the method! This solution allows me to process bees at an overall turnaround rate of less than five minutes per sample of 10 bees!
Figure 1. This photo shows the necessary equipment for a Quick Squash--5 bees, a plain microscope slide, 5 custom-made thin plastic cover slips, a table knife, and a paper towel.
The size of the cover slips is critical--they must be narrow enough not to touch at the edges, in order to keep the individual gut slurries from mixing. The easiest solution is to cut off-the-shelf plastic microscopy cover slips in half with scissors. You can then just discard them after use (cost about 20C//10-bee sample), or wash and reuse (use your mite shaker jar).
Update Feb 2019: I prefer to recycle rather than discard. But when I looked at costs, getting a large order of #1 thickness glass cover slips works out to only about a penny a slip. At Amazon: Karter Scientific 211Z2 Standard Microscope Cover Slip, #1 Thick, 22x22mm, 200pk (Case of 2000).
Be sure to order #1 thickness cover slips, since thicker cover slips won't allow you to focus upon the spores.
The other thing is that you don't need to make custom cover slips at all. Three standard glass cover slips will fit across a slide, and can be discarded after use if you don't want to wash them (although they wash easily in warm water with a tiny bit of dishwashing detergent).
But if you don't have plastic cover slips at hand, don't despair! You can make cover slips out of clear plastic scrap around the home--but only some plastics will work; I've experimented with several. Clear plastic transparency sheets unfortunately refract light in such a way that they make nosema spores look like little rectangles, so they don't fit the bill.
The heavy blister packs from the hardware store are too thick to focus through--a cover slip for 400x viewing needs to be thin. But then I found just the thing--the clear lid from a tub of the Colonel's Kentucky mashed potatoes (get the gravy too, so you get an extra lid). Cut it into 11mm x 22mm rectangles--they work perfectly! You can wash them in soapy water, rinse, blot, and reuse until they get scratchy.
Practical tip: Cut a whole bunch of cover slips and keep them in a custard dish for easy pick up--this greatly expedites the slide prep time. Look for thin clear plastic with the #1 recycling symbol for polyethylene terephthalate:
Beekeeper Health Breakthrough: Wracked as I was by images of beekeepers stuffing themselves with mashed potatoes in order to be able to monitor nosema levels, I forayed to the grocery to see if I could recommend a more healthful suggestion. To my great relief, I found that the rectangular containers for the nutritious "Baby Mixed Greens" are also made from PETE, and make excellent cover slips!
Figure 2. Hold a bee by the head/thorax, then use the table knife to "milk" the gut contents (or the gut itself) out of its abdomen directly onto the slide. Use the knife tip to mash the material in a droplet of water in order to distribute any spores into the macerate. Then remove any excess bee tissue, leaving a thin slurry (note the stinger and rectum on the slide, and on the towel to the right). Finally, place a cover slip over the drop of slurry. In this photo, I've completed two preps at the top (neither contained much pollen). I'm working on the third, which will make a more opaque slurry.
The technique of "milking" the bee's abdomen by rocking a flat blade from front to rear will quickly cause the discharge of the gut contents, or with increased pressure, the gut itself. It is critical to thoroughly crush and mash these in a little water--I wet the tip of the knife blade in a stream of water if necessary--until you create a cloudy, but not opaque, macerate. Tip: it's critical to be able to press the knife tip down flat against the slide, so work with the slide near the edge of a raised cutting board, so that your knuckles can drop below the work surface level. Be careful to keep the macerate on the portion of the slide that will be under each cover slip. Then be sure to flip off any thick chunks of excess tissue, especially the sting or any dark pieces of exoskeleton, or they will space the cover slip up too high. Clean the knife tip under running water, and wipe it on the dry towel between each bee. With practice, this entire process takes only a few seconds!
Repeat the process down the slide, exercising caution to wipe the blade thoroughly between bees, and not allowing any liquid to run from sample to sample. The separate cover slips keep the samples from mixing. After you've crushed and covered 5 gut samples, then fold the towel over the slide and press down firmly and evenly to set all the cover slips down flat, and to absorb any liquid that might otherwise get onto the microscope lens.
Figure 3. Presto--you now have a 5-bee gut sample ready to view under a scope. It's then a simple matter to glance at each of the samples in turn to check for nosema spores. This technique works for either freshly-killed or preserved bees.
At this point is really helps to have a scope with an adjustable stage (having turnable knobs to move the slide around). Then you can easily move from one cover slip to the next, and quickly scan up and down each slip if necessary. It's also very easy to see whether you've gotten nurse bees or foragers, since each gut squash clearly shows any contained pollen (Figs. 4 and 5).
Figure 4. Close up of the differences between squashes containing pollen (center) and those from without. This sample was taken from the entrance on a cold November morning with minimal flight. See the following photos for how the two left-hand squashes looked under the scope. Two out of 5 of these bees were infected.
Squashed bee guts, especially the midgut, are typically either free of nosema, or strongly infected, as above.
Figure 5. This is a view of the orange-colored center squash shown above. This bee is only moderately infected with Nosema ceranae, and the gut also contains some orange-centered rust fungus spores-which are unhealthy for bees to consume.
Figure 6. A close up from a gut packed full of "fried eggs." It took me a while, but I finally identified these spores as being from rust fungus.
It took me quite a while, but I eventually identified the "fried eggs" in the bees' guts as being spores from a blackberry rust fungus. In the photo above, you can see the fluorescent-orange spores packed as beebread-this is not pollen! The fungus tricks the bees into gathering its spores. Note the dying larvae next to this abundant beebread-although this colony appears to have abundant beebread, in fact, the fungal spores are unhealthy to the hive. In my area, hives full of such spores go downhill, unless we feed them all the pollen sub that they will eat. See "Fried Eggs" Identified!
Back to nosema sampling, one of the major beauties of the Quick Squash method is how quick it is, since you don't need to count spores at all (Fig. 7)!
Practical application: After a bit of practice, my turnaround time for the entire process of preparing, viewing, and recording results for 10 bees (two 5-bee slides) is just over four minutes if I don't fumble something along the way. Tip: have plenty of precut cover slips at hand in a small bowl.
Figure 7. This is a view of the far left-hand squash from an older bee, whose gut does not contain pollen. Even though the preparation looked nearly clear to the naked eye, it is easy to see the degree of nosema infection.
Viewing individual bees gives you a much better idea of just how greatly the gut contents of bees vary from bee to bee within the same hive! Sometimes each of the 5 gut contents look completely different. All that I can say is that bees have a lot of different things going on in their guts, and numerous infections, most of which I can't identify (Fig. 8).
Figure 8. This poor bee is suffering from both Nosema ceranae and what appears to be a Malpighamoeba mellificae infection (the larger oval cysts). Amoeba infection is not something that most beekeepers even consider, but I find it commonly in failing hives.
Malpighamoeba mellificae in the Malphigian tubules of bees ©️ Institut fur Saat - und Pflanzgut, Pflanzenschutzdienst und Bienen Abteilung Bienenkunde und Bienenschutz -
I'm not a microbiologist, and have trouble differentiating yeast cells in the gut from amoeba cysts. Here's a photo of beebread to which I added a weak sucrose solution, and allowed to ferment. I'm guessing that the cells between the pollen grains are yeasts. If anyone can help me, please let me know!
This method takes less time than a standard hemacytometer count, yet provides you far more useful information.
Economic analysis: A scope (which will last the rest of your life) costs less than the rental rate for two hives in almonds. You can easily run a dozen of these samples in an hour, which would give you a good idea of the infection rate for the weaker hives a 50-hive apiary. This method can quickly let you know if you have a serious nosema problem. On the other hand, bottle of fumagillin to unnecessarily treat those 50 hives would set you back $140, plus syrup and labor.
Update: time and again I've had beekeepers tell me that they've been trying to control dysentery by feeding fumagillin. When I ask them to send me bee samples, I often find that there is no nosema present, suggesting that they've been blaming the wrong suspect! As far as I can tell, nosema does not cause dysentery-this is a common misconception. Dysentery can spread nosema in the hive, but it doesn't appear to be an indicator of nosema.
There is nothing new about knowing that measuring the infection rate is a better assessment of nosema infection than that of taking spore counts--Dr. White made that clear back in 1919, and it has been confirmed again and again. The problem has always been that it is simply too tedious to individually squash hundreds of bees (Dr. White individually squashed and microscopically viewed over 3000 bees). What has always been lacking is a time-efficient way to determine the infection rate, and that is what I tried to develop with this "Quick Squash" method. Shy of an automated device, this method may be the best practical assessment of colony infection rate, and appears to have a reasonable degree of accuracy.
Validation
OK, so this past week I took samples from the strongest hives and from dinks in some of my yards, and have so far processed a total of 40 samples (I still have a backlog at press time, and favored the samples from weak hives). I've graphed the results below (Fig. 9):
Figure 9. Distribution of nosema prevalence in the weakest and strongest hives in my apiaries in early December, based upon 10-bee samples taken from under the lid or outside combs. In none of the strong hives were more than 1 bee out of 10 infected; whereas the majority of the weak hives scored at least 1 or more infected bees out of 10, and 40% scored 2 or more positives.
The preliminary data above strongly suggest that Nosema ceranae infection is associated with colony weakness in my own operation, which is not surprising, based upon the vast body of previous research on the negative effects of nosema! At this point in time, I am rather disillusioned with any field research findings based upon spore counts, and hope that other researchers follow the lead of Dr. Mariano Higes and include the percentage of infected bees.
Practical application: The point of the above graph is that up 'til this point, I have never been able to correlate N. ceranae infection intensity, based upon spore counts, with either colony health or production. But when I switched to a different assessment method--quantifying nosema prevalence based upon the number of infected bees in a sample of 10--the relationship jumps right out!
Summary (Completely Subject To Revision):
Early spring and early fall are likely the most appropriate times to sample, or during winter if you're going to almonds. No need to look for nosema in July or August, as it normally "disappears" during that time.
Take samples any time of year from any colonies or yards that appear to not be performing well--lagging, poor weight gain, lack of foragers or bees over the brood. I'm not sure whether it's worthwhile to routinely bother with taking nosema samples, provided that your colonies are not under stress, and so long as they are kicking butt.
Brush a dozen bees from under the lid or an outside comb into a ziplock bag, and add a glug of rubbing alcohol (for long-term storage use bottles and additional alcohol, or freeze). If you wish to label the sample, make sure the marker is alcohol resistant, or write with a pencil and put the label inside the bag.
(Alternate assessment) Process about 50 bees by the ziplock method (see Sick Bees Part 12). If you see fewer than about 5 spores in a field of view (about 1M equivalent), then you've got nothing to worry about. If more, go to the next step.
From each sample, prepare two slides of 5 bees each per the "Quick Squash" method in this article.
Interpret the entire 10-bee sample as follows:
0-1/10 positive for spores-likely safe
3/10-likely moderate infection
4/10-likely serious infection
>4/10- very likely serious
Be concerned any time that you hit 2 or more positive bees out of 5.
The odds of hitting 3 or more bees out of 10 climbs rapidly with infection rate--to a definitive 95% chance once half the bees in the hive are infected!
6. I feel that it is likely not worth the effort to sample more than 10 bees from any single hive-10 bees should give you a fairly close estimate of infection prevalence in that hive. Better to spend the time sampling more hives!
7. Important: don't base any management decisions upon only a single sample! Keep sampling until you are comfortable with the consistency of the results.
I realize that I just threw a lot of numbers at you, but in practice the method is really intuitive. It's very much like playing poker--your brain easily grasps the probabilities of getting either one ace or four in a hand. Chances are that you'll get more positive hits from colonies with a serious nosema infection, and few or no hits from healthy colonies.
Processing bee samples by this "Quick Squash" method offers an easy way for beekeepers to monitor whether nosema is actually a problem in their operations. It takes me less time to process a 10-bee sample than it does to do a single hemacytometer count, but the results of this method are much more meaningful from a practical standpoint. The "old school" researchers found this method to be a reliable assessment of the seriousness of nosema infection for N. apis; I suspect (subject to verification) that it may also prove to be the best for N. ceranae.
It sometimes seems that beekeepers need to reinvent the wheel. Anyway, I just came up with this quick method and really like it! My sons mastered the technique in a couple of tries. My favorite part is that I no longer need to count spores--a quick glance gives you a yes/no for infection. I'd be a happy guy if I never had to count another varroa mite or nosema spore--I'd much rather be counting all the money I'll be making from my healthy hives!
I feel that it is time for a paradigm shift in the way that we assess the impact of nosema infection upon colonies--moving from spore counting back to determining the proportion of infected bees! To that end, this method is practical and surprisingly quick, and gives you a much better idea of what's actually happening in the hive. I'd really appreciate hearing your results or suggestions for improvement if you try it (randy@randyoliver.com).
More Details--Web Version
I'm not looking to belabor the point of the reliability, or lack thereof, of spore counts, but I feel that this is an important enough issue to the beekeeping industry, in light of potential reduced honey production, increased colony mortality, and the cost of treatment, that interested beekeepers have a thorough understanding of the strong and weak points of various sampling methods.
The key question then is whether researchers, testing labs, and beekeepers can all agree upon a "standardized" method of testing, so that we can all compare results and recommendations. The current problem is that spore counts, even from the same colony, are frustratingly variable, depending upon the time of day at which the bee samples are taken (Fig. 1), the weather conditions, the place in the hive from which they are taken, the number of bees in the sample, how they are processed (mortar and pestle, filtration, squashing, etc.), how they are viewed (simple microscopy or hemacytometer), and even then counts are largely based upon the pure chance of whether or not one gets one or more highly-infected old bees in the sample!
Figure 1. Spore counts of four 25-bee samples taken each day from the same hive--from the entrance or the inside, and at either 9:30am or 12:30 pm. Note that counts on the same day varied from nearly zero to 10M spores--testament to the inherent variability of spore counts! It is also unlikely that the infection level varied as greatly from week to week as the data suggest. This finding really makes me question the comparability of spore counts unless they are taken at exactly the same time of day, under similar weather conditions, and from the same place in the hive each time! Data reworked from Meana (2010).
The colony sampled in Figure 1 was presumably moderately-infected, but in apparent good health. The researchers concluded, "This strong variation in the spore count was not associated with signs of illness and indeed, the colony was apparently as healthy (asymptomatic) as any other. It would thus appear that the spore count is not useful to measure the state of a colony's health [emphasis mine]." I echo this conclusion (as do a number of other studies), since while monitoring nosema counts in my own operation over the past four years, I have been unable to detect any correlation between spore counts and colony health, productivity, nor survival.
The above authors conclude that "the mean proportion of infected bees may be a more reliable method to establish colony health." This suggestion goes right back to Dr. White's findings at the beginning of the last century, and has withstood the test of time. I guarantee that looking at the individual gut contents of a sample of 10 bees gives one a much better feeling as to the severity of nosema infection in that hive!
From Where Should We Take Samples?
Figure 2. Spore counts vs. percent infection for house and field bees, n = 30 for each sample; all samples taken at 12:30pm. Data reworked from Higes (2008). Note that spore counts roughly reflect the percent infection rate for either group, but that spore counts of house bees may not be a particularly good indicator of the infection rate of field bees, which is likely the best assessment of the impact of nosema upon colony health. On the other hand, in this data set, the infection rates of both house and field bees roughly tracked each other. This data set suggests that spore counts of field bees is the most sensitive measure of the degree of nosema infection in a hive.
Experts' Opinions
Smart and Sheppard (2011) concluded that: "Based on these findings, we speculate that bees collected from the inner hive cover represent a mixture of age classes of bees and, depending on the goals of the sampler, may provide a better estimate of the whole colony mean infection level than sampling just foragers.
So I asked Dr. Brian Johnson, who had considerable experience with tracking bees in observation hives. He told me:
"The bees just under the lid tend to be older middle age bees, while the bees on the outside combs are mostly middle age bees with smaller numbers of nurses and foragers. In general, the foragers are near the entrance, the nurses are in the brood zone, and the middle age bees are everywhere, but with a slight bias for the honey zone."
I also asked the preeminent bee behavioralist, Dr. Tom Seeley. His response:
"Interesting question. The only information that I have regarding the age distribution of bees who are spending time just under the lid or on one of the outer combs (i.e., ones without brood) comes from a study that I did back in 1982. In it, I mapped out the locations (in a large observation hive) of various activities and at the same time I took data on the age distributions of the bees performing these tasks. These results make it clear that the middle-aged bees are mainly working in the peripheral (outside the brood nest) regions of the nest. So if bees are collected from these areas during the day, then they will be mainly middle-age and forager-age bees. At night, the percentage of forager-age bees will be higher. You've probably seen in observation hives how the foragers literally hang out in the edge areas of a hive at night."
Finally, there is one more piece of supportive evidence for taking samples from under the lid: Moeller (1956) found that "nosema-infected bees congregate in and above warm brood areas."
Conclusions
Hey, I'll leave the conclusions up to you. Today, I did some spore counts of 20-bee samples of piles dead bees from the front of three hives in one yard. They had little nosema--about 5 spores per field of view, so approx. 1M/bee. So not enough spores to indicate that a 10-bee squash would be useful. Since the bees were dead, it would have entailed rehydration in order to do gut squashes.
I also did some Quick Squashes of bees from under the lid for other hives. Each method has its advantages and limitations. The smart beekeeper understands them!
Next Month
Nosema: The Smoldering Epidemic
Acknowledgements
I wish to thank my wife Stephanie for her patience, and helpful comments on my manuscripts (she chokes on math and graphs, and is immensely helpful to me for making my charts more user friendly). As always Peter Borst helped with the research for this article. A special thanks to Dr. Jose Villa, as mentioned previously. Thanks to Dr. Jerry Bromenshenk for his helpful suggestions. And a big thanks to Drs. Mariano Higes, Aranzazu Meana, and Raquel Martin-Hernandez for their diligent work on nosema! For financial support toward this research, I've very appreciative of Joe Traynor, Heitkam's Honey Bees, Jester Bee Company, the Virginia State Beekeepers Assoc, and individual beekeepers Paul Limbach, Chris Moore, and Keith Jarret.
References
Botias, C, et al (2011) Critical aspects of the Nosema spp. diagnostic sampling in honey bee (Apis mellifera L.) colonies. Parasitology Research (in press).
Fingler BG, WT Nash, and TI Szabo (1982) A comparison of two techniques for the measurement of nosema disease in honey bee colonies wintered in Alberta, Canada. ABJ 122(5):369-371.
Forsgren, E, and I Fries (2010) Comparative virulence of Nosema ceranae and Nosema apis in individual European honey bees. Veterinary Parasitology 170: 212-217.
Frazier, MT, et al (2000) A sequential sampling scheme for detecting infestation levels of tracheal mites (Heterostigmata: Tarsonemidae) in honey bee (Hymenoptera: Apidae) colonies. Journal of Economic Entomology 93(3):551-558.
Higes, M, et al (2008) How natural infection by Nosema ceranae causes honeybee colony collapse. Environ Microbiol 10: 2659-2669.
Mattila HR, and GW Otis (2007) Dwindling pollen resources trigger the transition to broodless populations of long-lived honeybees each autumn. Ecol Entomol 32:496-505.
Meana, A, et al (2010) The reliability of spore counts to diagnose Nosema ceranae infections in honey bees. Journal of Apicultural Research and Bee World 49(2): 212-214.
Moeller, F.E., 1956. The behavior of nosema infected bees affecting their position in the winter cluster. J. Econ. Entomol. 49 (6), 743-745.
Oliver, R (2008) The Nosema Twins Part 3: Sampling. ABJ 148(2): 149-154. https://scientificbeekeeping.com/the-nosema-twins-part-3-sampling/
Porrini, MP, et al (2011) Nosema ceranae development in Apis mellifera: influence of diet and infective inoculum. Journal of Apicultural Research 50(1): 35-41
Smart, MD and WS Sheppard (2011, in press) Nosema ceranae in age cohorts of the western honey bee (Apis mellifera). J. Invertebr. Pathol. doi:10.1016/j.jip.2011.09.009
Tomasko, M. Finley, J. Harkness, W. Rajotte, E. 1993. A sequential sampling scheme for detecting the presence of tracheal mite (Acarapis woodi) infestations in honey bee (Apis mellifera L.) colonies. Penn. State College of Agricultural Sciences, Agricultural Experiment Station Bulletin 871.
Traver, B., and RD Fell (2011a) Prevalence and infection intensity of Nosema in honey bee (Apis mellifera L.) colonies in Virginia. J Invertebr Pathol 107 (1):43-49.
Traver, BE MR Williams, and RD Fell (2011b; in press) Comparison of within hive sampling and seasonal activity of Nosema ceranae in honey bee colonies. Journal of Invertebrate Pathology.
White, GF (1919) Nosema-Disease. USDA Bulletin No. 780.
Category: Nosema Summaries and Updates, Sampling
Tags: infection, n. apis, N. ceranae, nosema apis, Nosema cereanae, squash | nosema apis Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/nosema-apis/ |
2012 Almond Pollination Update
First published in: American Bee Journal, April 2012
2012 Almond Pollination Update
ScientificBeekeeping.com
First Published in ABJ in April 2012
Randy Oliver
Who woulda thunk, what with all the lousy weather last spring, widespread summer drought, the reports of massive queen failures, the disastrous honey crop, and the high winter losses of the past few years, that there would have been enough colonies for almond pollination this winter? But to most everyone's surprise, there was!
It seems like a lifetime ago that I wrote my first article for ABJ-on the status of almond pollination, way back in 2007! I'm typing these words during the middle of almond bloom 2012, and just spent the day in the orchards tending to my hives. The bloom today is on strong, and the weather perfect, with several varieties simultaneously in bloom (Fig. 1), which augurs well for a good harvest.
Figure 1. Almonds in bloom in the Central Valley last season. The cool, damp weather extended the bloom for the longest duration in memory; both growers and beekeepers were surprised that a record crop was set! For you trivia buffs, the average tree last year set 7,353 individual nuts (I have not personally confirmed that figure).
Back in 2007, there had been a sea change in the beekeeping industry, shifting from primarily being honey producers, to instead depending upon pollination rental income from a single crop in California. The Golden State is now host to a million out-of-state bee hives which come to celebrate Valentine's Day in the almond orchards. These immigrant pollinators outnumber California hives two to one. They arrive by pickup truck, flatbeds, and semi trailers, bringing with them every new strain of pest and pathogen from the far corners of the country, do their job (paying taxes to California as of last year), and then leave.
The big question each winter since 2004/2005 is whether there will be enough colonies to fulfill the pollination demand, and just how much growers are willing to pay for those hives.
More trivia: it took about 1.5 million colonies of bees to pollinate 750,000 bearing acres of almond trees, producing nearly 2 billion pounds of nutmeats. That means that on average, every colony pollinated about 1333 lbs of nuts, and at a wholesale price of about $2/lb, each colony's efforts contributed to a gross return to the grower of $2666.00! If we divide that value by the approximate number of bees in an 8-frame colony (14,000), that means that each individual bee, on average, pollinated 19C/ worth of nuts. And at a $150 per hive rental rate, each bee rented at 1C/ for a month's wages.
Supply And Demand
The supply of bees this season for almonds just barely met demand--it was neither short nor long. This indicates that the supply and demand market worked perfectly. It also indicates that the current offered rental rates are likely something that both growers and beekeepers can bank on, provided that the growers keep planting new acreage, that the world continues to crave almond nutmeats, and that colony winter mortality doesn't suddenly go up to 50% or drop back to the 5-10% that we enjoyed prior to our bees having to share their blood with the varroa mite.
Adam Smith's "invisible hand of the market" is clearly working as expected. The pollination needs of the growers are being met, and beekeepers are receiving adequate monetary incentive to supply enough colonies to continue to meet the growers' needs.
So how does this unregulated and inefficient market manage to work so well to reach equilibrium? It's driven by the simple bidding of almond growers against each other for a service that beekeepers are willing to provide. The economic demand for hives is relatively "inelastic"--growers need bees in order to set a crop, independent of the price. But the important thing to keep in mind is that the beekeepers do not set the average price for pollination contracts--it's impossible for us to rig prices, since there is no way to keep beekeepers from undercutting one another (otherwise, in this inelastic market, we'd all be charging $200 per hive). Rather, beekeepers respond to the price that growers offer and adjust the number of colonies that they run based upon the degree of profitability of hauling them to almonds. It's up to the growers to offer enough incentive for beekeepers to ramp up their numbers.
Just prior to bloom each year, we see the extremes: if the supply of bees is "long," desperate out-of-state beekeepers trying to recoup hauling costs for hives for which they couldn't find placement will advertize them for as low as $80 (the lowest price that I heard of this year). On the other hand, should supply be short, growers desperate to fulfill the crop insurance requirement for placing two 6-frame colonies per acre (USDA 2010) will bid the price up to $200 per hive (happened last year). The funny thing is that the next season the growers only remember the lowest advertized price; conversely, the beekeepers all remember the highest! The reality is that those extreme last-minute prices paid for a few hives only represent a drop in the bucket, and have little to do with the setting of a fair price for the other 99% already in place.
So the market, after some oscillations in recent years, seems to have settled upon a figure of around $140-$160 per 8-frame colony, sometimes with bonuses for stronger hives. At this price, Dave Mendes may find it worth the cost and hassle to haul thousands of hives from Florida to California (and is even more attractive for me hauling them the mere 100 miles to the orchards that I pollinate).
Colony Collapse And The Price Of Rentals
CCD has been a mixed blessing for beekeepers--it caused disastrous losses for some, but has also grabbed the public's attention about the plight of bees and beekeepers. Such attention has made it a tiny bit easier for almond growers to swallow the incredible jump in pollination prices since 2004 (Fig. 2). But the good news for those growers is that by dint of hard work and ingenuity, beekeepers have generally managed to supply enough hives each year. Most of us long-time almond pollinators have good relations with our growers, and certainly do not feel that we are gouging them. I want my growers to get rich-so that they are able to pay me a sustainable price for my hives! It appears that an inflation-adjusted price of around $150 is sustainable.
A recent economic analysis of almond pollination prices (Rucker 2012) concludes:
"Based on media reports, attentive readers who have tracked the issue might infer that managed U.S. honey bee populations are nearly gone. Our examination of the operation of pollination markets leads us to conclude that beekeepers are savvy entrepreneurs who use their wealth of knowledge of the particular circumstances of time and place--acquired over their lifetimes of work--to adapt quickly to changing market conditions. Not only was there not a failure of bee-related markets, but they adapted quickly and effectively to the changes induced by the appearance of Colony Collapse Disorder."
Figure 2. Acres of bearing almond trees in California (left scale, in thousands) vs. pollination rental rate (right scale, in dollars). Note that it wasn't any sudden surge in demand that caused prices to skyrocket--it was due to the sudden relative shortage of bees. Sources: Doug Flohr (2011), USDA, NASS, California Field Office, by permission; Almond Board of California; 2012 estimate.
The abrupt rise in pollination rental rates from 2005-2008 was a supply and demand "adjustment." Although increased acreage of bearing almond orchards indeed increased the demand somewhat, it certainly wasn't the main cause for the abrupt increase in prices--that was due to lack of supply--the number of colonies available for rent. The California State Beekeepers survey estimated that the winter mortality rate in 2004/2005 doubled from the previous year's 15 percent to 30 percent (Sumner 2006). The resulting shortage of bees caused prices to start climbing. Then in 2005/2006, "On the heels of the 2005 shortage, some almond growers wished to secure their bees early for 2006" (Mussen 2006), and things started to get exciting!
Up until that winter, the growers had been able to bluff the beekeepers into thinking that there was no way that they could possibly afford to pay another penny for hive rent. But then, anticipating another shortage, they suddenly they went into a bidding frenzy for the short supply of available bees, driving the price up to an unheard of $150. The growers had been forced to tip their hand, and we stunned beekeepers got a taste of what the growers were really willing and able to pay for bees. There was no turning back!
Increased Winter Mortality
That high winter mortality rate continued to persist through last year (it appears to have abated somewhat this season). As much as we'd like to blame it on a single cause, in reality there were a number of reasons. The high fall/winter losses for 2004/2005 and 2005/2006 can largely be attributed to the failure of miticides (and beekeeper management) to control varroa, and to poor late-summer forage in some regions (Mussen 2006). (We may see a return of major mite issues next fall if are unable to adjust to the unavailability of a current popular miticide).
Additionally, as I'm pointing out in my articles on Nosema ceranae, that parasite also likely started adding an additional degree of stress about that time. Plus, in 2005/2006, some operations (including my own) suffered from a serious epidemic of "corn-yellow EFB-like" sick brood and unusual sudden collapses. Then in 2006/2007 Dave Hackenberg became the industry spokesperson for the syndrome that came to be known as Colony Collapse Disorder.
Folk rushed to place their bets upon what caused CCD--blaming everything from cell phones or jet chemtrails, to genetically-modified crops or systemic pesticides, to previously unnamed viruses. Since CCD issues seem to be abating this year, a number of those suspects can likely be exonerated. What is important to keep in mind is that beekeepers, given enough economic incentive, figure out how to deal with things.
Rucker explains: "What should be understood is that the state of the honey bee population--numbers, vitality, and economic output--are the products of not just the impact of disease but also the economic decisions made by beekeepers and farmers."
If beekeepers' primary income is from almond pollination, then they are going to do whatever it takes to ramp up their numbers. As Sumner (2006) pointed out, many of those colonies are likely to be "unemployed" for the rest of the season, and must be maintained at considerable expense by trucking them to good forage if you can find it, or by costly supplemental feeding. Sumner predicted, "The result is that rather than receiving half or one third of their annual revenue from almonds, many commercial pollinators may now require almonds to cover most of their annual cost of colony maintenance. If this scenario develops as described, we may expect the pollination fee for almonds to remain high." Sumner was clearly prophetic.
As you can see by the graph above, due to the infusion of additional money from the almond industry, the beekeeping industry quickly responded to the problem of 30% winter losses; by 2008/2009 pollination prices had restabilized, but at a considerably higher set point.
So let's take a look at the various market forces involved, specifically the demand for bees, based upon the amount of bearing acreage, and the supply of bees, which is largely determined by the wholesale price of honey and the amount of winter mortality.
The Beekeepers' Situation
When honey prices were low, and winter losses starting hitting 35%, beekeeping for many became unprofitable. The almond growers stepped up and threw the beekeepers a lifeline in the form of higher rental income from pollination. And for that we beekeepers should be immensely grateful. In the past two years I've even heard beekeepers saying that times now are pretty good--with both honey and pollination prices at historically high levels, they are actually making money (myself included).
And then comes this year, with a completely unexpected full supply of bees for almonds! CCD seems to have largely disappeared (which is why "Disappearing Disease" used to be called just that--the disease would spontaneously disappear). The question now is, will there be an excess supply of bees next season exerting downward pressure on rental rates?
A projected shortage of strong colonies is the main bargaining chip for beekeepers. But that doesn't mean that lack of shortage is going to drive down pollination rates to any great extent, since the degree of supply directly reflects the return on investment to beekeepers. In order to maintain high colony numbers, commercial beekeepers today spend a fortune on trucking, queen replacement, medications, pollen supplements, and syrup; not to mention about twice as much labor per hive as back in the day.
A typical migratory pollinator nowadays may need to replace 50-70% of his colonies over the course of a season. The "three P's"--pathogens, pesticides, and poor nutrition are a deadly combination to bee health, and the necessary crowding of hives exacerbates the problems.
The need to make up replacement colonies from splits eats into income that might have otherwise been made from the unsplit hives (Harmon 2011). And it's much more expensive to try to build up your operation late in the season in time for almond pollination, than it would be to work instead with the normal honey bee seasonal cycle and split colonies on natural pollen flows in early spring (too late for almonds). So unless there's enough reward in the almond orchards, it simply won't be worth it for beekeepers to maintain the numbers of strong hives that the growers desire.
But there are always some beekeepers who for some danged reason or another just give their bees away in almonds! Beekeepers could learn from the almond industry. At a recent almond growers' convention (Waycott 2012), Brian Ezell from Paramount Farms explained that:
"Growers & Sellers must place value in what we produce. Buyers do not expect our industry to sell below the cost of production, but they will gladly let us!
Growers must draw the line on acceptable grower returns. There is never a reason to sell any...almond below the cost of production."
Beekeepers should take this sage advice to heart! Those who rent hives at less than the cost of production destabilize the market and hurt us all.
There is a term used in economics: the "marginal cost of production"-the cost of producing one more unit of a particular good. In the case of the supply of hives for almonds, that would be the cost to add one additional strong hive to the overall supply of bees (including the placement cost required to get them in and out of the orchard). In an expanding market, such as the demand for hives in almonds, the price paid by the buyer must allow the supplier to recoup his marginal cost of production.
So what's the cost of production of a new hive? I don't know how much it takes for the rest of you to produce an additional hive for almonds, but I figure over $200, so that fact alone suggests that colony rental rates won't be dropping much.
But is it fair to compare the marginal cost of production to something that is merely rented out? Perhaps we should rather be looking at the "return on assets"--in the case of beekeepers, the question would be, is running an additional hive a good "investment"? Data from an informal survey by Dr. Eric Mussen (2009) suggested that at that time it cost a beekeeper about $180 to maintain an 8-frame hive for a year--and costs have gone nowhere but up since then. Granted, that hive, if well managed and if the weather cooperates, may return some income from honey or other pollination contracts, but many beekeepers base their colony count upon a break-even in almonds. So if a temporary glut of hives occurs, my guess is that the supply will quickly adjust downward the next year.
There is also the "reserve pool" of potential hives that are not normally brought to almond pollination (these are akin to the "carryout" reserve of commodity crops). These hives belong to honey producers who simply don't find the price offered for almond contracts to be worth the time, trouble, cost, and risk to haul them to California. This reserve acts as a stabilizing force for the market price--should the growers suddenly get desperate due to a major shortage and start offering $200, then that would be enough motivation for some of those reserve hives to get put onto trucks. Conversely, if the offered bid dropped to only $100, even more hives would pass on almond pollination, and instead spend the winter resting (along with their owners).
Bottom line: the number of colonies available for rent reflects the degree of profitability to the beekeeper. Both the marginal cost of production and the return on assets suggest that the sustainable price for almond rental fees for 8-frame colonies will remain at around the current price, and adjust upward for inflation.
The Growers' Situation
The cost of production for almonds is currently approaching $4000 per acre if you calculate it by the book (Klonsky 2011, 2011), although that high theoretical cost should be taken with a grain of salt. Renting two hives per acre at $140/hive accounts for about 7% of theoretical production costs--in the same ballpark as either irrigation or fertilizer.
However, grower return per acre is pretty good-at last year's average yield per acre of 2600 lbs and the current farm gate price for nut meats of about $2 per lb, the average grower enjoys a net return of $1200/acre (over total operating costs), or $2700/acre (over cash operating costs, excluding land and trees) (Klonsky 2011). When you take into consideration that the grower would lose money on every acre without bees, it's easy to see why they are (begrudgingly) willing to pay $150 or more for colony rent (of course growers begrudged paying me $12/hive when I first began pollinating, and have begrudged every price increase since).
So what does the crystal ball say about future demand for colonies in almonds?
Projected Acreage
A recent presentation to growers on the economics of almond production (Harp 2011) projected that the world demand for almonds will require about 30-40,000 additional bearing acres in California per year, which in turn will require an additional 60-80,000 8-frame colonies. This projected additional demand should help to support pollination prices.
Sure there's some concern about the new "self-fertile" cultivars decreasing the demand for bees, but those varieties still require at least a colony per acre to be cost effective (Northcutt 2011), so no one is expecting them to make much of an impact for the foreseeable future.
Stocking Rate
The thing that I can't understand is why some growers shoot themselves in the foot by shorting themselves on bees. I picked up a new contract this season--a beautiful, by-the-book 15-yr orchard that yielded less than 2000 lbs/acre. But the grower had only been contracting for one 7-frame colony per acre, figuring that his neighbor rented enough bees to cover one end of his orchard (adjacent growers consider this sort of getting a free ride akin to thievery).
When I began pollinating almonds, growers rented two hives of bees per acre and were happy to obtain 1000 lbs of harvested nutmeats per acre. Today, state-of-the-art orchards harvest 4000 or more pounds from the same acre! Four times as much yield means that four times as many nuts are set per acre, meaning that at least four times as many blossoms must be pollinated per acre. Yet the average hive stocking rate is still set at only two hives per acre, even though average colony strength hasn't substantially changed (Sheesley 1970). Honey bee foraging behavior hasn't changed, so I wonder if we are expecting today's bee to do four times as much work as yesterday's bee?
Recent research by Dr. Frank Eischen indicates that at peak bloom of early cultivars, there was much better nut set at 2 colonies per acre compared to 1 colony; and for late cultivars better at 1 colony/acre as compared to 0.77 (which is the range that the grower in the test was willing to allow). His findings strongly suggest that growers are seriously not renting enough bees per acre to realize the full potential nut set.
Practical application: Dr. Eischen's findings strongly suggest that growers are not contracting for enough bees per acre in order to realize the full potential nut set, especially in the newer high-density orchards and for the densely-flowering hardshell cultivars. As growers get educated to this fact the demand for bees should increase.
At the U.C. experimental almond research station that I've pollinated for over 25 years (Fig. 4), the average bee stocking rate has been 18-20 frames of bees per acre of mature trees, or the equivalent of two 9-10 frame colonies. But you don't have to guess as to whether the stocking rate for any particular orchard is adequate--it's easy to check for yourself! In a fully-stocked orchard, the bees will have completely stripped the pollen from the blossoms by early afternoon each day (Fig. 3).
Practical application: I suggest to my growers that they confirm that they are getting optimum pollination by checking the blossoms for pollen in the afternoon at peak bloom.
Figure 3. Early bloom on a cold morning in Arbuckle this spring. My son Ian at work in the background; our bees at work in the foreground. Note that the pollen has not yet been stripped from these blossoms. At full bloom, recent data from Dr. Eischen suggest that growers may not be renting enough colonies per acre.
Without adequate pollination, the grower may forego some portion of the potential yield of that orchard. Smart growers go ahead and contract for bees a bit on the heavy side as a form of risk management should the weather not cooperate--in an orchard heavily stocked with bees, a good crop can be set during brief breaks in the weather.
Practical application: stocking an adequate amount of strong colonies per acre is an effective form of risk management for growers should poor pollination weather occur during bloom.
Although growers balk at spending more on hive rental, they should do the math! Say that an orchard is yielding 2000 lbs at two hives per acre. It follows that with nutmeats selling at $2 a pound, an increased yield of merely 4% would easily pay for an additional hive at $140. Dr. Eischen's data suggest that growers may be missing out on far larger percentages of yield than that! I just don't understand why a grower who has invested some $2500 in fixed costs per acre would short himself on bees at the most critical time for nut set!
Practical application: the beekeeping industry is doing a poor job at educating growers as to optimal stocking densities. If we were to invest some money into research and grower education, both parties would benefit!
Figure 4. At the Nickels Soil Laboratory in Arbuckle, U.C. researchers experiment with every combination of rootstocks and almond cultivars, planting density, type of pruning, methods of irrigation, fertilization, etc. I've been pollinating this orchard long enough to see plots get planted, the trees grow to maturity, and then be ripped out and the plot replanted!
Every spring I speak with grad students at the Nickels Lab who are marking off individual blossoms, monitoring soil probes, etc. Such research has allowed growers to increase production from 1000 lbs to an average 2600 lbs per acre, with 4000+ lbs expected in the near future! The research station is self-sustaining--they make enough from the sales of harvested almonds to cover their costs and pay the staff. Would I be frivolous to suggest that some of our bee research stations follow a similar model?
Frame Strength
The question often arises, what is the most efficient colony strength for almond pollination hives? And furthermore, what is a 10-frame colony worth relative to 4-framer, as far as the actual amount of pollination work that gets done?
There are plenty of opinions based upon what someone thinks, but not a whole lot of firm data. In my 2007 article, I plotted out a graph derived from a bunch of unpublished UC Davis data. It suggested that the relationship between frame strength (from 4 to 16 frames of bees) and actual pollination work was directly proportional--i.e., that a 12-frame colony would do as much work as three 4-framers. Of course, nearly everyone was incredulous.
So I found the best published data sets to date--a large 1970 study of 256 colonies, and a meticulous 2007 study of 83 colonies. Both studies used the amount of pollen removed by a pollen trap as a proxy for the number of blossoms visited by the foragers of that colony. One may argue fine points, but shy of netting off acres of almonds, the amount of trapped pollen is probably a fairly reliable indicator of pollination performance.
I reworked the data --setting the amount of pollen trapped by 4-frame colonies as the baseline to which pollen collection by colonies of other strengths could be compared. In the graph below (Fig. 5), I set the amount of pollen collected by 4-framers at 100%; if a larger colony collected three times that amount, then it would be rated at 300%. Interpretation tip: If there were indeed an optimal colony size, the bars would form a curve, peaking at that strength.
Figure 5. Pollen collection as a function of colony frame strength, relative to that of 4-framers. The green line is the hypothetical relationship that pollen collection is directly proportional to frame strength, rather than being more efficient at any particular colony size. And that is pretty much what the actual data indicates over the range from 3 -16 frames! These hard data sets indicate that a single 12-frame hive is likely worth at least as much to the grower as three 4-framers! Data reworked from Sheesley and Poduska (1970), 256 colonies, five orchards, two years combined data; and Eischen (2007), 83 colonies.
The above findings will come as a surprise to those of us (including myself) who assumed that stronger colonies would have a greater percentage of field bees, and would thus be relatively more effective pollinators per frame of bees. The data also suggest that pollination value continues to increase linearly clear up to at least 16 frame strength! By rights, then, if 4-frame colonies are renting for $100, then a 16-framer should rent for $400. That's going to be a hard sell, no matter how robust the data!
Practical application: again, unless beekeepers educate growers with firm economic data, we may not be paid fairly for strong colonies.
OK, you say, but strong colonies, due to their larger cluster size, must certainly fly better earlier in the morning or in cool weather! Luckily, Dr. Eischen also collected data comparing the number of returning pollen-carrying foragers in morning and evening, which I also reworked. In addition, I included his calculations for the number of grams of pollen trapped per frame of bees. To interpret the graph below (Fig. 6), for each color of bars, look to see if there is a curve indicating an optimal colony size for pollination efficiency.
Figure 6. Eischen's 2007 data, reworked. I divided both returning pollen forager rate and pollen collected per day by average colony frame strength during bloom in order to get pollination rates per frame of bees. Surprisingly again, the per-bee morning and afternoon foraging rates were highest for the 7-framers. On the other hand, the highest rate of actual pollen collection (as measured by pollen traps) was by the 10-frame colonies.
Well, more surprises again--it appears that a larger proportion of bees in the smaller colonies actually foraged for pollen! Lots of us would have lost money on that bet, but I put a great deal of faith in any of Dr. Eischen's well designed and meticulous studies (Fig. 7)! The astute reader may have noticed that the two graphs have different bottom axes. In the first graph, pollen collection was plotted against initial field grading, rounded to the nearest frame at the beginning of bloom. In the second graph, I plotted it against the more accurate average of actual measured frame strength over the entire course of bloom. I did this since not all of the colonies in the study grew in strength during the bloom.
Bottom line: it looks like a frame of bees performs approximately the frame amount of pollination work regardless of the size of the colony, suggesting that two 4-framers would provide about as much pollination service as a single 8-framer. If anything, pollination efficiency appears to be greatest in 8- to 12-frame colonies, which comes as no surprise, as this is around the size at which a colony is typically feeding the greatest proportion of brood.
Practical application: the implications of the above data sets are that growers are either paying far too much for 4-frame colonies, or far too little for 12-framers (I personally favor the latter interpretation).
Figure 7. Dr. Frank Eischen of the USDA ARS at work in the almonds this season--preparing to net off a branch to measure bee pollination rates. The bee industry owes Dr. Eischen a debt of gratitude for his valuable practical research on mite control, Small Hive Beetle, and almond pollination. Photo courtesy Kodua Galieti, whose images can be seen at koduaphotography.com.
And even those growers who are paying bonuses for stronger colonies may not be compensating beekeepers adequately. I had the choice this year between several different contracts (Table 1):
Contract
Strength Specified
Payment
Payment Per Frame of Bees
A
4-frame average
$100
$25.00
B
6-frame average
$125
$20.83
C
8-frame average, 6-frame min
$145
$18.12
D
5-frame min, 11-frame max
$165 max
$15.00 max
E
12-frame average
$175
$14.58
Table 1. Comparison of payment per frame of bees, depending upon the contract. Note that in the current market, the beekeeper really has little incentive to produce strong colonies. Other than saving a bit on trucking, you get paid more per bee the weaker the colony!
Traditionally, it used to be worth it to me to combine my 4-framers with my 8-framers, and contract for 12-frame colonies at a premium price (thus saving on trucking). There is no longer much incentive for me to do so, since the current market rewards the beekeeper for the number of boxes, rather than for the numbers of bees in those boxes.
So some beekeepers stick to the "Domino's Pizza model"--forget busting your butt to produce premium colonies that growers aren't willing to pay proportionately more for. Rather, offer them the minimum quality that they'll accept, for what appears to be a cheap price. After all, they are only screwing themselves!
Grower Education
I hope that Dr. Gordon Wardell, who has been collecting data on nut yield vs. average colony frame strength, will be able to share those important economic figures with the industry some day (hint, hint). My suggestion to the almond growers would be to shift from renting numbers of hives to numbers of frames of bees per acre.
To that end, I drew up a new contract this year for one of my more enlightened growers: I guaranteed a specific number of frames per acre (18), independent of the number of hives that I used to fill the contract. For validation, I invited my grower to inspect as many drops as he wished with me, to ensure that I met the guarantee. This contract allowed me great latitude as to how to fill each drop, and could easily have had a proportional penalty written in for failure to reach the target. Since I came up a little short on hives in February, I ran all my 12-framers to this contract, and then cleaned up by renting all my weaker hives at a high per-frame rate to other growers.
Such a contract may become a model for the future. But for now, there is unfortunately a disproportionately low return for providing extra-strong colonies, and I'm tired of all the feeding and work necessary to produce them!
Fungicides
Almonds are susceptible to a variety of fungal diseases, especially in the Central and North Valleys, which receive more rain than down south. Following wet weather, the sounds of tractor-mounted blowers, crop-duster biplanes, and helicopters are common in the orchards, spraying right over our hives (Fig. 8). Although such fungicides are touted as being harmless to bees, after a spray we may observe entombed pollen, brood issues, and adult bee dwindling.
Figure 8. I snapped this photo of John Miller's hives as they were being thoroughly fogged with fungicide in the middle of the day. Although fungicides do not normally cause significant overt adult bee mortality, the surfactant adjuvants in the tank mix sure can! Such spraying may also cause negative effects upon brood, beebread fermentation, and overall colony health. Growers can mitigate these problems somewhat by spraying after dusk.
Of special concern to the California queen breeders are the queen cell losses that some see when raising queens from colonies that had been exposed to the fungicide PristineO. Dr. Gloria Degrandi-Hoffman of the Tucson Bee Lab recently presented the results of their research, which found negative effects from Pristine upon queen production.
On the other hand, I've seen legitimate research by BASF, the manufacturer of Pristine, which indicates that the active ingredient has little effect upon bee brood. At the last California Queen Breeders meeting, representatives from BASF, to their great credit, pledged to work with us to get to the root of the reported problems. The company has stationed Dr. Christof Schneider, one of their bee specialists from Germany, in California to monitor pesticide levels in pollen and to run studies in almonds. I applaud this sort of cooperative work between beekeepers and the chemical industry!
Some researchers have suggested that the problem may be due to pesticide synergies or surfactants added to the tank mixes. I also suggested that we should consider that no researchers have investigated whether there are synergies between the toxic amygdalin in almond pollen and common pesticides.
Eco-Terrorism In The Valley
As if you didn't already have enough things to worry about, this January right in the heart of almond country, animal rights extremists perpetrated an act of terrorism by using kerosene and digital timers to incinerate fourteen parked cattle trucks at a major feedlot [1, 2]. Such destruction is a tactic used by those who feel that "Arson, property destruction, burglary and theft are 'acceptable crimes' when used for the animal cause" [2a].
What has the above got to do with beekeepers? Well, if you didn't already know, "bees are abused and exploited for their honey, wax and other derivatives" [3]. There is "cruelty in the honey industry" [4]. "Many people who understand the cruelty involved in factory farming and are morally opposed to eating meat find it less obvious that the lowly honeybee should also be of ethical concern...Like all factory farming, beekeeping has morphed into an industrial process which puts profits ahead of animal concerns" [5].
Your beekeeping operation could be the next target of some extremist!
One of the problems of the blogosphere is that folk concerned about legitimate issues can, by stretching the truth just a wee bit, incite those itching to destroy something to do so for some ostensibly "just cause." The destruction of Harris Farms' trucks should serve as a warning to all beekeepers that there are those out there who are under the impression that we abuse our bees-"Like other factory-farmed animals, honeybees are victims of unnatural living conditions, genetic manipulation, and stressful transportation" [6].
The press coverage of CCD has opened an opportunity for some to blame commercial beekeeping practices as the cause of death of our unfortunate charges. I am surprised by the number of blogs on the web by well-meaning folk who earnestly believe that, "There honestly is no escaping the harsh realities of methods within the commercial honey production process and the cruelty the bees themselves are forced to endure during such times" [7].
I read this after my sons and I had worked in the rain for a week to feed thousands of dollars worth of carefully-prepared and nutritious pollen supplement to my hungry hives, gently brushing the bees aside so that we didn't squash them. Heck, in this instance, I literally treated my bees better than my own children! (Fig. 9). But you'd never know it if your only source of information was the Internet!
Figure 9. My sons feeding pollen supplement to hungry colonies in the rain prior to moving to almonds. We use a pine bough to "tickle" the bees so that they move down between the frames. Some of my recent research strongly suggests that you don't want to squash bees when you're feeding pollen supplement (more later)!
Practical application: it's up to beekeepers to educate the public as to the truth about how much we care for our bees' well-being, and that we only make a living if we treat them well!
The Future
The reality is this: almond growers are doing pretty well these days. The projected world demand for tree nuts is strong, and almonds are the cheapest and most versatile among them. Indeed, one of the industry concerns is that sales of nuts are so strong that packers are having trouble maintaining a comfortable "carryout"--a minimum inventory to act as a cushion should there be a short crop!
California holds a virtual monopoly on world production of almonds, so long as our water holds out (there is no snowpack in the Sierra this winter). And the world loves almonds! They are not only a tasty confection, but also good for you.
Despite some record almond crops in recent years, prices to growers remain profitable. Grower Bill Harp (2011), speaking to the Almond Board, reports that projected 10-20% grower returns on assets are possible with the expected almond supply and demand fundamentals (this is in an economy where any return on assets is a good thing). The bee industry will continue to hitch a ride on that wagon.
Bottom line: The near future looks pretty rosy for both almond growers and beekeepers.
Good Sources Of Information
You can track the weather and progress of bloom at the Blue Diamond website http://www.bluediamond.com/applications/in-the-field/index.cfm?navid=101).
Project Apism http://projectapism.org has two great webpages of interest to almond pollinators:
The Cummings Report http://projectapism.org/content/view/64/49/ written by almond grower and industry insider Dan Cummings, and the
Bee Status Report http://projectapism.org/content/view/93/49/
Your $1 per hive donation to Project Apism will help to support beekeeper-funded practical research.
Hilltop Ranch posts almond updates at http://www.hilltopranch.com/2012/02/almond-update-25/
References
Carman, Hoy (2011) The estimated impact of bee colony collapse disorder on almond pollination fees. ARE Update 14(5): 9-11.
Eischen, FA, RH Graham, R Rivera & J Traynor (2007) The effect of colony size and composition on almond pollen collection. http://projectapism.org/component/option,com_docman/task,doc_download/gid,40/Itemid,44/
Flohr, D (2011) 2011 Almond Forecast http://www.hilltopranch.com/wp-content/uploads/2011/05/almond-industry-historical-data-from-nass.pdf
Harp, B, et al (2011) Economics of Almond Production. (Broken Link!) http://www.almondboard.com/Handlers/Documents/Economics%20of%20Almond%20Production.pdf
Klonsky, KA, et al (2011) Sample costs to establish an orchard and produce almonds (flood). http://coststudies.ucdavis.edu/files/AlmondFloodVN2011.pdf
Klonsky, KA, et al (2011) Sample costs to establish an orchard and produce almonds (microsprinkler). http://coststudies.ucdavis.edu/files/AlmondSprinkleVN2011.pdf
Ludwig, G (2009) Present & Future Beekeeping: "Almonds" http://www.usda.gov/oce/forum/2009_Speeches/Presentations/Ludwig.pdf
Mussen, EC (2006) Chaotic almond pollination. (Broken Link!) http://entomology.ucdavis.edu/faculty/mussen/JanFeb2006.pdf
Mussen, EC (2009) How much does it cost to keep commercial honey bee colonies going in California? http://projectapism.org/content/view/83/27/
Northcutt, G (2011) Quest continues for self-fertile almond varieties. Tree Nut Farm Press 3(5).
Rabobank 2011 https://www.rabobankamerica.com/content/documents/news/2011/us_tree_nut_sales_to_remain_strong_in_coming_years.pdf
Rucker, RR & WN Thurman (2012) Colony collapse disorder: The market response to bee disease. http://www.perc.org/files/ps50.pdf
Rucker, RR, WT Thurmon and Michael Burgett (2011) Colony collapse: The economic consequences of bee disease. http://economics.clemson.edu/files/ccd-paper-full-package-apr14-2011.pdf
Sheesley, B and B Poduska (1970) strong honeybee colonies prove value in almond pollination. California Agriculture. August 1970: 4-6.
Sumner, DA and H Boriss (2006) Bee-conomics and the Leap in Pollination Fees. http://aic.ucdavis.edu/research1/bee-conomics.pdf
USDA (2010) Federal crop insurance corporation adjustment standards product administration and standards division handbook 2012 and succeeding crop years. http://www.rma.usda.gov/handbooks/25000/2012/12_25020-1h.pdf
Waycott, R, moderator (2012) The Economics of Growing Almonds. (Broken Link!) http://www.almondboard.com/Growers/Documents/The%20Economics%20of%20Growing%20Almonds.pdf
[1] (Broken Link!) http://www.fresnobee.com/2012/01/10/2677557/animal-rights-activists-take-credit.html
[2] http://www.animalliberationpressoffice.org/communiques/2012/2012-01-10_harrisranch.htm
[2a] http://activistcash.com/biography.cfm/b/1459-alex-pacheco
[3] (Broken Link!) http://www.think-differently-about-sheep.com/Animal-Rights-Bees.htm
[5] http://prime.peta.org/2009/01/but-what-about-honey-is-it-cruelty-free
[4] http://www.veganpeace.com/animal_cruelty/honey.htm
[7] http://veglin.hubpages.com/hub/Why-Honey-REALLY-isnt-Vegan
[6] http://www.peta.org/issues/animals-used-for-food/honey-from-factory-farmed-bees.aspx
Category: Almond Pollination
Tags: almond, pollination | pollination Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/pollination/ |
2012 Almond Pollination Update
First published in: American Bee Journal, April 2012
2012 Almond Pollination Update
ScientificBeekeeping.com
First Published in ABJ in April 2012
Randy Oliver
Who woulda thunk, what with all the lousy weather last spring, widespread summer drought, the reports of massive queen failures, the disastrous honey crop, and the high winter losses of the past few years, that there would have been enough colonies for almond pollination this winter? But to most everyone's surprise, there was!
It seems like a lifetime ago that I wrote my first article for ABJ-on the status of almond pollination, way back in 2007! I'm typing these words during the middle of almond bloom 2012, and just spent the day in the orchards tending to my hives. The bloom today is on strong, and the weather perfect, with several varieties simultaneously in bloom (Fig. 1), which augurs well for a good harvest.
Figure 1. Almonds in bloom in the Central Valley last season. The cool, damp weather extended the bloom for the longest duration in memory; both growers and beekeepers were surprised that a record crop was set! For you trivia buffs, the average tree last year set 7,353 individual nuts (I have not personally confirmed that figure).
Back in 2007, there had been a sea change in the beekeeping industry, shifting from primarily being honey producers, to instead depending upon pollination rental income from a single crop in California. The Golden State is now host to a million out-of-state bee hives which come to celebrate Valentine's Day in the almond orchards. These immigrant pollinators outnumber California hives two to one. They arrive by pickup truck, flatbeds, and semi trailers, bringing with them every new strain of pest and pathogen from the far corners of the country, do their job (paying taxes to California as of last year), and then leave.
The big question each winter since 2004/2005 is whether there will be enough colonies to fulfill the pollination demand, and just how much growers are willing to pay for those hives.
More trivia: it took about 1.5 million colonies of bees to pollinate 750,000 bearing acres of almond trees, producing nearly 2 billion pounds of nutmeats. That means that on average, every colony pollinated about 1333 lbs of nuts, and at a wholesale price of about $2/lb, each colony's efforts contributed to a gross return to the grower of $2666.00! If we divide that value by the approximate number of bees in an 8-frame colony (14,000), that means that each individual bee, on average, pollinated 19C/ worth of nuts. And at a $150 per hive rental rate, each bee rented at 1C/ for a month's wages.
Supply And Demand
The supply of bees this season for almonds just barely met demand--it was neither short nor long. This indicates that the supply and demand market worked perfectly. It also indicates that the current offered rental rates are likely something that both growers and beekeepers can bank on, provided that the growers keep planting new acreage, that the world continues to crave almond nutmeats, and that colony winter mortality doesn't suddenly go up to 50% or drop back to the 5-10% that we enjoyed prior to our bees having to share their blood with the varroa mite.
Adam Smith's "invisible hand of the market" is clearly working as expected. The pollination needs of the growers are being met, and beekeepers are receiving adequate monetary incentive to supply enough colonies to continue to meet the growers' needs.
So how does this unregulated and inefficient market manage to work so well to reach equilibrium? It's driven by the simple bidding of almond growers against each other for a service that beekeepers are willing to provide. The economic demand for hives is relatively "inelastic"--growers need bees in order to set a crop, independent of the price. But the important thing to keep in mind is that the beekeepers do not set the average price for pollination contracts--it's impossible for us to rig prices, since there is no way to keep beekeepers from undercutting one another (otherwise, in this inelastic market, we'd all be charging $200 per hive). Rather, beekeepers respond to the price that growers offer and adjust the number of colonies that they run based upon the degree of profitability of hauling them to almonds. It's up to the growers to offer enough incentive for beekeepers to ramp up their numbers.
Just prior to bloom each year, we see the extremes: if the supply of bees is "long," desperate out-of-state beekeepers trying to recoup hauling costs for hives for which they couldn't find placement will advertize them for as low as $80 (the lowest price that I heard of this year). On the other hand, should supply be short, growers desperate to fulfill the crop insurance requirement for placing two 6-frame colonies per acre (USDA 2010) will bid the price up to $200 per hive (happened last year). The funny thing is that the next season the growers only remember the lowest advertized price; conversely, the beekeepers all remember the highest! The reality is that those extreme last-minute prices paid for a few hives only represent a drop in the bucket, and have little to do with the setting of a fair price for the other 99% already in place.
So the market, after some oscillations in recent years, seems to have settled upon a figure of around $140-$160 per 8-frame colony, sometimes with bonuses for stronger hives. At this price, Dave Mendes may find it worth the cost and hassle to haul thousands of hives from Florida to California (and is even more attractive for me hauling them the mere 100 miles to the orchards that I pollinate).
Colony Collapse And The Price Of Rentals
CCD has been a mixed blessing for beekeepers--it caused disastrous losses for some, but has also grabbed the public's attention about the plight of bees and beekeepers. Such attention has made it a tiny bit easier for almond growers to swallow the incredible jump in pollination prices since 2004 (Fig. 2). But the good news for those growers is that by dint of hard work and ingenuity, beekeepers have generally managed to supply enough hives each year. Most of us long-time almond pollinators have good relations with our growers, and certainly do not feel that we are gouging them. I want my growers to get rich-so that they are able to pay me a sustainable price for my hives! It appears that an inflation-adjusted price of around $150 is sustainable.
A recent economic analysis of almond pollination prices (Rucker 2012) concludes:
"Based on media reports, attentive readers who have tracked the issue might infer that managed U.S. honey bee populations are nearly gone. Our examination of the operation of pollination markets leads us to conclude that beekeepers are savvy entrepreneurs who use their wealth of knowledge of the particular circumstances of time and place--acquired over their lifetimes of work--to adapt quickly to changing market conditions. Not only was there not a failure of bee-related markets, but they adapted quickly and effectively to the changes induced by the appearance of Colony Collapse Disorder."
Figure 2. Acres of bearing almond trees in California (left scale, in thousands) vs. pollination rental rate (right scale, in dollars). Note that it wasn't any sudden surge in demand that caused prices to skyrocket--it was due to the sudden relative shortage of bees. Sources: Doug Flohr (2011), USDA, NASS, California Field Office, by permission; Almond Board of California; 2012 estimate.
The abrupt rise in pollination rental rates from 2005-2008 was a supply and demand "adjustment." Although increased acreage of bearing almond orchards indeed increased the demand somewhat, it certainly wasn't the main cause for the abrupt increase in prices--that was due to lack of supply--the number of colonies available for rent. The California State Beekeepers survey estimated that the winter mortality rate in 2004/2005 doubled from the previous year's 15 percent to 30 percent (Sumner 2006). The resulting shortage of bees caused prices to start climbing. Then in 2005/2006, "On the heels of the 2005 shortage, some almond growers wished to secure their bees early for 2006" (Mussen 2006), and things started to get exciting!
Up until that winter, the growers had been able to bluff the beekeepers into thinking that there was no way that they could possibly afford to pay another penny for hive rent. But then, anticipating another shortage, they suddenly they went into a bidding frenzy for the short supply of available bees, driving the price up to an unheard of $150. The growers had been forced to tip their hand, and we stunned beekeepers got a taste of what the growers were really willing and able to pay for bees. There was no turning back!
Increased Winter Mortality
That high winter mortality rate continued to persist through last year (it appears to have abated somewhat this season). As much as we'd like to blame it on a single cause, in reality there were a number of reasons. The high fall/winter losses for 2004/2005 and 2005/2006 can largely be attributed to the failure of miticides (and beekeeper management) to control varroa, and to poor late-summer forage in some regions (Mussen 2006). (We may see a return of major mite issues next fall if are unable to adjust to the unavailability of a current popular miticide).
Additionally, as I'm pointing out in my articles on Nosema ceranae, that parasite also likely started adding an additional degree of stress about that time. Plus, in 2005/2006, some operations (including my own) suffered from a serious epidemic of "corn-yellow EFB-like" sick brood and unusual sudden collapses. Then in 2006/2007 Dave Hackenberg became the industry spokesperson for the syndrome that came to be known as Colony Collapse Disorder.
Folk rushed to place their bets upon what caused CCD--blaming everything from cell phones or jet chemtrails, to genetically-modified crops or systemic pesticides, to previously unnamed viruses. Since CCD issues seem to be abating this year, a number of those suspects can likely be exonerated. What is important to keep in mind is that beekeepers, given enough economic incentive, figure out how to deal with things.
Rucker explains: "What should be understood is that the state of the honey bee population--numbers, vitality, and economic output--are the products of not just the impact of disease but also the economic decisions made by beekeepers and farmers."
If beekeepers' primary income is from almond pollination, then they are going to do whatever it takes to ramp up their numbers. As Sumner (2006) pointed out, many of those colonies are likely to be "unemployed" for the rest of the season, and must be maintained at considerable expense by trucking them to good forage if you can find it, or by costly supplemental feeding. Sumner predicted, "The result is that rather than receiving half or one third of their annual revenue from almonds, many commercial pollinators may now require almonds to cover most of their annual cost of colony maintenance. If this scenario develops as described, we may expect the pollination fee for almonds to remain high." Sumner was clearly prophetic.
As you can see by the graph above, due to the infusion of additional money from the almond industry, the beekeeping industry quickly responded to the problem of 30% winter losses; by 2008/2009 pollination prices had restabilized, but at a considerably higher set point.
So let's take a look at the various market forces involved, specifically the demand for bees, based upon the amount of bearing acreage, and the supply of bees, which is largely determined by the wholesale price of honey and the amount of winter mortality.
The Beekeepers' Situation
When honey prices were low, and winter losses starting hitting 35%, beekeeping for many became unprofitable. The almond growers stepped up and threw the beekeepers a lifeline in the form of higher rental income from pollination. And for that we beekeepers should be immensely grateful. In the past two years I've even heard beekeepers saying that times now are pretty good--with both honey and pollination prices at historically high levels, they are actually making money (myself included).
And then comes this year, with a completely unexpected full supply of bees for almonds! CCD seems to have largely disappeared (which is why "Disappearing Disease" used to be called just that--the disease would spontaneously disappear). The question now is, will there be an excess supply of bees next season exerting downward pressure on rental rates?
A projected shortage of strong colonies is the main bargaining chip for beekeepers. But that doesn't mean that lack of shortage is going to drive down pollination rates to any great extent, since the degree of supply directly reflects the return on investment to beekeepers. In order to maintain high colony numbers, commercial beekeepers today spend a fortune on trucking, queen replacement, medications, pollen supplements, and syrup; not to mention about twice as much labor per hive as back in the day.
A typical migratory pollinator nowadays may need to replace 50-70% of his colonies over the course of a season. The "three P's"--pathogens, pesticides, and poor nutrition are a deadly combination to bee health, and the necessary crowding of hives exacerbates the problems.
The need to make up replacement colonies from splits eats into income that might have otherwise been made from the unsplit hives (Harmon 2011). And it's much more expensive to try to build up your operation late in the season in time for almond pollination, than it would be to work instead with the normal honey bee seasonal cycle and split colonies on natural pollen flows in early spring (too late for almonds). So unless there's enough reward in the almond orchards, it simply won't be worth it for beekeepers to maintain the numbers of strong hives that the growers desire.
But there are always some beekeepers who for some danged reason or another just give their bees away in almonds! Beekeepers could learn from the almond industry. At a recent almond growers' convention (Waycott 2012), Brian Ezell from Paramount Farms explained that:
"Growers & Sellers must place value in what we produce. Buyers do not expect our industry to sell below the cost of production, but they will gladly let us!
Growers must draw the line on acceptable grower returns. There is never a reason to sell any...almond below the cost of production."
Beekeepers should take this sage advice to heart! Those who rent hives at less than the cost of production destabilize the market and hurt us all.
There is a term used in economics: the "marginal cost of production"-the cost of producing one more unit of a particular good. In the case of the supply of hives for almonds, that would be the cost to add one additional strong hive to the overall supply of bees (including the placement cost required to get them in and out of the orchard). In an expanding market, such as the demand for hives in almonds, the price paid by the buyer must allow the supplier to recoup his marginal cost of production.
So what's the cost of production of a new hive? I don't know how much it takes for the rest of you to produce an additional hive for almonds, but I figure over $200, so that fact alone suggests that colony rental rates won't be dropping much.
But is it fair to compare the marginal cost of production to something that is merely rented out? Perhaps we should rather be looking at the "return on assets"--in the case of beekeepers, the question would be, is running an additional hive a good "investment"? Data from an informal survey by Dr. Eric Mussen (2009) suggested that at that time it cost a beekeeper about $180 to maintain an 8-frame hive for a year--and costs have gone nowhere but up since then. Granted, that hive, if well managed and if the weather cooperates, may return some income from honey or other pollination contracts, but many beekeepers base their colony count upon a break-even in almonds. So if a temporary glut of hives occurs, my guess is that the supply will quickly adjust downward the next year.
There is also the "reserve pool" of potential hives that are not normally brought to almond pollination (these are akin to the "carryout" reserve of commodity crops). These hives belong to honey producers who simply don't find the price offered for almond contracts to be worth the time, trouble, cost, and risk to haul them to California. This reserve acts as a stabilizing force for the market price--should the growers suddenly get desperate due to a major shortage and start offering $200, then that would be enough motivation for some of those reserve hives to get put onto trucks. Conversely, if the offered bid dropped to only $100, even more hives would pass on almond pollination, and instead spend the winter resting (along with their owners).
Bottom line: the number of colonies available for rent reflects the degree of profitability to the beekeeper. Both the marginal cost of production and the return on assets suggest that the sustainable price for almond rental fees for 8-frame colonies will remain at around the current price, and adjust upward for inflation.
The Growers' Situation
The cost of production for almonds is currently approaching $4000 per acre if you calculate it by the book (Klonsky 2011, 2011), although that high theoretical cost should be taken with a grain of salt. Renting two hives per acre at $140/hive accounts for about 7% of theoretical production costs--in the same ballpark as either irrigation or fertilizer.
However, grower return per acre is pretty good-at last year's average yield per acre of 2600 lbs and the current farm gate price for nut meats of about $2 per lb, the average grower enjoys a net return of $1200/acre (over total operating costs), or $2700/acre (over cash operating costs, excluding land and trees) (Klonsky 2011). When you take into consideration that the grower would lose money on every acre without bees, it's easy to see why they are (begrudgingly) willing to pay $150 or more for colony rent (of course growers begrudged paying me $12/hive when I first began pollinating, and have begrudged every price increase since).
So what does the crystal ball say about future demand for colonies in almonds?
Projected Acreage
A recent presentation to growers on the economics of almond production (Harp 2011) projected that the world demand for almonds will require about 30-40,000 additional bearing acres in California per year, which in turn will require an additional 60-80,000 8-frame colonies. This projected additional demand should help to support pollination prices.
Sure there's some concern about the new "self-fertile" cultivars decreasing the demand for bees, but those varieties still require at least a colony per acre to be cost effective (Northcutt 2011), so no one is expecting them to make much of an impact for the foreseeable future.
Stocking Rate
The thing that I can't understand is why some growers shoot themselves in the foot by shorting themselves on bees. I picked up a new contract this season--a beautiful, by-the-book 15-yr orchard that yielded less than 2000 lbs/acre. But the grower had only been contracting for one 7-frame colony per acre, figuring that his neighbor rented enough bees to cover one end of his orchard (adjacent growers consider this sort of getting a free ride akin to thievery).
When I began pollinating almonds, growers rented two hives of bees per acre and were happy to obtain 1000 lbs of harvested nutmeats per acre. Today, state-of-the-art orchards harvest 4000 or more pounds from the same acre! Four times as much yield means that four times as many nuts are set per acre, meaning that at least four times as many blossoms must be pollinated per acre. Yet the average hive stocking rate is still set at only two hives per acre, even though average colony strength hasn't substantially changed (Sheesley 1970). Honey bee foraging behavior hasn't changed, so I wonder if we are expecting today's bee to do four times as much work as yesterday's bee?
Recent research by Dr. Frank Eischen indicates that at peak bloom of early cultivars, there was much better nut set at 2 colonies per acre compared to 1 colony; and for late cultivars better at 1 colony/acre as compared to 0.77 (which is the range that the grower in the test was willing to allow). His findings strongly suggest that growers are seriously not renting enough bees per acre to realize the full potential nut set.
Practical application: Dr. Eischen's findings strongly suggest that growers are not contracting for enough bees per acre in order to realize the full potential nut set, especially in the newer high-density orchards and for the densely-flowering hardshell cultivars. As growers get educated to this fact the demand for bees should increase.
At the U.C. experimental almond research station that I've pollinated for over 25 years (Fig. 4), the average bee stocking rate has been 18-20 frames of bees per acre of mature trees, or the equivalent of two 9-10 frame colonies. But you don't have to guess as to whether the stocking rate for any particular orchard is adequate--it's easy to check for yourself! In a fully-stocked orchard, the bees will have completely stripped the pollen from the blossoms by early afternoon each day (Fig. 3).
Practical application: I suggest to my growers that they confirm that they are getting optimum pollination by checking the blossoms for pollen in the afternoon at peak bloom.
Figure 3. Early bloom on a cold morning in Arbuckle this spring. My son Ian at work in the background; our bees at work in the foreground. Note that the pollen has not yet been stripped from these blossoms. At full bloom, recent data from Dr. Eischen suggest that growers may not be renting enough colonies per acre.
Without adequate pollination, the grower may forego some portion of the potential yield of that orchard. Smart growers go ahead and contract for bees a bit on the heavy side as a form of risk management should the weather not cooperate--in an orchard heavily stocked with bees, a good crop can be set during brief breaks in the weather.
Practical application: stocking an adequate amount of strong colonies per acre is an effective form of risk management for growers should poor pollination weather occur during bloom.
Although growers balk at spending more on hive rental, they should do the math! Say that an orchard is yielding 2000 lbs at two hives per acre. It follows that with nutmeats selling at $2 a pound, an increased yield of merely 4% would easily pay for an additional hive at $140. Dr. Eischen's data suggest that growers may be missing out on far larger percentages of yield than that! I just don't understand why a grower who has invested some $2500 in fixed costs per acre would short himself on bees at the most critical time for nut set!
Practical application: the beekeeping industry is doing a poor job at educating growers as to optimal stocking densities. If we were to invest some money into research and grower education, both parties would benefit!
Figure 4. At the Nickels Soil Laboratory in Arbuckle, U.C. researchers experiment with every combination of rootstocks and almond cultivars, planting density, type of pruning, methods of irrigation, fertilization, etc. I've been pollinating this orchard long enough to see plots get planted, the trees grow to maturity, and then be ripped out and the plot replanted!
Every spring I speak with grad students at the Nickels Lab who are marking off individual blossoms, monitoring soil probes, etc. Such research has allowed growers to increase production from 1000 lbs to an average 2600 lbs per acre, with 4000+ lbs expected in the near future! The research station is self-sustaining--they make enough from the sales of harvested almonds to cover their costs and pay the staff. Would I be frivolous to suggest that some of our bee research stations follow a similar model?
Frame Strength
The question often arises, what is the most efficient colony strength for almond pollination hives? And furthermore, what is a 10-frame colony worth relative to 4-framer, as far as the actual amount of pollination work that gets done?
There are plenty of opinions based upon what someone thinks, but not a whole lot of firm data. In my 2007 article, I plotted out a graph derived from a bunch of unpublished UC Davis data. It suggested that the relationship between frame strength (from 4 to 16 frames of bees) and actual pollination work was directly proportional--i.e., that a 12-frame colony would do as much work as three 4-framers. Of course, nearly everyone was incredulous.
So I found the best published data sets to date--a large 1970 study of 256 colonies, and a meticulous 2007 study of 83 colonies. Both studies used the amount of pollen removed by a pollen trap as a proxy for the number of blossoms visited by the foragers of that colony. One may argue fine points, but shy of netting off acres of almonds, the amount of trapped pollen is probably a fairly reliable indicator of pollination performance.
I reworked the data --setting the amount of pollen trapped by 4-frame colonies as the baseline to which pollen collection by colonies of other strengths could be compared. In the graph below (Fig. 5), I set the amount of pollen collected by 4-framers at 100%; if a larger colony collected three times that amount, then it would be rated at 300%. Interpretation tip: If there were indeed an optimal colony size, the bars would form a curve, peaking at that strength.
Figure 5. Pollen collection as a function of colony frame strength, relative to that of 4-framers. The green line is the hypothetical relationship that pollen collection is directly proportional to frame strength, rather than being more efficient at any particular colony size. And that is pretty much what the actual data indicates over the range from 3 -16 frames! These hard data sets indicate that a single 12-frame hive is likely worth at least as much to the grower as three 4-framers! Data reworked from Sheesley and Poduska (1970), 256 colonies, five orchards, two years combined data; and Eischen (2007), 83 colonies.
The above findings will come as a surprise to those of us (including myself) who assumed that stronger colonies would have a greater percentage of field bees, and would thus be relatively more effective pollinators per frame of bees. The data also suggest that pollination value continues to increase linearly clear up to at least 16 frame strength! By rights, then, if 4-frame colonies are renting for $100, then a 16-framer should rent for $400. That's going to be a hard sell, no matter how robust the data!
Practical application: again, unless beekeepers educate growers with firm economic data, we may not be paid fairly for strong colonies.
OK, you say, but strong colonies, due to their larger cluster size, must certainly fly better earlier in the morning or in cool weather! Luckily, Dr. Eischen also collected data comparing the number of returning pollen-carrying foragers in morning and evening, which I also reworked. In addition, I included his calculations for the number of grams of pollen trapped per frame of bees. To interpret the graph below (Fig. 6), for each color of bars, look to see if there is a curve indicating an optimal colony size for pollination efficiency.
Figure 6. Eischen's 2007 data, reworked. I divided both returning pollen forager rate and pollen collected per day by average colony frame strength during bloom in order to get pollination rates per frame of bees. Surprisingly again, the per-bee morning and afternoon foraging rates were highest for the 7-framers. On the other hand, the highest rate of actual pollen collection (as measured by pollen traps) was by the 10-frame colonies.
Well, more surprises again--it appears that a larger proportion of bees in the smaller colonies actually foraged for pollen! Lots of us would have lost money on that bet, but I put a great deal of faith in any of Dr. Eischen's well designed and meticulous studies (Fig. 7)! The astute reader may have noticed that the two graphs have different bottom axes. In the first graph, pollen collection was plotted against initial field grading, rounded to the nearest frame at the beginning of bloom. In the second graph, I plotted it against the more accurate average of actual measured frame strength over the entire course of bloom. I did this since not all of the colonies in the study grew in strength during the bloom.
Bottom line: it looks like a frame of bees performs approximately the frame amount of pollination work regardless of the size of the colony, suggesting that two 4-framers would provide about as much pollination service as a single 8-framer. If anything, pollination efficiency appears to be greatest in 8- to 12-frame colonies, which comes as no surprise, as this is around the size at which a colony is typically feeding the greatest proportion of brood.
Practical application: the implications of the above data sets are that growers are either paying far too much for 4-frame colonies, or far too little for 12-framers (I personally favor the latter interpretation).
Figure 7. Dr. Frank Eischen of the USDA ARS at work in the almonds this season--preparing to net off a branch to measure bee pollination rates. The bee industry owes Dr. Eischen a debt of gratitude for his valuable practical research on mite control, Small Hive Beetle, and almond pollination. Photo courtesy Kodua Galieti, whose images can be seen at koduaphotography.com.
And even those growers who are paying bonuses for stronger colonies may not be compensating beekeepers adequately. I had the choice this year between several different contracts (Table 1):
Contract
Strength Specified
Payment
Payment Per Frame of Bees
A
4-frame average
$100
$25.00
B
6-frame average
$125
$20.83
C
8-frame average, 6-frame min
$145
$18.12
D
5-frame min, 11-frame max
$165 max
$15.00 max
E
12-frame average
$175
$14.58
Table 1. Comparison of payment per frame of bees, depending upon the contract. Note that in the current market, the beekeeper really has little incentive to produce strong colonies. Other than saving a bit on trucking, you get paid more per bee the weaker the colony!
Traditionally, it used to be worth it to me to combine my 4-framers with my 8-framers, and contract for 12-frame colonies at a premium price (thus saving on trucking). There is no longer much incentive for me to do so, since the current market rewards the beekeeper for the number of boxes, rather than for the numbers of bees in those boxes.
So some beekeepers stick to the "Domino's Pizza model"--forget busting your butt to produce premium colonies that growers aren't willing to pay proportionately more for. Rather, offer them the minimum quality that they'll accept, for what appears to be a cheap price. After all, they are only screwing themselves!
Grower Education
I hope that Dr. Gordon Wardell, who has been collecting data on nut yield vs. average colony frame strength, will be able to share those important economic figures with the industry some day (hint, hint). My suggestion to the almond growers would be to shift from renting numbers of hives to numbers of frames of bees per acre.
To that end, I drew up a new contract this year for one of my more enlightened growers: I guaranteed a specific number of frames per acre (18), independent of the number of hives that I used to fill the contract. For validation, I invited my grower to inspect as many drops as he wished with me, to ensure that I met the guarantee. This contract allowed me great latitude as to how to fill each drop, and could easily have had a proportional penalty written in for failure to reach the target. Since I came up a little short on hives in February, I ran all my 12-framers to this contract, and then cleaned up by renting all my weaker hives at a high per-frame rate to other growers.
Such a contract may become a model for the future. But for now, there is unfortunately a disproportionately low return for providing extra-strong colonies, and I'm tired of all the feeding and work necessary to produce them!
Fungicides
Almonds are susceptible to a variety of fungal diseases, especially in the Central and North Valleys, which receive more rain than down south. Following wet weather, the sounds of tractor-mounted blowers, crop-duster biplanes, and helicopters are common in the orchards, spraying right over our hives (Fig. 8). Although such fungicides are touted as being harmless to bees, after a spray we may observe entombed pollen, brood issues, and adult bee dwindling.
Figure 8. I snapped this photo of John Miller's hives as they were being thoroughly fogged with fungicide in the middle of the day. Although fungicides do not normally cause significant overt adult bee mortality, the surfactant adjuvants in the tank mix sure can! Such spraying may also cause negative effects upon brood, beebread fermentation, and overall colony health. Growers can mitigate these problems somewhat by spraying after dusk.
Of special concern to the California queen breeders are the queen cell losses that some see when raising queens from colonies that had been exposed to the fungicide PristineO. Dr. Gloria Degrandi-Hoffman of the Tucson Bee Lab recently presented the results of their research, which found negative effects from Pristine upon queen production.
On the other hand, I've seen legitimate research by BASF, the manufacturer of Pristine, which indicates that the active ingredient has little effect upon bee brood. At the last California Queen Breeders meeting, representatives from BASF, to their great credit, pledged to work with us to get to the root of the reported problems. The company has stationed Dr. Christof Schneider, one of their bee specialists from Germany, in California to monitor pesticide levels in pollen and to run studies in almonds. I applaud this sort of cooperative work between beekeepers and the chemical industry!
Some researchers have suggested that the problem may be due to pesticide synergies or surfactants added to the tank mixes. I also suggested that we should consider that no researchers have investigated whether there are synergies between the toxic amygdalin in almond pollen and common pesticides.
Eco-Terrorism In The Valley
As if you didn't already have enough things to worry about, this January right in the heart of almond country, animal rights extremists perpetrated an act of terrorism by using kerosene and digital timers to incinerate fourteen parked cattle trucks at a major feedlot [1, 2]. Such destruction is a tactic used by those who feel that "Arson, property destruction, burglary and theft are 'acceptable crimes' when used for the animal cause" [2a].
What has the above got to do with beekeepers? Well, if you didn't already know, "bees are abused and exploited for their honey, wax and other derivatives" [3]. There is "cruelty in the honey industry" [4]. "Many people who understand the cruelty involved in factory farming and are morally opposed to eating meat find it less obvious that the lowly honeybee should also be of ethical concern...Like all factory farming, beekeeping has morphed into an industrial process which puts profits ahead of animal concerns" [5].
Your beekeeping operation could be the next target of some extremist!
One of the problems of the blogosphere is that folk concerned about legitimate issues can, by stretching the truth just a wee bit, incite those itching to destroy something to do so for some ostensibly "just cause." The destruction of Harris Farms' trucks should serve as a warning to all beekeepers that there are those out there who are under the impression that we abuse our bees-"Like other factory-farmed animals, honeybees are victims of unnatural living conditions, genetic manipulation, and stressful transportation" [6].
The press coverage of CCD has opened an opportunity for some to blame commercial beekeeping practices as the cause of death of our unfortunate charges. I am surprised by the number of blogs on the web by well-meaning folk who earnestly believe that, "There honestly is no escaping the harsh realities of methods within the commercial honey production process and the cruelty the bees themselves are forced to endure during such times" [7].
I read this after my sons and I had worked in the rain for a week to feed thousands of dollars worth of carefully-prepared and nutritious pollen supplement to my hungry hives, gently brushing the bees aside so that we didn't squash them. Heck, in this instance, I literally treated my bees better than my own children! (Fig. 9). But you'd never know it if your only source of information was the Internet!
Figure 9. My sons feeding pollen supplement to hungry colonies in the rain prior to moving to almonds. We use a pine bough to "tickle" the bees so that they move down between the frames. Some of my recent research strongly suggests that you don't want to squash bees when you're feeding pollen supplement (more later)!
Practical application: it's up to beekeepers to educate the public as to the truth about how much we care for our bees' well-being, and that we only make a living if we treat them well!
The Future
The reality is this: almond growers are doing pretty well these days. The projected world demand for tree nuts is strong, and almonds are the cheapest and most versatile among them. Indeed, one of the industry concerns is that sales of nuts are so strong that packers are having trouble maintaining a comfortable "carryout"--a minimum inventory to act as a cushion should there be a short crop!
California holds a virtual monopoly on world production of almonds, so long as our water holds out (there is no snowpack in the Sierra this winter). And the world loves almonds! They are not only a tasty confection, but also good for you.
Despite some record almond crops in recent years, prices to growers remain profitable. Grower Bill Harp (2011), speaking to the Almond Board, reports that projected 10-20% grower returns on assets are possible with the expected almond supply and demand fundamentals (this is in an economy where any return on assets is a good thing). The bee industry will continue to hitch a ride on that wagon.
Bottom line: The near future looks pretty rosy for both almond growers and beekeepers.
Good Sources Of Information
You can track the weather and progress of bloom at the Blue Diamond website http://www.bluediamond.com/applications/in-the-field/index.cfm?navid=101).
Project Apism http://projectapism.org has two great webpages of interest to almond pollinators:
The Cummings Report http://projectapism.org/content/view/64/49/ written by almond grower and industry insider Dan Cummings, and the
Bee Status Report http://projectapism.org/content/view/93/49/
Your $1 per hive donation to Project Apism will help to support beekeeper-funded practical research.
Hilltop Ranch posts almond updates at http://www.hilltopranch.com/2012/02/almond-update-25/
References
Carman, Hoy (2011) The estimated impact of bee colony collapse disorder on almond pollination fees. ARE Update 14(5): 9-11.
Eischen, FA, RH Graham, R Rivera & J Traynor (2007) The effect of colony size and composition on almond pollen collection. http://projectapism.org/component/option,com_docman/task,doc_download/gid,40/Itemid,44/
Flohr, D (2011) 2011 Almond Forecast http://www.hilltopranch.com/wp-content/uploads/2011/05/almond-industry-historical-data-from-nass.pdf
Harp, B, et al (2011) Economics of Almond Production. (Broken Link!) http://www.almondboard.com/Handlers/Documents/Economics%20of%20Almond%20Production.pdf
Klonsky, KA, et al (2011) Sample costs to establish an orchard and produce almonds (flood). http://coststudies.ucdavis.edu/files/AlmondFloodVN2011.pdf
Klonsky, KA, et al (2011) Sample costs to establish an orchard and produce almonds (microsprinkler). http://coststudies.ucdavis.edu/files/AlmondSprinkleVN2011.pdf
Ludwig, G (2009) Present & Future Beekeeping: "Almonds" http://www.usda.gov/oce/forum/2009_Speeches/Presentations/Ludwig.pdf
Mussen, EC (2006) Chaotic almond pollination. (Broken Link!) http://entomology.ucdavis.edu/faculty/mussen/JanFeb2006.pdf
Mussen, EC (2009) How much does it cost to keep commercial honey bee colonies going in California? http://projectapism.org/content/view/83/27/
Northcutt, G (2011) Quest continues for self-fertile almond varieties. Tree Nut Farm Press 3(5).
Rabobank 2011 https://www.rabobankamerica.com/content/documents/news/2011/us_tree_nut_sales_to_remain_strong_in_coming_years.pdf
Rucker, RR & WN Thurman (2012) Colony collapse disorder: The market response to bee disease. http://www.perc.org/files/ps50.pdf
Rucker, RR, WT Thurmon and Michael Burgett (2011) Colony collapse: The economic consequences of bee disease. http://economics.clemson.edu/files/ccd-paper-full-package-apr14-2011.pdf
Sheesley, B and B Poduska (1970) strong honeybee colonies prove value in almond pollination. California Agriculture. August 1970: 4-6.
Sumner, DA and H Boriss (2006) Bee-conomics and the Leap in Pollination Fees. http://aic.ucdavis.edu/research1/bee-conomics.pdf
USDA (2010) Federal crop insurance corporation adjustment standards product administration and standards division handbook 2012 and succeeding crop years. http://www.rma.usda.gov/handbooks/25000/2012/12_25020-1h.pdf
Waycott, R, moderator (2012) The Economics of Growing Almonds. (Broken Link!) http://www.almondboard.com/Growers/Documents/The%20Economics%20of%20Growing%20Almonds.pdf
[1] (Broken Link!) http://www.fresnobee.com/2012/01/10/2677557/animal-rights-activists-take-credit.html
[2] http://www.animalliberationpressoffice.org/communiques/2012/2012-01-10_harrisranch.htm
[2a] http://activistcash.com/biography.cfm/b/1459-alex-pacheco
[3] (Broken Link!) http://www.think-differently-about-sheep.com/Animal-Rights-Bees.htm
[5] http://prime.peta.org/2009/01/but-what-about-honey-is-it-cruelty-free
[4] http://www.veganpeace.com/animal_cruelty/honey.htm
[7] http://veglin.hubpages.com/hub/Why-Honey-REALLY-isnt-Vegan
[6] http://www.peta.org/issues/animals-used-for-food/honey-from-factory-farmed-bees.aspx
Category: Almond Pollination
Tags: almond, pollination | almond Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/almond/ |
"Fried Eggs" Identified!
"Fried Eggs" Identified!
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in Feb 2012
I mentioned in my previous article that I've been seeing an unidentified organism that looked like "fried eggs" in the guts of bees from my operation in the California foothills (Figure 1). I sent out requests to a number of researchers for ideas as to what it was. Thanks to Antonio Gomez Pajuelo of Consultores Apicolas in Spain for identifying them as rust fungus spores.
Figure 1. These "fried eggs" have a distinctive pattern of tiny spikes on their outer shell, which helped to identify them as some sort of rust fungus spore. What appeared to be the process of cell division in this photo may have actually been the process of digestion! Photo by the author.
Upon further research, I found that beekeepers have long reported bees gathering rust spores and packing them into their pollen baskets, and that a number of scientific papers had been written on the subject (it always pays to dig into the older literature). The rusts are a large group of parasitic fungi with complicated life cycles. They infect quite a number of different plants, often forming reddish spore masses on the undersides of leaves. Bees have been observed collecting spores from a number of genera of rusts, including Uromyces, Puccinia, Caeoma, and Melampsora (Fig. 2),
Figure 2. Spores of the Poplar Rust Melampsora, which is commonly collected by bees. It's not clear whether rust spores in general are harmful to bees. Photo courtesy www.bioimages.org.uk, ©️ Malcolm Storey.
A.J. Cook reported in 1885 that bees in New York were gathering spores from blackberry rust "with great apparent greed." Of interest is that the last two seasons, I had noticed unusual infestations of fluorescent orange rust on our invasive Himalaya blackberries in the foothills. I hadn't put it together previously, but I had also noticed bees bringing in loads of a brilliant orange "pollen" that I'd never noticed before (by the time I got the dang things ID'd, I could no longer find that orange "pollen" to check under the 'scope). Blackberry rust is generally attributed to Caeoma, but I found that UC Davis extension (Bolda 2011) reported we have a new invasion of orange rust of blackberries caused by two other fungi--Arthuriomyces and Gymnoconia (Fig. 3).
Figure 3. An orange rust on blackberry. This looks like the same thing that I saw around my apiaries. Photo courtesy Mark Boulda.
Something that I find intriguing is that some rust fungi produce sugary secretions for the purpose of attracting insects in order to help disperse their spores (Wackers 2005). Even more fascinating is a potential explanation for the day-glow orange spore masses of blackberry rust. Shaw (1980), studying the collection of rust spores by honey bees, found that the spore masses reflected ultraviolet light of a wavelength to which bees are highly sensitive. So the fungus may be "intentionally" using bees to its advantage!
Bees consume rust spores readily; during our fall pollen dearth I often find bee guts packed with them. Schmidt (1984) found that bees in cages consumed Uromyces rust spores as readily as they did dandelion pollen, despite it being low in protein. The question then is whether rust spores are of any nutritional value to bees, or, since I often find them associated with sick colonies, whether they cause actual harm to the bees (my sampling is admittedly biased towards colonies in poor health).
Above is a photo of a typical comb filled with beebread consisting of rust fungus spores. Note the lousy brood pattern and the dying brood. When the colony is feeding upon this beebread, it goes downhill quickly. However, if we feed the hive several pounds of high-quality pollen sub, it will turn around immediately and grow again.
Antonio Pajuelo (pers comm) also reports a correlation between the consumption of poplar rust spores and colony mortality, but doesn't know whether it is due to spore toxicity or lack of better nutrition. It may be that the collection of rust spores is due to the lack of more attractive and nutritious floral pollen, and as such would simply be a generic indicator of poor colony nutritional status.
On the other hand, Schmidt (1987) found that caged bees fed Uromyces spores as a sole protein source actually had their lifespan reduced compared to those fed sugar syrup only--strongly suggesting that the spores were toxic. The spore-fed bees lived about 20 days less than those fed the most nutritious pollens!
Practical application: it may be wise to feed pollen supplement if you observe your bees collecting rust spores.
Acknowledgements
Thanks to Antonio Pajuelo and all the other researchers who helped with trying to put a name to these organisms. And a big thanks to Peter Borst and Juanse Barros for plying through Google Images in the search for the identity of these spores, and Dr. Jose Villa for digging up the old literature.
References
Bolda, M (2011) Orange rust emerging again in blackberry. http://cesantacruz.ucdavis.edu/?blogpost=4660&blogasset=16664
Cooke, AJ (1885) Fungus spores for bee bread: A new kind of pollen. Gleanings in Bee Culture July 1885 pp. 455-456.
Schmidt, JO and BE Johnson (1984) Pollen feeding preference of Apis mellifera, a polylectic bee. The Southwestern Entomologist. 9(1).
Schmidt, JO, SC Thoenes and MD Levin (1987) Survival of honey bees, Apis mellifera (Hymenoptera: apidae), fed various pollen sources. Annals of the Entomological Society of America 80(2): 176-183.
Shaw, DE (1980) Collection of neurospora by honeybees. Trans. British Mycol Soc. 74 (3): 459-464.
Wackers, FL, J Bruin (2005) Plant-provided food for carnivorous insects: a protective mutualism. Cambridge Univ. Press.
Category: Nosema ceranae
Tags: fried eggs, Nosema cereanae | Nosema cereanae Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/nosema-cereanae/ |
Sick Bees - Part 16: The "Quick Squash" Method for Determining Nosema Prevalence in a Colony
Infection Prevalence
Sequential Sampling
A Neat Little Shortcut
Validation
Summary (completely subject to revision)
More Details
Next Month
Acknowledgements
References
2019 Quick Nosema Prevalence Assessment Method
First published in ABJ February 2012
Updated March 13, 2019
Randy Oliver
Since the discovery of Nosema ceranae, I and many other beekeepers and researchers have been frustrated by the tedium and apparent futility of counting nosema spores, since many of us haven't seen any meaningful relationship between spore counts and colony health or production. I strongly suspect that the issue is not that N. ceranae does not cause problems, but rather that our methodology for assessing the degree of infection has been flawed.
The quickest way that I've found to determine the degree of nosema infection in a hive is to do a 2-step sampling.
Step 1: open the hive and take a sample of about 50 workers from an outer frame, or from under the hive cover. These bees can be salvaged from an alcohol wash for varroa. Set at least 15 bees aside for the time being, and use the rest for the next step.
I now typically use only 10 bees. This is based upon the thorough research on Nosema apis by GF White in the early 1900s. What he found was that individually sampling 10 bees in order to determine the prevalence of nosema infection in the house bees gave the best indication of its biological relevance-a finding later suggested by Cameron Jack in Colony Level Prevalence and Intensity of Nosema ceranae in Honey Bees (Apis mellifera L.).
Be sure to read https://scientificbeekeeping.com/the-seasonality-of-nosema-ceranae/
Step 2: place at least 25 of the bees in a ziplock sandwich bag, and roll a round jar over them to crush their guts thoroughly. Then add about 3 mL of water for every 10 bees in the sample, and massage the bag in your fingers until you've homogenized all the gut contents into the water, creating a semi-opaque suspension (not too clear, not too thick). For details on this step, see https://scientificbeekeeping.com/sick-bees-part-13-simple-microscopy-of-nosema/
Step 3: immediately place a drop of the suspension on a slide, drop on a cover slip, and view under the scope. Scan a few fields of view for nosema spores. If you don't see any (or only one or two), that indicates that the infection prevalence of that sample of bees was zero-end of assessment.
On the other hand, if you see spores in the sample, then perform 10 individual bee gut squashes from the remaining bees in the original sample in order to determine the biological relevance of the infection prevalence in the colony-details below.
Infection Prevalence
The current "standard" method for monitoring nosema "level" in hives is to determine the mean spore count per bee in an aggregate sample (of typically 10-100 bees). The method is relatively quick and gives the sort of quantifiable numbers that scientists love. Unfortunately, as noted by Meana (2010), "the spore count is not directly related to the parasite burden and health status of whole colonies naturally infected by N. ceranae under field conditions."
Spore counts certainly have their uses, such as quantifying the progress of nosema infection in individual bees in cage trials by researchers. They are also appropriate as a method for "discovery sampling." For example, one can "discover" whether nosema is present to any extent in an apiary by taking an aggregate sample of say ten bees from the entrance of every hive and determining the mean spore count. If the count is less than 1M (1 million spores per bee), then nosema is likely not a problem in the sampled hives.
The point that I'm trying to make about sampling for nosema is that we are well beyond the "discovery" phase. Rennich (2011) found N. ceranae in at least half of all random bee samples taken in the U.S. during winter and spring.
So instead of "discovery" sampling, what we need to do is to shift to the most meaningful way to measure the potential impact of nosema upon colony health--the proportion of infected bees. Of the various terms used to describe this measure--"proportion of infected bees in a sample," "percent infected," or "infection rate"- I prefer the term used by epidemiologists: "prevalence."
Practical application: I henceforth plan to use the term "prevalence" as the measure of the proportion of bees infected by nosema. For example, if 2 bees out of 10 were infected, that would be a prevalence of 20%.
There is a strong case to be made for shifting our assessment of nosema infection from "intensity" (as measured by spore counts) to "prevalence" (the percent of bees actually infected). The only problem with determining prevalence is that most of us choke at the thought of having to inspect jillions of bees one at a time. Luckily, there are practical shortcuts:
Sequential Sampling
In my last article, I proposed that even a small sample of bees might be adequate for making management decisions. I'm immensely grateful to Dr. Jose Villa of the Baton Rouge Bee Lab for bringing to my attention that I was reinventing the wheel--this sort of decision making process, based upon small sample sizes, already has a fancy name: it's called "sequential sampling," and was develped as a time-saving method for quality control inspections during World War II. Furthermore, Dr. Villa dug into the library and forwarded me existing "Decision Tables" for tracheal mite sampling produced by Tomasko (1993).
Dr. Maryann Frazier (2000), following up on Tomasko's work, discussed the situation regarding the assement of tracheal mite prevalence as opposed to "parasite load" (analagous to spore counts). It is remarkable in that it almost exactly mirrors today's situation with nosema! And in her paper she validated the accuracy of sequential sampling.
Sequential sampling is all about the tradeoff between tedium (the number of bees that you need to squash and view) and confidence (the error rate which you are willing to accept). And it appears that for our purposes, I estimated the minimum number of bees to sample right on the nose!
So let's set some arbitrary parameters for our decision making:
An infection prevalence of 10% is "tolerable."
A prevalence of 30-40% is "intolerable."
We'll accept a 20% error rate for overestimating the prevalence.
But we won't accept an error rate above 10% for underestimating the prevalence.
We'll use the above parameters to set our treatment thresholds--below 10% prevalence, don't treat; above 30%, treat. The math gets complex, but here's the gist of the outcome:
Practical application: it appears that in order to make a decision whether to treat or not, that a couple of 5-bee samples should be adequate, interpreted as follows:
0 positive bees out of 5, or no more than 1 positive out of 10 indicates < 10% infection
3 positive bees out of 5, or at least 4 positives out of 10 indicates > 30% infection
Any number of positive bees lying between these cutoffs (e.g., 2 bees out of 5, or 3 out of 10) is not enough to make a firm decision, but suggests an infection level that lies in the gray zone. But I doubt that going beyond a 10-bee sample is worth the effort--I'd just move on to the next sample.
With true sequential sampling, you'd keep sampling until you hit a critical number of positive or negative bees in order to make a treatment decision. However, my limited experience suggests that we hit a point of diminishing returns after viewing 10 bees.
Update July 5, 2012 Beekeeper Ruary Rudd (ruaryrudd@iol.ie) has developed a great Excel spreadsheet for sequential sampling. You can write him for a copy-thanks Ruary!
So I've got us down to sampling a maximum of 10-bees. But even so, I must advise you that nosema infection appears to exist in "pockets" of bees in the hive, so any single small sample is inadequate for making an apiary-level decision (Botias 2011). Therefore, it's necessary to process a number of samples. What's been holding us back from determining actual nosema prevalence is the lack of a quick method for processing a number of samples of 10 bees!
Nosema apis becomes a serious problem if about a third of the bees in a hive become infected. It appears that Nosema ceranae may be a problem at even a lower prevalence.
A Neat Little Shortcut
Since I really wanted to find a quicker way to prepare and view the 200 bees for the validation table in the previous article, I racked my brain trying to figure out a technique for speeding things up, and finally hit upon a relatively simple procedure (Figures 1,2, and 3). I've now got over 400 individual gut squashes under my belt, and am pretty excited about the method! This solution allows me to process bees at an overall turnaround rate of less than five minutes per sample of 10 bees!
Figure 1. This photo shows the necessary equipment for a Quick Squash--5 bees, a plain microscope slide, 5 custom-made thin plastic cover slips, a table knife, and a paper towel.
The size of the cover slips is critical--they must be narrow enough not to touch at the edges, in order to keep the individual gut slurries from mixing. The easiest solution is to cut off-the-shelf plastic microscopy cover slips in half with scissors. You can then just discard them after use (cost about 20C//10-bee sample), or wash and reuse (use your mite shaker jar).
Update Feb 2019: I prefer to recycle rather than discard. But when I looked at costs, getting a large order of #1 thickness glass cover slips works out to only about a penny a slip. At Amazon: Karter Scientific 211Z2 Standard Microscope Cover Slip, #1 Thick, 22x22mm, 200pk (Case of 2000).
Be sure to order #1 thickness cover slips, since thicker cover slips won't allow you to focus upon the spores.
The other thing is that you don't need to make custom cover slips at all. Three standard glass cover slips will fit across a slide, and can be discarded after use if you don't want to wash them (although they wash easily in warm water with a tiny bit of dishwashing detergent).
But if you don't have plastic cover slips at hand, don't despair! You can make cover slips out of clear plastic scrap around the home--but only some plastics will work; I've experimented with several. Clear plastic transparency sheets unfortunately refract light in such a way that they make nosema spores look like little rectangles, so they don't fit the bill.
The heavy blister packs from the hardware store are too thick to focus through--a cover slip for 400x viewing needs to be thin. But then I found just the thing--the clear lid from a tub of the Colonel's Kentucky mashed potatoes (get the gravy too, so you get an extra lid). Cut it into 11mm x 22mm rectangles--they work perfectly! You can wash them in soapy water, rinse, blot, and reuse until they get scratchy.
Practical tip: Cut a whole bunch of cover slips and keep them in a custard dish for easy pick up--this greatly expedites the slide prep time. Look for thin clear plastic with the #1 recycling symbol for polyethylene terephthalate:
Beekeeper Health Breakthrough: Wracked as I was by images of beekeepers stuffing themselves with mashed potatoes in order to be able to monitor nosema levels, I forayed to the grocery to see if I could recommend a more healthful suggestion. To my great relief, I found that the rectangular containers for the nutritious "Baby Mixed Greens" are also made from PETE, and make excellent cover slips!
Figure 2. Hold a bee by the head/thorax, then use the table knife to "milk" the gut contents (or the gut itself) out of its abdomen directly onto the slide. Use the knife tip to mash the material in a droplet of water in order to distribute any spores into the macerate. Then remove any excess bee tissue, leaving a thin slurry (note the stinger and rectum on the slide, and on the towel to the right). Finally, place a cover slip over the drop of slurry. In this photo, I've completed two preps at the top (neither contained much pollen). I'm working on the third, which will make a more opaque slurry.
The technique of "milking" the bee's abdomen by rocking a flat blade from front to rear will quickly cause the discharge of the gut contents, or with increased pressure, the gut itself. It is critical to thoroughly crush and mash these in a little water--I wet the tip of the knife blade in a stream of water if necessary--until you create a cloudy, but not opaque, macerate. Tip: it's critical to be able to press the knife tip down flat against the slide, so work with the slide near the edge of a raised cutting board, so that your knuckles can drop below the work surface level. Be careful to keep the macerate on the portion of the slide that will be under each cover slip. Then be sure to flip off any thick chunks of excess tissue, especially the sting or any dark pieces of exoskeleton, or they will space the cover slip up too high. Clean the knife tip under running water, and wipe it on the dry towel between each bee. With practice, this entire process takes only a few seconds!
Repeat the process down the slide, exercising caution to wipe the blade thoroughly between bees, and not allowing any liquid to run from sample to sample. The separate cover slips keep the samples from mixing. After you've crushed and covered 5 gut samples, then fold the towel over the slide and press down firmly and evenly to set all the cover slips down flat, and to absorb any liquid that might otherwise get onto the microscope lens.
Figure 3. Presto--you now have a 5-bee gut sample ready to view under a scope. It's then a simple matter to glance at each of the samples in turn to check for nosema spores. This technique works for either freshly-killed or preserved bees.
At this point is really helps to have a scope with an adjustable stage (having turnable knobs to move the slide around). Then you can easily move from one cover slip to the next, and quickly scan up and down each slip if necessary. It's also very easy to see whether you've gotten nurse bees or foragers, since each gut squash clearly shows any contained pollen (Figs. 4 and 5).
Figure 4. Close up of the differences between squashes containing pollen (center) and those from without. This sample was taken from the entrance on a cold November morning with minimal flight. See the following photos for how the two left-hand squashes looked under the scope. Two out of 5 of these bees were infected.
Squashed bee guts, especially the midgut, are typically either free of nosema, or strongly infected, as above.
Figure 5. This is a view of the orange-colored center squash shown above. This bee is only moderately infected with Nosema ceranae, and the gut also contains some orange-centered rust fungus spores-which are unhealthy for bees to consume.
Figure 6. A close up from a gut packed full of "fried eggs." It took me a while, but I finally identified these spores as being from rust fungus.
It took me quite a while, but I eventually identified the "fried eggs" in the bees' guts as being spores from a blackberry rust fungus. In the photo above, you can see the fluorescent-orange spores packed as beebread-this is not pollen! The fungus tricks the bees into gathering its spores. Note the dying larvae next to this abundant beebread-although this colony appears to have abundant beebread, in fact, the fungal spores are unhealthy to the hive. In my area, hives full of such spores go downhill, unless we feed them all the pollen sub that they will eat. See "Fried Eggs" Identified!
Back to nosema sampling, one of the major beauties of the Quick Squash method is how quick it is, since you don't need to count spores at all (Fig. 7)!
Practical application: After a bit of practice, my turnaround time for the entire process of preparing, viewing, and recording results for 10 bees (two 5-bee slides) is just over four minutes if I don't fumble something along the way. Tip: have plenty of precut cover slips at hand in a small bowl.
Figure 7. This is a view of the far left-hand squash from an older bee, whose gut does not contain pollen. Even though the preparation looked nearly clear to the naked eye, it is easy to see the degree of nosema infection.
Viewing individual bees gives you a much better idea of just how greatly the gut contents of bees vary from bee to bee within the same hive! Sometimes each of the 5 gut contents look completely different. All that I can say is that bees have a lot of different things going on in their guts, and numerous infections, most of which I can't identify (Fig. 8).
Figure 8. This poor bee is suffering from both Nosema ceranae and what appears to be a Malpighamoeba mellificae infection (the larger oval cysts). Amoeba infection is not something that most beekeepers even consider, but I find it commonly in failing hives.
Malpighamoeba mellificae in the Malphigian tubules of bees ©️ Institut fur Saat - und Pflanzgut, Pflanzenschutzdienst und Bienen Abteilung Bienenkunde und Bienenschutz -
I'm not a microbiologist, and have trouble differentiating yeast cells in the gut from amoeba cysts. Here's a photo of beebread to which I added a weak sucrose solution, and allowed to ferment. I'm guessing that the cells between the pollen grains are yeasts. If anyone can help me, please let me know!
This method takes less time than a standard hemacytometer count, yet provides you far more useful information.
Economic analysis: A scope (which will last the rest of your life) costs less than the rental rate for two hives in almonds. You can easily run a dozen of these samples in an hour, which would give you a good idea of the infection rate for the weaker hives a 50-hive apiary. This method can quickly let you know if you have a serious nosema problem. On the other hand, bottle of fumagillin to unnecessarily treat those 50 hives would set you back $140, plus syrup and labor.
Update: time and again I've had beekeepers tell me that they've been trying to control dysentery by feeding fumagillin. When I ask them to send me bee samples, I often find that there is no nosema present, suggesting that they've been blaming the wrong suspect! As far as I can tell, nosema does not cause dysentery-this is a common misconception. Dysentery can spread nosema in the hive, but it doesn't appear to be an indicator of nosema.
There is nothing new about knowing that measuring the infection rate is a better assessment of nosema infection than that of taking spore counts--Dr. White made that clear back in 1919, and it has been confirmed again and again. The problem has always been that it is simply too tedious to individually squash hundreds of bees (Dr. White individually squashed and microscopically viewed over 3000 bees). What has always been lacking is a time-efficient way to determine the infection rate, and that is what I tried to develop with this "Quick Squash" method. Shy of an automated device, this method may be the best practical assessment of colony infection rate, and appears to have a reasonable degree of accuracy.
Validation
OK, so this past week I took samples from the strongest hives and from dinks in some of my yards, and have so far processed a total of 40 samples (I still have a backlog at press time, and favored the samples from weak hives). I've graphed the results below (Fig. 9):
Figure 9. Distribution of nosema prevalence in the weakest and strongest hives in my apiaries in early December, based upon 10-bee samples taken from under the lid or outside combs. In none of the strong hives were more than 1 bee out of 10 infected; whereas the majority of the weak hives scored at least 1 or more infected bees out of 10, and 40% scored 2 or more positives.
The preliminary data above strongly suggest that Nosema ceranae infection is associated with colony weakness in my own operation, which is not surprising, based upon the vast body of previous research on the negative effects of nosema! At this point in time, I am rather disillusioned with any field research findings based upon spore counts, and hope that other researchers follow the lead of Dr. Mariano Higes and include the percentage of infected bees.
Practical application: The point of the above graph is that up 'til this point, I have never been able to correlate N. ceranae infection intensity, based upon spore counts, with either colony health or production. But when I switched to a different assessment method--quantifying nosema prevalence based upon the number of infected bees in a sample of 10--the relationship jumps right out!
Summary (Completely Subject To Revision):
Early spring and early fall are likely the most appropriate times to sample, or during winter if you're going to almonds. No need to look for nosema in July or August, as it normally "disappears" during that time.
Take samples any time of year from any colonies or yards that appear to not be performing well--lagging, poor weight gain, lack of foragers or bees over the brood. I'm not sure whether it's worthwhile to routinely bother with taking nosema samples, provided that your colonies are not under stress, and so long as they are kicking butt.
Brush a dozen bees from under the lid or an outside comb into a ziplock bag, and add a glug of rubbing alcohol (for long-term storage use bottles and additional alcohol, or freeze). If you wish to label the sample, make sure the marker is alcohol resistant, or write with a pencil and put the label inside the bag.
(Alternate assessment) Process about 50 bees by the ziplock method (see Sick Bees Part 12). If you see fewer than about 5 spores in a field of view (about 1M equivalent), then you've got nothing to worry about. If more, go to the next step.
From each sample, prepare two slides of 5 bees each per the "Quick Squash" method in this article.
Interpret the entire 10-bee sample as follows:
0-1/10 positive for spores-likely safe
3/10-likely moderate infection
4/10-likely serious infection
>4/10- very likely serious
Be concerned any time that you hit 2 or more positive bees out of 5.
The odds of hitting 3 or more bees out of 10 climbs rapidly with infection rate--to a definitive 95% chance once half the bees in the hive are infected!
6. I feel that it is likely not worth the effort to sample more than 10 bees from any single hive-10 bees should give you a fairly close estimate of infection prevalence in that hive. Better to spend the time sampling more hives!
7. Important: don't base any management decisions upon only a single sample! Keep sampling until you are comfortable with the consistency of the results.
I realize that I just threw a lot of numbers at you, but in practice the method is really intuitive. It's very much like playing poker--your brain easily grasps the probabilities of getting either one ace or four in a hand. Chances are that you'll get more positive hits from colonies with a serious nosema infection, and few or no hits from healthy colonies.
Processing bee samples by this "Quick Squash" method offers an easy way for beekeepers to monitor whether nosema is actually a problem in their operations. It takes me less time to process a 10-bee sample than it does to do a single hemacytometer count, but the results of this method are much more meaningful from a practical standpoint. The "old school" researchers found this method to be a reliable assessment of the seriousness of nosema infection for N. apis; I suspect (subject to verification) that it may also prove to be the best for N. ceranae.
It sometimes seems that beekeepers need to reinvent the wheel. Anyway, I just came up with this quick method and really like it! My sons mastered the technique in a couple of tries. My favorite part is that I no longer need to count spores--a quick glance gives you a yes/no for infection. I'd be a happy guy if I never had to count another varroa mite or nosema spore--I'd much rather be counting all the money I'll be making from my healthy hives!
I feel that it is time for a paradigm shift in the way that we assess the impact of nosema infection upon colonies--moving from spore counting back to determining the proportion of infected bees! To that end, this method is practical and surprisingly quick, and gives you a much better idea of what's actually happening in the hive. I'd really appreciate hearing your results or suggestions for improvement if you try it (randy@randyoliver.com).
More Details--Web Version
I'm not looking to belabor the point of the reliability, or lack thereof, of spore counts, but I feel that this is an important enough issue to the beekeeping industry, in light of potential reduced honey production, increased colony mortality, and the cost of treatment, that interested beekeepers have a thorough understanding of the strong and weak points of various sampling methods.
The key question then is whether researchers, testing labs, and beekeepers can all agree upon a "standardized" method of testing, so that we can all compare results and recommendations. The current problem is that spore counts, even from the same colony, are frustratingly variable, depending upon the time of day at which the bee samples are taken (Fig. 1), the weather conditions, the place in the hive from which they are taken, the number of bees in the sample, how they are processed (mortar and pestle, filtration, squashing, etc.), how they are viewed (simple microscopy or hemacytometer), and even then counts are largely based upon the pure chance of whether or not one gets one or more highly-infected old bees in the sample!
Figure 1. Spore counts of four 25-bee samples taken each day from the same hive--from the entrance or the inside, and at either 9:30am or 12:30 pm. Note that counts on the same day varied from nearly zero to 10M spores--testament to the inherent variability of spore counts! It is also unlikely that the infection level varied as greatly from week to week as the data suggest. This finding really makes me question the comparability of spore counts unless they are taken at exactly the same time of day, under similar weather conditions, and from the same place in the hive each time! Data reworked from Meana (2010).
The colony sampled in Figure 1 was presumably moderately-infected, but in apparent good health. The researchers concluded, "This strong variation in the spore count was not associated with signs of illness and indeed, the colony was apparently as healthy (asymptomatic) as any other. It would thus appear that the spore count is not useful to measure the state of a colony's health [emphasis mine]." I echo this conclusion (as do a number of other studies), since while monitoring nosema counts in my own operation over the past four years, I have been unable to detect any correlation between spore counts and colony health, productivity, nor survival.
The above authors conclude that "the mean proportion of infected bees may be a more reliable method to establish colony health." This suggestion goes right back to Dr. White's findings at the beginning of the last century, and has withstood the test of time. I guarantee that looking at the individual gut contents of a sample of 10 bees gives one a much better feeling as to the severity of nosema infection in that hive!
From Where Should We Take Samples?
Figure 2. Spore counts vs. percent infection for house and field bees, n = 30 for each sample; all samples taken at 12:30pm. Data reworked from Higes (2008). Note that spore counts roughly reflect the percent infection rate for either group, but that spore counts of house bees may not be a particularly good indicator of the infection rate of field bees, which is likely the best assessment of the impact of nosema upon colony health. On the other hand, in this data set, the infection rates of both house and field bees roughly tracked each other. This data set suggests that spore counts of field bees is the most sensitive measure of the degree of nosema infection in a hive.
Experts' Opinions
Smart and Sheppard (2011) concluded that: "Based on these findings, we speculate that bees collected from the inner hive cover represent a mixture of age classes of bees and, depending on the goals of the sampler, may provide a better estimate of the whole colony mean infection level than sampling just foragers.
So I asked Dr. Brian Johnson, who had considerable experience with tracking bees in observation hives. He told me:
"The bees just under the lid tend to be older middle age bees, while the bees on the outside combs are mostly middle age bees with smaller numbers of nurses and foragers. In general, the foragers are near the entrance, the nurses are in the brood zone, and the middle age bees are everywhere, but with a slight bias for the honey zone."
I also asked the preeminent bee behavioralist, Dr. Tom Seeley. His response:
"Interesting question. The only information that I have regarding the age distribution of bees who are spending time just under the lid or on one of the outer combs (i.e., ones without brood) comes from a study that I did back in 1982. In it, I mapped out the locations (in a large observation hive) of various activities and at the same time I took data on the age distributions of the bees performing these tasks. These results make it clear that the middle-aged bees are mainly working in the peripheral (outside the brood nest) regions of the nest. So if bees are collected from these areas during the day, then they will be mainly middle-age and forager-age bees. At night, the percentage of forager-age bees will be higher. You've probably seen in observation hives how the foragers literally hang out in the edge areas of a hive at night."
Finally, there is one more piece of supportive evidence for taking samples from under the lid: Moeller (1956) found that "nosema-infected bees congregate in and above warm brood areas."
Conclusions
Hey, I'll leave the conclusions up to you. Today, I did some spore counts of 20-bee samples of piles dead bees from the front of three hives in one yard. They had little nosema--about 5 spores per field of view, so approx. 1M/bee. So not enough spores to indicate that a 10-bee squash would be useful. Since the bees were dead, it would have entailed rehydration in order to do gut squashes.
I also did some Quick Squashes of bees from under the lid for other hives. Each method has its advantages and limitations. The smart beekeeper understands them!
Next Month
Nosema: The Smoldering Epidemic
Acknowledgements
I wish to thank my wife Stephanie for her patience, and helpful comments on my manuscripts (she chokes on math and graphs, and is immensely helpful to me for making my charts more user friendly). As always Peter Borst helped with the research for this article. A special thanks to Dr. Jose Villa, as mentioned previously. Thanks to Dr. Jerry Bromenshenk for his helpful suggestions. And a big thanks to Drs. Mariano Higes, Aranzazu Meana, and Raquel Martin-Hernandez for their diligent work on nosema! For financial support toward this research, I've very appreciative of Joe Traynor, Heitkam's Honey Bees, Jester Bee Company, the Virginia State Beekeepers Assoc, and individual beekeepers Paul Limbach, Chris Moore, and Keith Jarret.
References
Botias, C, et al (2011) Critical aspects of the Nosema spp. diagnostic sampling in honey bee (Apis mellifera L.) colonies. Parasitology Research (in press).
Fingler BG, WT Nash, and TI Szabo (1982) A comparison of two techniques for the measurement of nosema disease in honey bee colonies wintered in Alberta, Canada. ABJ 122(5):369-371.
Forsgren, E, and I Fries (2010) Comparative virulence of Nosema ceranae and Nosema apis in individual European honey bees. Veterinary Parasitology 170: 212-217.
Frazier, MT, et al (2000) A sequential sampling scheme for detecting infestation levels of tracheal mites (Heterostigmata: Tarsonemidae) in honey bee (Hymenoptera: Apidae) colonies. Journal of Economic Entomology 93(3):551-558.
Higes, M, et al (2008) How natural infection by Nosema ceranae causes honeybee colony collapse. Environ Microbiol 10: 2659-2669.
Mattila HR, and GW Otis (2007) Dwindling pollen resources trigger the transition to broodless populations of long-lived honeybees each autumn. Ecol Entomol 32:496-505.
Meana, A, et al (2010) The reliability of spore counts to diagnose Nosema ceranae infections in honey bees. Journal of Apicultural Research and Bee World 49(2): 212-214.
Moeller, F.E., 1956. The behavior of nosema infected bees affecting their position in the winter cluster. J. Econ. Entomol. 49 (6), 743-745.
Oliver, R (2008) The Nosema Twins Part 3: Sampling. ABJ 148(2): 149-154. https://scientificbeekeeping.com/the-nosema-twins-part-3-sampling/
Porrini, MP, et al (2011) Nosema ceranae development in Apis mellifera: influence of diet and infective inoculum. Journal of Apicultural Research 50(1): 35-41
Smart, MD and WS Sheppard (2011, in press) Nosema ceranae in age cohorts of the western honey bee (Apis mellifera). J. Invertebr. Pathol. doi:10.1016/j.jip.2011.09.009
Tomasko, M. Finley, J. Harkness, W. Rajotte, E. 1993. A sequential sampling scheme for detecting the presence of tracheal mite (Acarapis woodi) infestations in honey bee (Apis mellifera L.) colonies. Penn. State College of Agricultural Sciences, Agricultural Experiment Station Bulletin 871.
Traver, B., and RD Fell (2011a) Prevalence and infection intensity of Nosema in honey bee (Apis mellifera L.) colonies in Virginia. J Invertebr Pathol 107 (1):43-49.
Traver, BE MR Williams, and RD Fell (2011b; in press) Comparison of within hive sampling and seasonal activity of Nosema ceranae in honey bee colonies. Journal of Invertebrate Pathology.
White, GF (1919) Nosema-Disease. USDA Bulletin No. 780.
Category: Nosema Summaries and Updates, Sampling
Tags: infection, n. apis, N. ceranae, nosema apis, Nosema cereanae, squash | infection Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/infection/ |
"Fried Eggs" Identified!
"Fried Eggs" Identified!
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in Feb 2012
I mentioned in my previous article that I've been seeing an unidentified organism that looked like "fried eggs" in the guts of bees from my operation in the California foothills (Figure 1). I sent out requests to a number of researchers for ideas as to what it was. Thanks to Antonio Gomez Pajuelo of Consultores Apicolas in Spain for identifying them as rust fungus spores.
Figure 1. These "fried eggs" have a distinctive pattern of tiny spikes on their outer shell, which helped to identify them as some sort of rust fungus spore. What appeared to be the process of cell division in this photo may have actually been the process of digestion! Photo by the author.
Upon further research, I found that beekeepers have long reported bees gathering rust spores and packing them into their pollen baskets, and that a number of scientific papers had been written on the subject (it always pays to dig into the older literature). The rusts are a large group of parasitic fungi with complicated life cycles. They infect quite a number of different plants, often forming reddish spore masses on the undersides of leaves. Bees have been observed collecting spores from a number of genera of rusts, including Uromyces, Puccinia, Caeoma, and Melampsora (Fig. 2),
Figure 2. Spores of the Poplar Rust Melampsora, which is commonly collected by bees. It's not clear whether rust spores in general are harmful to bees. Photo courtesy www.bioimages.org.uk, ©️ Malcolm Storey.
A.J. Cook reported in 1885 that bees in New York were gathering spores from blackberry rust "with great apparent greed." Of interest is that the last two seasons, I had noticed unusual infestations of fluorescent orange rust on our invasive Himalaya blackberries in the foothills. I hadn't put it together previously, but I had also noticed bees bringing in loads of a brilliant orange "pollen" that I'd never noticed before (by the time I got the dang things ID'd, I could no longer find that orange "pollen" to check under the 'scope). Blackberry rust is generally attributed to Caeoma, but I found that UC Davis extension (Bolda 2011) reported we have a new invasion of orange rust of blackberries caused by two other fungi--Arthuriomyces and Gymnoconia (Fig. 3).
Figure 3. An orange rust on blackberry. This looks like the same thing that I saw around my apiaries. Photo courtesy Mark Boulda.
Something that I find intriguing is that some rust fungi produce sugary secretions for the purpose of attracting insects in order to help disperse their spores (Wackers 2005). Even more fascinating is a potential explanation for the day-glow orange spore masses of blackberry rust. Shaw (1980), studying the collection of rust spores by honey bees, found that the spore masses reflected ultraviolet light of a wavelength to which bees are highly sensitive. So the fungus may be "intentionally" using bees to its advantage!
Bees consume rust spores readily; during our fall pollen dearth I often find bee guts packed with them. Schmidt (1984) found that bees in cages consumed Uromyces rust spores as readily as they did dandelion pollen, despite it being low in protein. The question then is whether rust spores are of any nutritional value to bees, or, since I often find them associated with sick colonies, whether they cause actual harm to the bees (my sampling is admittedly biased towards colonies in poor health).
Above is a photo of a typical comb filled with beebread consisting of rust fungus spores. Note the lousy brood pattern and the dying brood. When the colony is feeding upon this beebread, it goes downhill quickly. However, if we feed the hive several pounds of high-quality pollen sub, it will turn around immediately and grow again.
Antonio Pajuelo (pers comm) also reports a correlation between the consumption of poplar rust spores and colony mortality, but doesn't know whether it is due to spore toxicity or lack of better nutrition. It may be that the collection of rust spores is due to the lack of more attractive and nutritious floral pollen, and as such would simply be a generic indicator of poor colony nutritional status.
On the other hand, Schmidt (1987) found that caged bees fed Uromyces spores as a sole protein source actually had their lifespan reduced compared to those fed sugar syrup only--strongly suggesting that the spores were toxic. The spore-fed bees lived about 20 days less than those fed the most nutritious pollens!
Practical application: it may be wise to feed pollen supplement if you observe your bees collecting rust spores.
Acknowledgements
Thanks to Antonio Pajuelo and all the other researchers who helped with trying to put a name to these organisms. And a big thanks to Peter Borst and Juanse Barros for plying through Google Images in the search for the identity of these spores, and Dr. Jose Villa for digging up the old literature.
References
Bolda, M (2011) Orange rust emerging again in blackberry. http://cesantacruz.ucdavis.edu/?blogpost=4660&blogasset=16664
Cooke, AJ (1885) Fungus spores for bee bread: A new kind of pollen. Gleanings in Bee Culture July 1885 pp. 455-456.
Schmidt, JO and BE Johnson (1984) Pollen feeding preference of Apis mellifera, a polylectic bee. The Southwestern Entomologist. 9(1).
Schmidt, JO, SC Thoenes and MD Levin (1987) Survival of honey bees, Apis mellifera (Hymenoptera: apidae), fed various pollen sources. Annals of the Entomological Society of America 80(2): 176-183.
Shaw, DE (1980) Collection of neurospora by honeybees. Trans. British Mycol Soc. 74 (3): 459-464.
Wackers, FL, J Bruin (2005) Plant-provided food for carnivorous insects: a protective mutualism. Cambridge Univ. Press.
Category: Nosema ceranae
Tags: fried eggs, Nosema cereanae | fried eggs Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/fried-eggs/ |
A New Large-Scale Trial of Clothianidin
First published in: American Bee Journal, September, 2012
A New Large-Scale Trial of Clothianidin
Randy Oliver and Brett Adee
First published in ABJ September 2012
The process for approving a new pesticide is similar to that of approving a new drug. In the case of a drug, randomized controlled clinical trials are run to demonstrate efficacy and safety. Then once the drug is approved for use, it essentially undergoes a more extensive "uncontrolled trial," in which regulators watch for reports of adverse effects, which, if they are problematic, could result in either relabeling of the drug, or its withdrawal from the market.
Due to reports of adverse effects from the neonicotinoids, both the EPA and Canada's Pest Management Regulatory Agency (PMRA) are reevaluating the registrations of these insecticides [1]. PMRA has called for Bayer to expand one of the original studies used for the registration of clothianidin as a seed treatment for canola. That study [2], performed in 2005-2006, has been questioned on a few points, mainly:
1. Due to the small plot sizes, bees could have foraged off the test plantings and avoided the treated crop, or been exposed to insecticide residues from other flora.
Clothianidin residues showed up in some nectar samples from the control colonies, indicating that the control bees foraged to some extent on the treated plots, thus compromising the controls.
Figure 1. Canola is a favored plant for systemic insecticide studies, since bees avidly forage on its nectar and pollen, both of which contain residues of the seed treatments (typically <2ppb). Virtually all canola seed is treated with fungicides plus the neonicotinoid clothianidin.
Canola seed is normally treated with fungicides to ensure adequate germination, so it is easy for seed companies to also add clothianidin to control the devastating flea beetle, which attacks the young plants. The effectiveness of this environmentally-friendly treatment (no spraying necessary) has allowed growers to massively expand canola plantings over the past 15 years--to the current 20 million acres.
Bayer CropScience grows hybrid canola seed in Canada, and in an ironic twist, is thereby the largest renter of honey bee pollination services in Canada, and is thus highly motivated to ensure that the product does not harm bees. In late June, Bayer invited representatives of the regulatory agencies, Canadian and U.S. beekeepers (including the authors), seed suppliers, and grain growers to the University of Guelph to familiarize us with the experiment, and to solicit our input on the design.
This new trial should be of interest to U.S. commercial beekeepers, since about a quarter of commercial hives spend the summer in the Dakotas [3]. Canola is becoming a favored crop in the prairies, with over a million acres (1700 square miles) to be planted in North Dakota alone this year.
Since virtually all canola seed is treated with clothianidin or its precursor, thiamethoxam, this trend suggests that plenty of colonies will be ingesting residues in their diet (Figure 1).
The crop protection companies[1] typically hire independent investigators to run field trials of their products in order to avoid charges of conflict of interest (Figure 2). For this trial, they again hired University of Guelph environmental scientists Drs. Cynthia Scott-Dupree and Chris Cutler to repeat their previous study in more and larger plots (Figure 3). Bayer scientist Dr. Dave Fischer (Environmental Toxicology and Risk Assessment) presented details of this ambitious study, designed to eliminate any questions about the original studies:
1. The scientists went to great effort to locate ten widely separated 2 hectare (5 acre) plots in which to plant canola, with the added requirements that no other canola, and little competing forage, would be growing within normal flight range (10 km) (Brett and I confirmed that the test plots appeared to be surrounded largely by forest or agricultural land without competing forage).
2. The distance between plots would prevent any cross-plot foraging, so that the researchers would know that any canola pollen in the hives would have necessarily come from the test plot.
3. The researchers are trapping pollen to confirm the degree of foraging on the canola plots.
4. The stocking rate was low enough that each 2 hectare plot should provide adequate forage for the 4 colonies.
5. The ten plots should increase the statistical strength of the study.
During the tour, Dr. Fischer solicited comments from all invitees to make sure that we were satisfied with the protocol. We (Brett and Randy) raised several questions, which were answered to our satisfaction. All parties were receptive to our comments. We suggested a change in protocol, which was subsequently implemented-we asked the researchers to change the holding yard to which the colonies were to be moved after bloom to a non agricultural area in order to eliminate any further exposure to clothianidin (as from soybeans or corn). This would ensure that the control group was truly a clothianidin-free control. Overall, we found both the Bayer reps and the investigators willing and determined to run an honest and unquestionable trial.
[1] I hesitate to call the Plant Protection Products companies "chemical companies" anymore, as the leading companies are moving into biological products, genetics, and RNAi technology.
Figure 2. In order to avoid implications of bias, plant protection product companies routinely hire independent scientists to perform the required field trials of their products. Principal investigator Dr. Scott-Dupree's bio reads, ""My research interests include integrated management of insect pests in horticultural, fruit, field and greenhouse crops using environmentally compatible control methods, insecticide resistance management, and the impact of agro-ecosystems on non-target organisms, including beneficial insects such as honey bees, bumble bees, native bees and natural enemies or biological control agents of insect pests."
The investigators randomly chose half the plots to plant with clothianidin-treated seed; the other half serve as controls, and were sprayed for flea beetles a month before bees were introduced. The field technicians paid great attention to detail to make sure that each field was planted in an identical manner.
Four colonies were placed in the center of each field at the beginning of bloom, fitted with both pollen traps (normally open) and dead bee traps. Each plot provides enough forage for four colonies, and the pollen will be analyzed to determine whether bees foraged off site, and to quantify any pesticides present in the pollen (nectar will also be tested).
Figure 3. Principal investigators Drs. Cynthia Scott-Dupree and Chris Cutler next to one of the test colonies fitted with a dead bee trap in front. Four hives were placed at the center of each 5-acre field of canola, with no other canola, and little other forage, within flight range.
Periodically the research teams (composed of grad students) will pull each brood frame from each hive, and photograph it to be analyzed by a fancy (and expensive) computer program which quantifies the coverage by adult bees, as well as the amount of sealed brood (Fig. 4).
Figure 4. This specially-designed system will be used to photograph both sides of each frame in the field (with and then without bee coverage). A computer program then determines the number of bees and area of sealed brood.
At the point where only 25% of bloom remains, all the hives will be removed from their test plots and taken to a single non agricultural fall/winter yard to track colony overwinter survival. The research teams will collect data on colony weight, honey yield, adult bee mortality, brood production, colony strength (adult bee coverage), queen events, and residues in nectar, honey, pollen, and wax. The entire trial with be performed following GLP's--the highest standard of laboratory practices, with meticulous recordkeeping of every single detail.
To us, the study design appears sound, and should address the "deficiencies" of the 2006 trial for which EPA downgraded it from "core" to "supplemental" [4]. An important point for critics to keep in mind is that this study is being performed in the full light of day, and any concerned party is free to contact either the researchers or Bayer CropScience if they have any questions.
If all goes well, the results of this study should answer questions about the impact, if any, upon colony population and productivity, from the seed treatment of canola with clothianidin (Poncho). These colonies will be followed through the winter, so that any short- or long-term effects should be observed.
Over the course of the day-long tour and dinner, all parties involved--the Bayer scientists, the government regulators, the seed companies, the growers, and the beekeepers--had ample opportunity to openly discuss issues and solutions. We were able to speak candidly with a number of Bayer environmental scientists from Germany, Canada, and the U.S., who all confirmed the high interest that Bayer has in developing bee-friendly products. Over dinner, I asked Dr. Christian Maus (Global Pollinator Safety Manager for Bayer CropScience) whether Bayer was concerned about finding out something negative when they run a new trial. He replied that if indeed there was a problem with one of their products, Bayer would want to be the first to know of it!
Throughout the tour, the atmosphere was very positive for working together to support the growers, while at the same time protecting bee health. Our overall impression was that Bayer is acting in good faith and that Drs. Cutler and Scott-Dupree are earnestly conducting a well-designed trial that should detect any measureable effect of clothianidin upon colony productivity and survival.
References
[1] Health Canada (2012) Re-evaluation of Neonicotinoid Insecticides http://www.hc-sc.gc.ca/cps-spc/pubs/pest/_decisions/rev2012-02/index-eng.php
[2] Cutler GC and CD Scott-Dupree (2007) Exposure to clothianidin seed treated canola has no long-term impact on honey bees. J Econ Entomol 100:765-772 (Broken Link!) http://dspace.lib.uoguelph.ca/xmlui/bitstream/handle/10214/2621/32546.pdf?sequence=1
[3] (Broken Link!) http://usda01.library.cornell.edu/usda/current/Hone/Hone-03-30-2012.pdf
[4] http://www.epa.gov/opp00001/about/intheworks/clothianidin-response-letter.pdf
Category: Pesticide Issues
Tags: canola, clothianidin, insecticides, neonicotinoids, pesticide | canola Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/canola/ |
A New Large-Scale Trial of Clothianidin
First published in: American Bee Journal, September, 2012
A New Large-Scale Trial of Clothianidin
Randy Oliver and Brett Adee
First published in ABJ September 2012
The process for approving a new pesticide is similar to that of approving a new drug. In the case of a drug, randomized controlled clinical trials are run to demonstrate efficacy and safety. Then once the drug is approved for use, it essentially undergoes a more extensive "uncontrolled trial," in which regulators watch for reports of adverse effects, which, if they are problematic, could result in either relabeling of the drug, or its withdrawal from the market.
Due to reports of adverse effects from the neonicotinoids, both the EPA and Canada's Pest Management Regulatory Agency (PMRA) are reevaluating the registrations of these insecticides [1]. PMRA has called for Bayer to expand one of the original studies used for the registration of clothianidin as a seed treatment for canola. That study [2], performed in 2005-2006, has been questioned on a few points, mainly:
1. Due to the small plot sizes, bees could have foraged off the test plantings and avoided the treated crop, or been exposed to insecticide residues from other flora.
Clothianidin residues showed up in some nectar samples from the control colonies, indicating that the control bees foraged to some extent on the treated plots, thus compromising the controls.
Figure 1. Canola is a favored plant for systemic insecticide studies, since bees avidly forage on its nectar and pollen, both of which contain residues of the seed treatments (typically <2ppb). Virtually all canola seed is treated with fungicides plus the neonicotinoid clothianidin.
Canola seed is normally treated with fungicides to ensure adequate germination, so it is easy for seed companies to also add clothianidin to control the devastating flea beetle, which attacks the young plants. The effectiveness of this environmentally-friendly treatment (no spraying necessary) has allowed growers to massively expand canola plantings over the past 15 years--to the current 20 million acres.
Bayer CropScience grows hybrid canola seed in Canada, and in an ironic twist, is thereby the largest renter of honey bee pollination services in Canada, and is thus highly motivated to ensure that the product does not harm bees. In late June, Bayer invited representatives of the regulatory agencies, Canadian and U.S. beekeepers (including the authors), seed suppliers, and grain growers to the University of Guelph to familiarize us with the experiment, and to solicit our input on the design.
This new trial should be of interest to U.S. commercial beekeepers, since about a quarter of commercial hives spend the summer in the Dakotas [3]. Canola is becoming a favored crop in the prairies, with over a million acres (1700 square miles) to be planted in North Dakota alone this year.
Since virtually all canola seed is treated with clothianidin or its precursor, thiamethoxam, this trend suggests that plenty of colonies will be ingesting residues in their diet (Figure 1).
The crop protection companies[1] typically hire independent investigators to run field trials of their products in order to avoid charges of conflict of interest (Figure 2). For this trial, they again hired University of Guelph environmental scientists Drs. Cynthia Scott-Dupree and Chris Cutler to repeat their previous study in more and larger plots (Figure 3). Bayer scientist Dr. Dave Fischer (Environmental Toxicology and Risk Assessment) presented details of this ambitious study, designed to eliminate any questions about the original studies:
1. The scientists went to great effort to locate ten widely separated 2 hectare (5 acre) plots in which to plant canola, with the added requirements that no other canola, and little competing forage, would be growing within normal flight range (10 km) (Brett and I confirmed that the test plots appeared to be surrounded largely by forest or agricultural land without competing forage).
2. The distance between plots would prevent any cross-plot foraging, so that the researchers would know that any canola pollen in the hives would have necessarily come from the test plot.
3. The researchers are trapping pollen to confirm the degree of foraging on the canola plots.
4. The stocking rate was low enough that each 2 hectare plot should provide adequate forage for the 4 colonies.
5. The ten plots should increase the statistical strength of the study.
During the tour, Dr. Fischer solicited comments from all invitees to make sure that we were satisfied with the protocol. We (Brett and Randy) raised several questions, which were answered to our satisfaction. All parties were receptive to our comments. We suggested a change in protocol, which was subsequently implemented-we asked the researchers to change the holding yard to which the colonies were to be moved after bloom to a non agricultural area in order to eliminate any further exposure to clothianidin (as from soybeans or corn). This would ensure that the control group was truly a clothianidin-free control. Overall, we found both the Bayer reps and the investigators willing and determined to run an honest and unquestionable trial.
[1] I hesitate to call the Plant Protection Products companies "chemical companies" anymore, as the leading companies are moving into biological products, genetics, and RNAi technology.
Figure 2. In order to avoid implications of bias, plant protection product companies routinely hire independent scientists to perform the required field trials of their products. Principal investigator Dr. Scott-Dupree's bio reads, ""My research interests include integrated management of insect pests in horticultural, fruit, field and greenhouse crops using environmentally compatible control methods, insecticide resistance management, and the impact of agro-ecosystems on non-target organisms, including beneficial insects such as honey bees, bumble bees, native bees and natural enemies or biological control agents of insect pests."
The investigators randomly chose half the plots to plant with clothianidin-treated seed; the other half serve as controls, and were sprayed for flea beetles a month before bees were introduced. The field technicians paid great attention to detail to make sure that each field was planted in an identical manner.
Four colonies were placed in the center of each field at the beginning of bloom, fitted with both pollen traps (normally open) and dead bee traps. Each plot provides enough forage for four colonies, and the pollen will be analyzed to determine whether bees foraged off site, and to quantify any pesticides present in the pollen (nectar will also be tested).
Figure 3. Principal investigators Drs. Cynthia Scott-Dupree and Chris Cutler next to one of the test colonies fitted with a dead bee trap in front. Four hives were placed at the center of each 5-acre field of canola, with no other canola, and little other forage, within flight range.
Periodically the research teams (composed of grad students) will pull each brood frame from each hive, and photograph it to be analyzed by a fancy (and expensive) computer program which quantifies the coverage by adult bees, as well as the amount of sealed brood (Fig. 4).
Figure 4. This specially-designed system will be used to photograph both sides of each frame in the field (with and then without bee coverage). A computer program then determines the number of bees and area of sealed brood.
At the point where only 25% of bloom remains, all the hives will be removed from their test plots and taken to a single non agricultural fall/winter yard to track colony overwinter survival. The research teams will collect data on colony weight, honey yield, adult bee mortality, brood production, colony strength (adult bee coverage), queen events, and residues in nectar, honey, pollen, and wax. The entire trial with be performed following GLP's--the highest standard of laboratory practices, with meticulous recordkeeping of every single detail.
To us, the study design appears sound, and should address the "deficiencies" of the 2006 trial for which EPA downgraded it from "core" to "supplemental" [4]. An important point for critics to keep in mind is that this study is being performed in the full light of day, and any concerned party is free to contact either the researchers or Bayer CropScience if they have any questions.
If all goes well, the results of this study should answer questions about the impact, if any, upon colony population and productivity, from the seed treatment of canola with clothianidin (Poncho). These colonies will be followed through the winter, so that any short- or long-term effects should be observed.
Over the course of the day-long tour and dinner, all parties involved--the Bayer scientists, the government regulators, the seed companies, the growers, and the beekeepers--had ample opportunity to openly discuss issues and solutions. We were able to speak candidly with a number of Bayer environmental scientists from Germany, Canada, and the U.S., who all confirmed the high interest that Bayer has in developing bee-friendly products. Over dinner, I asked Dr. Christian Maus (Global Pollinator Safety Manager for Bayer CropScience) whether Bayer was concerned about finding out something negative when they run a new trial. He replied that if indeed there was a problem with one of their products, Bayer would want to be the first to know of it!
Throughout the tour, the atmosphere was very positive for working together to support the growers, while at the same time protecting bee health. Our overall impression was that Bayer is acting in good faith and that Drs. Cutler and Scott-Dupree are earnestly conducting a well-designed trial that should detect any measureable effect of clothianidin upon colony productivity and survival.
References
[1] Health Canada (2012) Re-evaluation of Neonicotinoid Insecticides http://www.hc-sc.gc.ca/cps-spc/pubs/pest/_decisions/rev2012-02/index-eng.php
[2] Cutler GC and CD Scott-Dupree (2007) Exposure to clothianidin seed treated canola has no long-term impact on honey bees. J Econ Entomol 100:765-772 (Broken Link!) http://dspace.lib.uoguelph.ca/xmlui/bitstream/handle/10214/2621/32546.pdf?sequence=1
[3] (Broken Link!) http://usda01.library.cornell.edu/usda/current/Hone/Hone-03-30-2012.pdf
[4] http://www.epa.gov/opp00001/about/intheworks/clothianidin-response-letter.pdf
Category: Pesticide Issues
Tags: canola, clothianidin, insecticides, neonicotinoids, pesticide | clothianidin Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/clothianidin/ |
A New Large-Scale Trial of Clothianidin
First published in: American Bee Journal, September, 2012
A New Large-Scale Trial of Clothianidin
Randy Oliver and Brett Adee
First published in ABJ September 2012
The process for approving a new pesticide is similar to that of approving a new drug. In the case of a drug, randomized controlled clinical trials are run to demonstrate efficacy and safety. Then once the drug is approved for use, it essentially undergoes a more extensive "uncontrolled trial," in which regulators watch for reports of adverse effects, which, if they are problematic, could result in either relabeling of the drug, or its withdrawal from the market.
Due to reports of adverse effects from the neonicotinoids, both the EPA and Canada's Pest Management Regulatory Agency (PMRA) are reevaluating the registrations of these insecticides [1]. PMRA has called for Bayer to expand one of the original studies used for the registration of clothianidin as a seed treatment for canola. That study [2], performed in 2005-2006, has been questioned on a few points, mainly:
1. Due to the small plot sizes, bees could have foraged off the test plantings and avoided the treated crop, or been exposed to insecticide residues from other flora.
Clothianidin residues showed up in some nectar samples from the control colonies, indicating that the control bees foraged to some extent on the treated plots, thus compromising the controls.
Figure 1. Canola is a favored plant for systemic insecticide studies, since bees avidly forage on its nectar and pollen, both of which contain residues of the seed treatments (typically <2ppb). Virtually all canola seed is treated with fungicides plus the neonicotinoid clothianidin.
Canola seed is normally treated with fungicides to ensure adequate germination, so it is easy for seed companies to also add clothianidin to control the devastating flea beetle, which attacks the young plants. The effectiveness of this environmentally-friendly treatment (no spraying necessary) has allowed growers to massively expand canola plantings over the past 15 years--to the current 20 million acres.
Bayer CropScience grows hybrid canola seed in Canada, and in an ironic twist, is thereby the largest renter of honey bee pollination services in Canada, and is thus highly motivated to ensure that the product does not harm bees. In late June, Bayer invited representatives of the regulatory agencies, Canadian and U.S. beekeepers (including the authors), seed suppliers, and grain growers to the University of Guelph to familiarize us with the experiment, and to solicit our input on the design.
This new trial should be of interest to U.S. commercial beekeepers, since about a quarter of commercial hives spend the summer in the Dakotas [3]. Canola is becoming a favored crop in the prairies, with over a million acres (1700 square miles) to be planted in North Dakota alone this year.
Since virtually all canola seed is treated with clothianidin or its precursor, thiamethoxam, this trend suggests that plenty of colonies will be ingesting residues in their diet (Figure 1).
The crop protection companies[1] typically hire independent investigators to run field trials of their products in order to avoid charges of conflict of interest (Figure 2). For this trial, they again hired University of Guelph environmental scientists Drs. Cynthia Scott-Dupree and Chris Cutler to repeat their previous study in more and larger plots (Figure 3). Bayer scientist Dr. Dave Fischer (Environmental Toxicology and Risk Assessment) presented details of this ambitious study, designed to eliminate any questions about the original studies:
1. The scientists went to great effort to locate ten widely separated 2 hectare (5 acre) plots in which to plant canola, with the added requirements that no other canola, and little competing forage, would be growing within normal flight range (10 km) (Brett and I confirmed that the test plots appeared to be surrounded largely by forest or agricultural land without competing forage).
2. The distance between plots would prevent any cross-plot foraging, so that the researchers would know that any canola pollen in the hives would have necessarily come from the test plot.
3. The researchers are trapping pollen to confirm the degree of foraging on the canola plots.
4. The stocking rate was low enough that each 2 hectare plot should provide adequate forage for the 4 colonies.
5. The ten plots should increase the statistical strength of the study.
During the tour, Dr. Fischer solicited comments from all invitees to make sure that we were satisfied with the protocol. We (Brett and Randy) raised several questions, which were answered to our satisfaction. All parties were receptive to our comments. We suggested a change in protocol, which was subsequently implemented-we asked the researchers to change the holding yard to which the colonies were to be moved after bloom to a non agricultural area in order to eliminate any further exposure to clothianidin (as from soybeans or corn). This would ensure that the control group was truly a clothianidin-free control. Overall, we found both the Bayer reps and the investigators willing and determined to run an honest and unquestionable trial.
[1] I hesitate to call the Plant Protection Products companies "chemical companies" anymore, as the leading companies are moving into biological products, genetics, and RNAi technology.
Figure 2. In order to avoid implications of bias, plant protection product companies routinely hire independent scientists to perform the required field trials of their products. Principal investigator Dr. Scott-Dupree's bio reads, ""My research interests include integrated management of insect pests in horticultural, fruit, field and greenhouse crops using environmentally compatible control methods, insecticide resistance management, and the impact of agro-ecosystems on non-target organisms, including beneficial insects such as honey bees, bumble bees, native bees and natural enemies or biological control agents of insect pests."
The investigators randomly chose half the plots to plant with clothianidin-treated seed; the other half serve as controls, and were sprayed for flea beetles a month before bees were introduced. The field technicians paid great attention to detail to make sure that each field was planted in an identical manner.
Four colonies were placed in the center of each field at the beginning of bloom, fitted with both pollen traps (normally open) and dead bee traps. Each plot provides enough forage for four colonies, and the pollen will be analyzed to determine whether bees foraged off site, and to quantify any pesticides present in the pollen (nectar will also be tested).
Figure 3. Principal investigators Drs. Cynthia Scott-Dupree and Chris Cutler next to one of the test colonies fitted with a dead bee trap in front. Four hives were placed at the center of each 5-acre field of canola, with no other canola, and little other forage, within flight range.
Periodically the research teams (composed of grad students) will pull each brood frame from each hive, and photograph it to be analyzed by a fancy (and expensive) computer program which quantifies the coverage by adult bees, as well as the amount of sealed brood (Fig. 4).
Figure 4. This specially-designed system will be used to photograph both sides of each frame in the field (with and then without bee coverage). A computer program then determines the number of bees and area of sealed brood.
At the point where only 25% of bloom remains, all the hives will be removed from their test plots and taken to a single non agricultural fall/winter yard to track colony overwinter survival. The research teams will collect data on colony weight, honey yield, adult bee mortality, brood production, colony strength (adult bee coverage), queen events, and residues in nectar, honey, pollen, and wax. The entire trial with be performed following GLP's--the highest standard of laboratory practices, with meticulous recordkeeping of every single detail.
To us, the study design appears sound, and should address the "deficiencies" of the 2006 trial for which EPA downgraded it from "core" to "supplemental" [4]. An important point for critics to keep in mind is that this study is being performed in the full light of day, and any concerned party is free to contact either the researchers or Bayer CropScience if they have any questions.
If all goes well, the results of this study should answer questions about the impact, if any, upon colony population and productivity, from the seed treatment of canola with clothianidin (Poncho). These colonies will be followed through the winter, so that any short- or long-term effects should be observed.
Over the course of the day-long tour and dinner, all parties involved--the Bayer scientists, the government regulators, the seed companies, the growers, and the beekeepers--had ample opportunity to openly discuss issues and solutions. We were able to speak candidly with a number of Bayer environmental scientists from Germany, Canada, and the U.S., who all confirmed the high interest that Bayer has in developing bee-friendly products. Over dinner, I asked Dr. Christian Maus (Global Pollinator Safety Manager for Bayer CropScience) whether Bayer was concerned about finding out something negative when they run a new trial. He replied that if indeed there was a problem with one of their products, Bayer would want to be the first to know of it!
Throughout the tour, the atmosphere was very positive for working together to support the growers, while at the same time protecting bee health. Our overall impression was that Bayer is acting in good faith and that Drs. Cutler and Scott-Dupree are earnestly conducting a well-designed trial that should detect any measureable effect of clothianidin upon colony productivity and survival.
References
[1] Health Canada (2012) Re-evaluation of Neonicotinoid Insecticides http://www.hc-sc.gc.ca/cps-spc/pubs/pest/_decisions/rev2012-02/index-eng.php
[2] Cutler GC and CD Scott-Dupree (2007) Exposure to clothianidin seed treated canola has no long-term impact on honey bees. J Econ Entomol 100:765-772 (Broken Link!) http://dspace.lib.uoguelph.ca/xmlui/bitstream/handle/10214/2621/32546.pdf?sequence=1
[3] (Broken Link!) http://usda01.library.cornell.edu/usda/current/Hone/Hone-03-30-2012.pdf
[4] http://www.epa.gov/opp00001/about/intheworks/clothianidin-response-letter.pdf
Category: Pesticide Issues
Tags: canola, clothianidin, insecticides, neonicotinoids, pesticide | pesticide Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/pesticide/ |
Neonicotinoids: Trying To Make Sense of the Science Part 1
First published in: American Bee Journal, August, 2012
Trying to Make Sense of It All
Look and You Shall Find It
Looking at Both Sides of the Issue
The Regulatory Gauntlet
A Balancing Act
Who Does the Testing?
Academic versus Field Applicable
Field Relevance
Problems in Methodology and Interpretation
Recent Studies
References
Neonicotinoids: Trying To Make Sense Of The Science
Part 1
Randy Oliver
ScientificBeekeeping.com
First published in ABJ August 2012
Science is all about trying to understand things. When a scientist gets a hunch about why is it that something happens, he puts his hypothesis to the test in an experiment. He may then publish the results, including his own interpretation of the data--at which point other scientists are duty bound to question every aspect of the study, as well as to attempt to replicate the original results. In the end, we hope to learn what is actually true.
And this is my intent, to get to the truths of the neonicotinoid issue. In this series of articles, I am essentially "thinking out loud." I find that the neonic issue is so emotionally charged that folk try to pigeonhole you as holding a black or white position, and then try to paint you as defending that position. Please let me be clear--I hold no position, and am not trying to defend anything! I'm simply asking that we stick to the facts, rather than playing to irrational fears and supposition. To that end I am intentionally taking on the role of "mythbuster," which is predictably rubbing some folk the wrong way. But if I can get people actually thinking, rather than merely parroting, then I feel that my efforts have been successful!
So how do we reconcile the conflicting reports on the neonics? Last month I reported from Ground Zero of neonicotinoid use, and found the majority of beekeepers to be doing just fine. On the other hand, there was a rash of reports this spring of apiaries suffering serious mortality from planting dust. And to further confuse the issue, several recent scientific studies have been interpreted as having demonstrated that neonics are going to be the death of bees.
Trying to Make Sense of It All
As I reported in my last article, many beekeepers feel strongly that the widespread use of the neonicotinoid insecticides has been a good thing--there are far fewer spray kills nowadays than back in the bad old days (in 1968 an estimated 83,000 colonies were lost to pesticides in California alone [1]). However, there remain several unresolved issues and unanswered questions about these insecticides:
There are occasional, but intolerable bee kills due to seed planting dust (especially so this year), from which individual beekeepers may suffer serious financial losses. This issue must be resolved!
Although there is a substantial amount of good field data indicating that neonic residues in pollen and nectar are generally at tolerable levels, in some instances higher concentrations have been found. These situations need to be clearly identified.
The long-term potential buildup of residues in soil must be carefully monitored.
The sky-high application rates of neonics for landscape uses (turf, ornamentals, homeowner use) and on flowering trees, and the resulting runoff into surface waters, is of legitimate concern.
The sublethal effects upon bee behaviors, such as memory, navigation, and age-related task allocation need to be further studied.
The interactions between these insecticides and the bee immune response to parasites such as mites, nosema, and viruses need to be thoroughly investigated.
Neonics have been shown to synergize with one particular class of fungicides. Other synergies should be explored, although there is no particular reason to suspect that neonics are unique in this matter.
All the above are things to be suspicious of, but to date there is no overwhelming evidence that any of them, save for the planting dust issue [2], generally cause serious problems. To date, no independent investigatory body has been able to confirm that the neonics are responsible for large-scale colony mortality [2].
Practical application: the scientific community and the regulatory bodies are well aware of the potential adverse effects of the neonicotinoids, are actively researching the issues above, and are in the process of reassessing their risks.
There is a growing public demand for more environmentally-friendly pesticides, which must be balanced against the real-world needs of agriculture for effective pest control products in order to feed a hungry world. Unfortunately, there are constraints due to cost and the expiration of patents that limit the actual amount of testing that can be done before regulators must make decisions as to whether a pesticide appears to be safe enough to be registered for use. Accordingly, the EPA often grants "conditional registration," which allows it to ask for continued testing under actual field conditions. This is a good thing, since approved uses of a conditionally-registered pesticide can be quickly revoked should problems appear.
This is where independent scientists take over from those of the pesticide industry, and follow their hunches to test for any suspected negative effects that the pesticide might cause to "off target" organisms, such as humans and honey bees. The confusing part to the public is that...
Look and You Shall Find It
As with anything, the more you look, the more you will find potential risks (just Google the words "dangers of" followed by any food, medicine, or household chemical). You can drive yourself crazy with "what ifs." The trick is to try to put all the findings into perspective.
Looking at Both Sides of the Issue
What I find, is that to be objective one must go out of one's way to investigate all of the evidence, and to listen carefully to the interpretations by all parties. I already had a thorough grounding in distrust of pesticides, having come of age shortly after the publication of Rachel Carson's seminal book, Silent Spring (which jumpstarted the environmental movement). I have a background in aquatic biology, and have clearly seen the devastating effects of pesticides and pollutants on downstream organisms. I'm deeply concerned about our overreliance upon pesticides and the resultant environmental consequences, well summarized by Dr. David Pimentel [3].
What I have also done, however, is to take a look at the issue through the eyes of the other stakeholders--the farmers and the companies that supply them with the plant protection products that they clamor for. I find that it often helps to play "Devil's Advocate" and argue the "other side's" position. I must admit that my doing so has gotten me into hot water with a number of beekeepers, but if our side can't rebut the other side's arguments, then we don't really have a good case, do we?
What I found was that there are dedicated people already trying to objectively sort out the evidence. These are the regulatory agencies, such as the EPA, which are assigned the difficult responsibility of deciding how best to balance environmental safety with the demands of agriculture--a difficult task to say the least!
The Regulatory Gauntlet
Manufacturers screen each newly-developed chemical for any potential uses, including that as a pesticide. For a chemical (whether natural or synthetic) to be registered as a pesticide, the registrant must demonstrate both its efficacy against one or more pests, as well as its relative safety to both humans and to the environment as a whole. To do so it must run a gauntlet of tiered levels of "risk assessment."
In general, a product is evaluated in a stepwise fashion, first (in the case of honey bees) to determine the degree of exposure (e.g., honey bees wouldn't be expected to get into cockroach bait), and then to quantify the toxicity of the product by both contact (spray or contamination of leaves) and orally (as in nectar, pollen, or water). Risk assessment has been updated to take into account exposure to residues from systemic pesticides (such as the neonicotinoids), which are absorbed by plants and distributed in plant tissues, rather than simply sitting on the surface (Fig. 1).
Figure 1. Routes of exposure to systemic insecticides and potential effects upon honey bee colonies. Diagram ©️ SETAC (2011) Pesticide Risk Assessment for Pollinators: Summary of a SETAC Pellston Workshop.
After determining whether there is a risk of bees being exposed to the product, the next tier of risk assessment is to determine the LD50 (median lethal dose) and the NOEL (no observed effects level) of the pesticide, for both oral and contact routes, and acute and chronic exposure, for adult bees as well as brood. Safety margins are then applied to decide whether the risks to either adult bees or brood indicate that additional testing is necessary to quantify sublethal effects. Testing is done first in the lab, then "semi field" (in enclosed screened tunnels over crop plants), and then under full field conditions (hives next to planted fields) (Fig. 2).
Figure 2. A simplified flow chart for the risk assessment of plant protection products. This diagram has since been updated to reflect the use of systemic insecticides (EPPO 2010, SETAC 2011). IGR means "insect growth regulator." The EPPO, EPA, and SETAC documents are freely available on the web--I suggest that interested beekeepers read them! Chart ©️ European and Mediterranean Plant Protection Organization (EPPO 2003), by permission.
Not all countries use exactly the same testing requirements, most notably that in the EU and Canada, the formulated product, as opposed to solely the active ingredient, must be tested (a position that I strongly support). I've sat with some of the principals and discussed the state of the art of testing. All parties (including Bayer) would like to improve the risk assessment protocols, and develop a standardized set which all countries (and manufacturers) alike could use. I suggest that interested readers download two recent (and free) documents on pesticide risk assessment for honey bees:
The 2008 International Symposium on Hazards of Pesticides To Bees [4], and
Pesticide Risk Assessment for Pollinators: Summary of a SETAC Pellston Workshop [5]
You may be surprised by how thoroughly every aspect of pesticide testing with regard to bees is being discussed!
Practical application: the regulatory process for risk assessment of pesticides is constantly improving, and is adjusting specifically for the case of systemic insecticides. The regulators are looking long and hard at the neonics [6], but objectively rather than emotionally.
A Balancing Act
Roughly 15% of agricultural crop losses are due to insects, 13% to fungus. Growers call for industry to provide plant protection products to keep them from losing their crops (just as beekeepers call for products to protect our bees from varroa). The plant protection product (PPP) industry tests perhaps 200,000 compounds for any one that it actually brings to market, at a typical cost of some $200 million for each new product [6]. The manufacturers need clear sets of rules in order to maintain the incentive to develop more ecologically-friendly pesticides.
The difficult balancing act between providing the PPP industry with rules, and the well-deserved scientific scrutiny of the effects of manmade pesticides in the environment are handled by regulatory agencies such as EPA and EPPO, with guidance from SETAC and The International Commission for Plant-Bee Relationships.
Practical application: I find it surprising that some advocates keep repeating that the regulatory agencies or the PPP industry are being negligent in looking out for the well being of honey bees--it only takes the slightest bit of homework to see that this claim is entirely untrue!
Who Does the Testing?
In general, after initial in-house testing, a manufacturer will generally shop out "core studies" to an independent lab or university researcher. Some will say that when an independent researcher is paid by the manufacturer to run a trial to test a product, that he is then hopelessly biased. I've spoken to a number of researchers, who take great offense at that suggestion! Or manufacturer may hire an independent company to run the trial. At the 2012 Eastern Apicultural Society conference, entomologist Jessica Lawrence from such a company (Eurofin) gave an impressive presentation on the nitpicky details that such a lab must follow in order to meet the highest standards of scientific testing [7].
The EPA even then does not take study conclusions at face value, but has its own reviewers go over them with a fine-toothed comb (for an example see [8]). They then thoroughly analyze all the available data prior to making a registration decision (see the 137-page document for the registration of clothianidin for some crops [9]).
Practical application: The point that I'm trying to get across is that, although the system is not perfect, I tend to trust the EPA's thorough evaluation of a pesticide more than that of some blogger who has simply read a few abstracts.
Academic versus Field Applicable
Something that confuses the issue is that many of the published studies are academic--of scientific interest, but not necessarily relevant to "real life" situations. The problem with extrapolating from lab tests is that doses which cause adverse effects to individual bees under laboratory conditions may not cause any measurable effect when given to normal free-flying colonies. A number of researchers have told me that there appears to be some sort of colony-level mitigation of the effects of the neonicotinoid insecticides.
EPPO (2012) "adopts the assumption that the most reliable risk assessment is based on data collected under conditions which most resemble normal practice, i.e. by field tests or by monitoring the product in use. Such studies are relatively expensive and difficult to conduct, but the results should be considered as decisive if there is any conflict with results from lower-tier testing (laboratory and semi-field testing)".
From my point of view, the best perspective is to not get distracted by the hypothetical, but rather to focus upon the two final arbiters of the effects of a pesticide upon colony health--the ability to maintain its population, and the ability to put on surplus honey. These two metrics (cluster size and weight gain) reflect the final calculus of all the potential effects of the pesticide, and are easily measured in the field.
Practical application: this is why I give such weight to the on-the-ground assessment of the effects of seed treatments upon bees by the beekeepers in the Corn Belt and on Canadian canola, who report good colony survival and honey production despite their bees foraging in landscapes with high neonicotinoid use.
Field Relevance
The actual measured amounts of neonic residues found in the nectar or pollen of treated plants are typically in the range of 0-3 ppb (rarely above 5 ppb) (EFSA 2012). However, researchers routinely test bees fed at levels of 25 - 400 ppb, in order to find out what kind of negative effects may occur. The problem is that in many cases, the researchers do not make clear that they are testing at residue levels that would not normally occur under "field relevant" conditions.
The thing to keep in mind is that the neonics are, like nicotine, stimulants. Their effect is similar to that of other stimulants such as the toxic alkaloid caffeine, with which 90% of U.S. adults intentionally dose themselves with on a daily basis.
As an analogy, suppose that you wanted to perform an experiment to determine the effects of the stimulant caffeine on the ability of downhill bicycle racers to negotiate a tricky course. A cup or two of coffee would likely enhance their performance; but imagine if you forced them to drink 10 or 40 cups (still "sublethal doses") before the race! Would you consider the results to be relevant to everyday real life?
Dr. James Cresswell [10] recently performed a meta-analysis of published research on the effects of neonicotinoids upon bees, in both laboratory and field trials. He then fitted dose-response curves to the data (Fig. 3), which suggested that there would be little expected bee mortality at field relevant doses (the paper is a free download, and worth reading).
Figure 3. Neonicotinoids are typically tested at doses higher than those to which bees would be normally exposed in the field via nectar or pollen. This is a legitimate method for identifying potential negative effects, but the results may not necessarily be relevant under field conditions. Graph roughly after Cresswell 2010.
On the other hand, Cresswell found that "Dietary imidacloprid at measured levels in nectar from two widespread crops is expected to reduce performance [e.g., navigation] in honey bees by between 6 and 11% (oilseed rape) and between 14 and 16% (sunflower). These findings raise renewed concern about the impact of systemic neonicotinoids on honey bees that forage in agriculturally intensive landscapes."
However, we must again compare those hypothetical performance reductions with reality--colonies in Canada make great honey crops on treated canola, as can bees in areas of treated corn and soy. The problem in reconciling these disparate reports is that several factors come into play in the field:
The dose makes the poison--field doses from seed treatments are typically (except in the case of planting dust) very low. They are intentionally designed to be so.
Bees metabolize neonicotinoids quickly [11], similar to the manner in which humans quickly metabolize nicotine, so that they appear to tolerate small doses well.
Bees appear to find neonicotinoid residues distasteful [12], and avoid drinking highly contaminated nectar. However, they may well bring home highly contaminated pollen or dust.
Just because an insecticide goes systemic in a plant, that doesn't mean that bees are constantly exposed to that product. Treated plants only produce contaminated nectar or pollen for a relatively short period of time each season. The rest of the season the bees would ignore those plants.
Several surveys of trapped pollen found that bees in agricultural areas often mainly collect pollen from plant species other than the treated crops. These findings suggest that bees may be avoiding the treated crops, and that nectar and pollen from the untreated plants would tend to dilute the insecticide residues. However, if the treated crop is the only plant in bloom, then the colony would be exposed to a greater degree (note, however, that colonies foraging on virtually undiluted treated canola appear to do fine).
The above factors would lead to the dilution of the insecticide within the hive.
Then there is the "colony effect." Even when fed extremely high doses of imidacloprid over a period of weeks or months, colonies may continue to thrive (Pettis 2012; Lu 2012; Galen Dively, pers comm).
This is not to say that exposure to high levels of planting dust can't result in sudden loss of a large portion of a colony's adult population!
Practical application: Just as drinking a couple of cups of coffee a day won't hurt you, a little bit of neonics in the diet don't appear to harm bees. The question then is always, "How great was the dose?" With modern analytical equipment, that is an easy question to answer by sampling the nectar, pollen, dust, or bees themselves. It is not hard to pin the problem on a specific pesticide if there is actual evidence, which is why it is so important for beekeepers to report adverse effects, and to make sure that samples are taken for analysis!
Problems in Methodology and Interpretation
To be frank, I find many studies on the neonics to exhibit obvious bias--those from the registrant tend to play down any adverse effects; to the contrary, some other labs are clearly on a mission to prove that neonics are the scourge of bees. Therefore, I find myself reading papers on this subject with an extremely critical eye. As an example of a well-designed and objectively interpreted study, I've included an arbitrarily-chosen free download in the references: (Aliouane 2009).
The first tier of testing for adverse effects involves laboratory trials with caged bees. One must keep in mind that the results of these studies must be qualified, in that it is difficult to duplicate the natural hive environment and social milieu with a handful of queenless, broodless bees in an incubator, so the results may not really apply to bees in real life. Dr. Geoff Williams has compiled a list of suggestions for the standardization of cage trials, soon to be published.
There are also inherent problems with tunnel and field trials, since it then becomes much more difficult to control extraneous variables, such as the impact of confined flight, weather, alternative forage, disease, and the finding of matching control plots. Often, unforeseen problems (Murphy's Law applies in scientific research) crop up during a study and the study is junked; in other cases, the researcher openly discusses the problems; but sometimes obvious problems are simply ignored in the write up. Here are a few of the typical questionable details that I see in studies:
I've already mentioned excessive dosing. Exaggerated dosing may help to point us toward avenues for further research, but should not necessarily be interpreted as having any field relevance. I suggest that you take a look at the dosing level in any study. Anything over 5 ppb in feed is likely not relevant to normal field exposure.
Decourtye [13] found that there were substantial differences in susceptibility between winter and summer bees. There may well also be race and patriline differences to be accounted for.
Lack of a "positive control"-that is, a dose of a known toxicant (typically the insecticide dimethoate) for comparison. Without a positive control, you really don't know how the effects of the tested product compare to those from a generic chemical stressor (such as a hive miticide or a natural plant toxin). Amusingly, I've spoken with researchers who included a 100 ppb dose of imidacloprid expecting it to be a positive control that would kill most of the bees, but found to their surprise that there was actually little effect at the colony leve!.
Additional solvents-some labs routinely use the solvent DMSO to first dissolve the neonicotinoid. When I checked with a toxicologist, he said that DMSO is dangerous to even have in a lab, since it greatly increases absorption of chemicals across membranes. Since the bee gut membrane is an effective barrier to neonicotinoids [14], I find such use of DMSO, which is not found in commercial neonic formulations, to be potentially problematic.
Test bees are often knocked out with CO2 or chilled on ice for easier handling. Both stresses can affect be behavior and survivability [15, 16].
Lack of control of stress due to parasites. Bees stressed by nosema or virus infection may be more susceptible to pesticide toxicity [17], indicating that in any testing of pesticides, the parasite load of the subject bees should be controlled for.
Improper incubation temperature of bees or brood. Bee behavior and longevity can be strongly influenced by incubation temperature [18, 19], yet in some studies, the test bees have been severely chilled.
Running tests solely on very young adult bees, rather than mixed age workers.
Lack of proper nutrition for caged, newly-emerged bees. Many trials start with bees that are emerged into a near-sterile environment. These "teneral adults" are generally deprived of the normal meal of jelly from a nurse bee (and the included inoculum of the critical endosymbiotic gut bacteria), nor are they fed beebread, or any other protein source. DeGrandi-Hoffman [20] demonstrated that young bees deprived of protein get hammered by DWV. DWV can strongly affect bee brain function.
In one widely-cited study, it appears that the researcher unknowingly starved the bees for sugar, yet claimed that their mortality was due to the insecticides [21].
Caged bees are generally not exposed to the normal queen and brood pheromones of the broodnest. We have no idea how such deprivation affects their behavior, physiology, or resistance to insecticides.
Imagine that if we wished to determine the effects of a pesticide on humans, but that we used as test subjects young children that had been ripped away from their families, chilled, starved, and held in isolation, then knocked out and revived, dosed with a stimulant and then watched to see how well they performed some arbitrary test. Would we feel that the results of such a test were applicable to the human community in the real world? Again, the question on any scientific study on bees is whether the results are field relevant.
Practical application: when I carefully scrutinize scientific papers, I find that a number suffer from (often inadvertent) flaws in methodology, or from overreaching interpretation of the results. Luckily, the majority of researchers are meticulous and methodical, and I am greatly impressed by their diligent work! Unfortunately, most beekeepers can't take the time to sort the good from the questionable.
Recent Studies
There have been several widely cited studies released in the last couple of years--I've indicated in the references those that are free downloads. For those few of you who still trust my judgment and objectivity, I'll give short summaries. Please note that I've often corresponded with the authors to get further details of their studies--in general, the researchers are happy to discuss their methodology and findings.
Nosema: Alaux (2009); Vidau (2011); Pettis (2012)--There is every reason to expect a synergy between insecticide stress and nosema infection; neonic treatment may either increase or decrease spore production, but appears to increase mortality in infected bees. However, such results may not be apparent at the colony level. In the Pettis study, after 10 weeks of feeding colonies pollen patties spiked at 5 or 20 ppb imidacloprid, "there was surprisingly no relationship between Nosema infection and imidacloprid treatment which would have been predicted by the lab study."
Chronic toxicity: Tennekes (2010a, b)--I discussed the paper and his alarming book at length with Dr. Tennekes. He points out legitimate concerns about high levels of residues in surface waters; however, the applicability of the Druckrey-Kupfmuller equation does not stand up to scrutiny, nor does his bird data.
Guttation fluid: Hoffmann (2012) found the guttation fluid droplets on treated melons could contain high levels of neonics. I corresponded with the author about his three studies in Arizona--alternate water sources were available, and he did not observe bees taking up the guttation droplets.
Imidacloprid and CCD: Lu (2012). I don't wish to belabor this paper's shortcomings (see ScientificBeekeeping.com for detailed questions). Scott Black, executive director of the Xerces Society for Invertebrate Conservation, called the study "fatally flawed," both in its design and its conclusions [22]. However, there were two clear conclusions that could be drawn from the study--(1) feeding colonies for four straight weeks with a half gallon of HFCS spiked with imidacloprid at field-realistic levels did not have any negative effects, and (2) then feeding the colonies with sky-high levels of the insecticide for another nine weeks straight still did not harm them enough to cause mortality during treatment or for three months afterward.
Planting dust: Krupke (2012) contained little new information-planting dust can cause bee mortality; the test colonies recovered (Greg Hunt, pers comm). Points out potential synergies with fungicides--there are also other pesticides in the dust. There is a large body of research already published on this issue--see Krupke's or Marzaro's (2011) references sections.
Bumblebees: Whitehorn (2012) found that bumblebee colonies fed realistic doses of imidacloprid gained less weight and produced fewer queens. This finding is of great interest, since solitary- and bumblebee colonies are more likely to be affected by pesticides than would be honey bees (due to the population reserve in the honey bee colony). This is of special concern, since native pollinators are already suffering greatly from habitat disturbance and introduced pathogens. "However, it is uncertain as to what extent the exposure situation in the study is representative to field conditions since bumblebees would need to forage for two weeks exclusively on imidacloprid-treated crops in order to be exposed to the same extent as in the study" EFSA (2012).
Homing ability: Henry (2012) glued RFID chips to foragers, fed them a substantial dose of thiamethoxam, released them up to a km away from their hives and recorded whether they made their way home. They then calculated that colonies should crash due to loss of foragers--a result not substantiated in, say, canola fields. Schneider (2012), using similar tracking chips, found that field-realistic doses of imidacloprid or clothianidin had no effect the number of foraging trips from the hive to the feeder, the duration of these foraging trips, and the time interval a bee spent inside the hive between foraging trips, but that much higher doses, as expected, did cause negative effects. The EFSA review (2012) states that "it should be noted that there are several uncertainties regarding these results, therefore, they should be considered with caution. In particular, in the studies from Henry et al and Schneider et al. bees consumed the total amount of active substance within a relatively short period and not administered over a longer period (i.e. a day). Depending on the substance properties and how fast the substance can be metabolised by the bees, this method of exposure could have led to more severe effects than what may occur when bees are foraging."
Sucrose responsiveness and waggle dancing: Eiri (2012) found that foragers treated with imidacloprid were less responsive to low sugar concentrations in offered droplets of syrup (intoxicated bees "liked" sweeter syrup). They also found that if bees were fed a 24 ppb (about 10x field realistic) dose of imidacloprid, the next day they performed fewer waggle dances (were they "hung over"?). Again, I must question the relevance of such high doses.
Other studies: I could fill the pages of this magazine several times over with my notes on hundreds of studies and my correspondence with various researchers, as I've really been trying to make sense of the neonicotinoids. I wish that I could give you cut and dried answers, but the science is not yet there. I'll continue my analysis in the next issue...
References
[1] Swift (1969), cited in McGregor (1976) Insect Pollination Of Cultivated Crop Plants. http://www.ars.usda.gov/SP2UserFiles/Place/53420300/OnlinePollinationHandbook.pdf]
[2] AFSSA (2009) Mortalites, effondrements et affaiblissements des colonies d'abeilles (Weakening, collapse and mortality of bee colonies). http://www.afssa.fr/Documents/SANT-Ra-MortaliteAbeilles.pdf. This free download, translated into English, is an excellent overall review of colony mortality in Europe by the French Food Safety Agency.
[3] Pimentel, D. (2001) Environmental effects of pesticides on public health, birds and other organisms. Rachel Carson and the Conservation Movement: Past Present and Future. Conference presented 10-12 August 2001, Shepherdstown, W.V. http://rachels-carson-of-today.blogspot.com/2011/02/environmental-effects-of-pesticides-on.html
[4] Oomen, PA and HM Thompson (Editors) (2009) Hazards of Pesticides to Bees: International Commission for Plant-Bee Relationships, Bee Protection Group, 10th International Symposium. http://www.jki.bund.de/fileadmin/dam_uploads/_veroeff/JKI_Archiv/JKI_Archiv_423.pdf. This document is a "must read" for anyone seriously interested in pesticide risk assessment for honey bees.
[5] Pesticide Risk Assessment for Pollinators: Summary of a SETAC Pellston Workshop http://www.setac.org/sites/default/files/executivesummarypollinators_20sep2011.pdf
[6] Whitford, F, et al (nd) The Pesticide Marketplace, Discovering and developing new product. (Broken Link!) http://www.ppp.purdue.edu/Pubs/PPP-71.pdf]
[7] http://www.eurofins.com/agroscienceservices/about-us/latest-news/beekeepers-open-day-at-cgrf,-nc.aspx]
[8] EPA (2003) Data evaluation record honey bee - Acute oral LD50 test http://www.epa.gov/pesticides/chem_search/cleared_reviews/csr_PC-044309_20-Mar-03_d.pdf
[9] EPA (2005) EFED Registration Chapter for Clothianidin for use on Potatoes and Grapes as a spray treatment and as a Seed Treatment for Sorghum and Cotton. http://www.epa.gov/pesticides/chem_search/cleared_reviews/csr_PC-044309_28-Sep-05_a.pdf
[10] Cresswell, JE (2011) A meta-analysis of experiments testing the effects of a neonicotinoid insecticide (imidacloprid) on honey bees. Ecotoxicology 20(1):149-57. Epub 2010 Nov 16.
[11] Suchail, S, et al (2004) Metabolism of imidacloprid in Apis mellifera. Pest Manag Sci 60:291-296.
[12] DEFRA (2007) Assessment of the Risk Posed to Honeybees by Systemic Pesticides, PS2322. Central Science Laboratory, (GB). http://randd.defra.gov.uk/Default.aspx?Menu=Menu&Module=More&Location=None&Completed=0&ProjectID=13502 This is a long download, but full of good data.
[13] Decourtye, A (2003) Learning performances of honeybees (Apis mellifera L) are differentially affected by imidacloprid according to the season. Pest Manag Sci 59: 269-278.
[14] Suchail, S, et al (2004) In vivo distribution and metabolisation of 14C-imidacloprid in different compartments of Apis mellifera L. Pest Manag Sci 60(11):1056-62.
[15] Ebadi, R, et al (1980) Effects of carbon dioxide and low temperature narcosis on honey bees Apis mellifera. Environmental Entomology 9: 144-147.
[16] Frost, E (2011) Effects of cold immobilization and recovery period on honeybee learning, memory, and responsiveness to sucrose. Journal of Insect Physiology 57: 1385-1390.
[17] Vidau C, et al. (2011) Exposure to sublethal doses of fipronil and thiacloprid highly increases mortality of honeybees previously infected by Nosema ceranae. PLoS ONE 6(6): e21550. doi:10.1371/journal.pone.0021550
[18] Tautz, J, et al (2003) Behavioral performance in adult honey bees is influenced by the temperature experienced during their pupal development. Proc Natl Acad Sci 100(12): 7343-7347.
[19] Medrzycki, P, et al (2010) Influence of brood rearing temperature on honey bee development and susceptibility to poisoning by pesticides. Journal of Apicultural Research 49(1): 52-59
[20] DeGrandi-Hoffman, G, et al (2010) The effect of diet on protein concentration, hypopharyngeal gland development and virus load in worker honey bees (Apis mellifera L.). Journal of Insect Physiology 56: 1184-1191.
[21] Schmuck, R (2004) Effects of a chronic dietary exposure of the honeybee Apis mellifera (Hymenoptera: Apidae) to imidacloprid. Arch. Environ. Contam. Toxicol. 47: 471-478.
[22] Nordhaus, H (2012) The honeybees are still dying. http://boingboing.net/2012/05/07/the-honeybees-are-still-dying.html
Alaux C, et al (2010) Interactions between Nosema microspores and a neonicotinoid weaken honeybees (Apis mellifera). Environ Microbiol 12:774-782. http://www.prodinra.inra.fr/prodinra/pinra/data/2011/03/PROD20116cf9b1b_20110315103742504.pdf
Aliouane, Y, et al (2009) Subchronic exposure of honeybees to sublethal doses of pesticides: effects on behavior. Environmental Toxicology and Chemistry 28 91): 113-122. This is a free download, and an excellent example of a rigorous and meticulous investigation into the sublethal effects of some insecticides, in which they freely admit to some surprising and unexplained negative results for thiamethoxam. http://cognition.ups-tlse.fr/productscientific/documents/papers/Aliouane%20ET&C%2008.pdf
EFSA (2012) Statement on the findings in recent studies investigating sub-lethal effects in bees of some neonicotinoids in consideration of the uses currently authorised in Europe. http://www.efsa.europa.eu/fr/efsajournal/doc/2752.pdf
Eiri, D and JC Nieh (2012) A nicotinic acetylcholine receptor agonist affects honey bee sucrose responsiveness and decreases waggle dancing. The Journal of Experimental Biology 215: 2022-2029.
EPPO (2003) EPPO Standards: Environmental risk assessment scheme for plant protection products, Chapter 10, Honeybees. OEPP/EPPO Bulletin 33: 99-101. http://archives.eppo.int/EPPOStandards/PP3_ERA/pp3-10(2).pdf?utm_source=archives.eppo.org&utm_medium=int_redirect
EPPO (2010) Environmental risk assessment scheme for plant protection products. Chapter 10: honeybees. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2338.2010.02419.x/pdf
Henry, M, et al (2012) A common pesticide decreases foraging success and survival in honey bees. Science 336 (6079): 348-350.
Hoffmann, EJ and SJ Castle (2012) Imidacloprid in melon guttation fluid: a potential mode of exposure for pest and beneficial organisms. J. Econ. Entomol. 105(1): 67-71.
Krupke CH, et al (2012) Multiple routes of pesticide exposure for honey bees living near agricultural fields. http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0029268
Marzaro, M, et al (2011) Lethal aerial powdering of honey bees with neonicotinoids from fragments of maize seed coat. Bulletin of Insectology 64 (1): 119-126. http://www.bulletinofinsectology.org/pdfarticles/vol64-2011-119-126marzaro.pdf
Pettis, JS, et al (2012) Pesticide exposure in honey bees results in increased levels of the gut pathogen Nosema. Naturwissenschaften 99(2):153-8. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3264871/?tool=pubmed
Schneider CW, et al (2012) RFID tracking of sublethal effects of two neonicotinoid insecticides on the foraging behavior of Apis mellifera. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0030023
Tennekes, H (2010a) The significance of the Druckrey-Kupfmuller equation for risk assessment--The toxicity of neonicotinoid insecticides to arthropods is reinforced by exposure time. Toxicology 276(1):1-4.
Tennekes, HA (2010b) The systemic insecticides: a disaster in the making. Weevers Walburg Communicatie.
Vidau C, et al (2011) Exposure to sublethal doses of fipronil and thiacloprid highly increases mortality of honeybees previously infected by Nosema ceranae. http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0021550
Whitehorn, P, et al (2012) Neonicotinoid pesticide reduces bumble bee colony growth and queen production. Science 336 (6079): 351-352.
Category: Pesticide Issues
Tags: neonicotinoids, testing | testing Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/testing/ |
Neonicotinoids: Trying To Make Sense of the Science - Part 2
First published in: American Bee Journal, September, 2012
Neonicotinoids: Trying To Make Sense Of The Science
Part 2
Randy Oliver
ScientificBeekeeping.com
First published in ABJ September 2012
"Scientists have largely remained silent when the public discussion turns to the trade-off of benefits and risks from chemicals. They are often unwilling to engage controversial issues that could endanger their funding and research...The public interprets the unwillingness of scientists to engage those who campaign against chemicals as an implicit validation of their dangers. Those who do speak out are often...branded as industry apologists. Maybe the best we can hope for is that brave scientists, scientifically literate journalists and government officials who are responsible for translating science into regulatory policy will take the public's best interest into account...[and] resist the irrational and often regressive impulse stirred by the scare tactics that are so common today." 1
Thanks For The Feedback!
Following the publication of my article "The Extinction of the Honey Bee?" 2 in which I pointed out that honey bees were thriving at Ground Zero of neonicotinoid use, I fully expected to be excoriated by the anti-neonicotinoid True Believers. But to my great surprise, I was instead deluged by letters of support from beekeepers and researchers worldwide! A few examples:
"I'm an amateur beekeeper in France and I want to tell you that I strongly believe that CCD is not caused by pesticides. Like you, I'd like to find the culprit but so far it remains a mystery."
"I liked your article because here in Germany we are facing a hard discussion with bee keepers and other organizations regarding neonicotinoids and feel similar as you that often any scientific idea is missing and that it is a political mission," from a researcher at the major agricultural science institute.
"Likewise in USA, in Europe the discussion is more and more polarized, and in the hands of activists rather than scientists," a bee researcher from the Netherlands.
Thanks, Randy, for acting as a mythbuster," from a beekeeper from the Corn Belt.
Fortified by your vote of support, allow me to return to what I hope is an objective analysis of the neonicotinoid debate.
Innate Distrust Of Chemicals
I came of age in the '60's, and was profoundly influenced by Rachel Carson's book Silent Spring, which detailed how humans were poisoning the environment with pesticides. I have always had an innate distrust of manmade chemicals. I became an environmental activist, subscribed to Mother Earth News and Organic Gardening, moved to the woods, and began a lifelong quest to "walk the walk"--going solar, avoiding pesticides and manmade toxins in my personal environment, creating an organic garden and orchard. I'm a lifelong member of the Sierra Club and The Nature Conservancy, and am considered in my community to be about as green as you can get.
When I first heard reports from France that some new insecticides--the neonicotinoids--were causing massive bee mortality, I of course assumed, "Here we go again--the corporate recklessness of the chemical industry, coupled with government regulators asleep at the switch, has created yet another environmental catastrophe." 3 So, having a background in biology and chemistry, in my usual manner I began to investigate the subject deeply.
Boy, was I in for an education! I read the literature from both sides of the pesticide debate, and got to know the principal players--the beekeeper anti-neonic advocates (who I fully respect), bee researchers, ecotoxicologists, farmers, and scientists from the chemical companies and the EPA. I soon found out who I could trust for accurate information, and who was so biased that I had to take anything they said with a grain of salt. I had thought that I knew something about pesticides; but in reality, how little I knew!
Why Neonicotinoids?
"Until the mid-20th century, pest insect control in agriculture relied on largely inorganic and botanical insecticides, which were inadequate. Then, the remarkable insecticidal properties of several organochlorines, organophosphates, methylcarbamates, and pyrethroids were discovered, leading to an arsenal of synthetic organics. The effectiveness of these insecticides, however, diminished over time due to the emergence of resistant insect strains with less sensitive molecular targets in their nervous systems. This created a critical need for a new type of neuroactive insecticide with a different yet highly sensitive target. Nicotine in tobacco extract was for centuries the best available agent to prevent sucking insects from damaging crops, although this alkaloid was hazardous to people and not very effective. The search for unusual structures and optimization revealed a new class of potent insecticides, known as neonicotinoids, which are similar to nicotine in their structure and action." 4
The neonicotinoids had three other distinct advantages:
They are far more toxic to insects than to mammals, making them much safer for humans.
They are absorbed by plants and translocated via the vascular system, giving effective control of sap sucking and boring insects which other sprayed insecticides might not contact.
They can be applied as seed treatments (Fig. 1), thus being a solution to the longstanding problem that roughly 99% of sprayed treatments never actually hit a target pest, and thus are unnecessarily dumped into the environment. 5
Figure 1. Treated seed, dyed for identification. The purple ones on the left are canola. Seed treatment has a very long history[i], and has been popular in the U.S. for about 40 years. Treatment can consist of any number of fungicides or insecticides, often in "cocktails." The neonicotinoids, since they are transported by the plant vascular system, lend themselves well to this application. The treatments are diluted as the plants grow--in canola, they no longer kill aphids or flea beetles by the time the plants have grown for a month, and by bloom time, are nontoxic to bees.
[i] Munkvold, G (2006) Seed Treatment http://www.extension.iastate.edu/Publications/CS16.pdf
The neonicotinoid insecticides have become widely popular with farmers, and when used as seed treatments, drenches, or attentively applied foliar sprays, appear to indeed be more environmentally friendly than the alternatives. However, the problem lies in the delicate balance between applying them in a manner that targets the pests, without harming "off target" species, such as bees and native pollinators. So let's look at some of the questioned adverse effects.
Sublethal Effects
I can't think of any researcher who has more thoroughly investigated the effects of the neonicotinoids upon honey bee behavior than Dr. Axel Decourtye in France. In an extensive and excellent recent review, 7 he summarizes research on behavior:
Learning performance: Field-relevant doses do not appear to negatively affect learning, but higher doses may. "In general, results from these studies cannot be extrapolated to natural conditions. Moreover, imidacloprid can also have facilitatory effects on learning performances that complicate the interpretation at an ecological level." Yes, you understood him-a low dose of neonic may help bees to learn!
Orientation: "The lowest observed effect concentration on the frequentation of feeding site was 50 [ppb]" (normal field-realistic doses are usually less than 5 ppb).
Foraging: "Although these studies showed the absence of effect of neonicotinoids on foraging of treated plants, perturbations of the foraging behavior on artificial feeder were revealed in other experiments. Thus, for example, it was found a quick decrease in the foraging activity in honey bee colonies at about 20 ppb of imidacloprid. This is probably due to the anti-feedant character of the compound." This is a key point--bees appear to avoid nectar with high concentrations of neonicotinoids. Decourtye does mention that doses at the high end of field relevance may affect bee communication within the hive.
Immune function:
Stress due to exposure to any insecticide could plausibly affect bee immune response to pathogens. I find the research along this line less than compelling. What struck me was the lack of dose response, inconsistency of effect upon nosema replication, and lack of effect in field colonies. I'm sure that we will see further research on this subject.
Some beekeepers have been confused by the action of imidacloprid against termites, thinking that it suppressed the general termite immune function. This does not appear to be the case, as explained by Ramakrishnan (1999) 8: "Collectively, this evidence indicates that imidacloprid did not disrupt termite cellular defense mechanisms, and further suggests that social behaviors are the primary defense against pathogen infection." The social behavior he refers to is grooming, by which termites clean fungal spores off their bodies to prevent infection. Since grooming does not appear to be critical for bee defense against the most common pathogens, I find it difficult to extrapolate the action of imidacloprid against termites to bees.
Social interactions and task allocation:
It is plausible that intoxication by neonics could affect bee social behavior or alter the normal progression of age-related tasks (as proposed by Dr. James Frazier). However, if this were the case, it should affect overall colony performance, which hasn't been observed.
Putting sublethal effects into perspective:
People get hung up on the word "toxin." Perhaps it would help to consider the neonics as "stimulants." As I type these words, I'm enjoying the effects of a sublethal dose of the toxic alkaloid caffeine (plants produce caffeine to poison herbivores). Two cups of coffee supplies about 1/40th of the human LD50 (median lethal dose). 9 The way I brew my java, I'm at the high end of a sublethal dose! And I'll dose myself again late this afternoon.
So why don't I die from caffeine toxicity? Because my body quickly degrades the toxin. The same thing happens with nicotine, and with the neonicotinoids in bees. Suchail 10, 11 found that ingested imidacloprid is rapidly passed to the bee's rectum and excreted or degraded within hours. Very little makes it into the blood or rest of the body. Only about 5% is absorbed into the brain or flight muscles, where it is converted to the more toxic olefin metabolite, which then disappears within a day. Although the metabolite is more toxic on a dosage basis, understand that little of it actually formed.
This is the main problem with the hypothesis of Dr. Henk Tennekes 12, whose widely-cited publications attempt to make a case for the application the Druckrey-Kupfmuller equation for chronic toxicity to the neonics. I've corresponded at length with Dr. Tennekes, and asked him to explain why the neonics, which are also rapidly degraded by the bee, would have any more chronic toxicity than nicotine would to a human smoker. There is enough nicotine in a pack of cigarettes to easily kill a human, yet no one dies from nicotine toxicity (I watched in perverse horror as my high school biology teacher injected a rat with nicotine--its death was not a pretty sight). The point is, that nicotine and neonics appear to be so rapidly metabolized, that there is no buildup in the body (as there is in the case of DDT), the binding to the nerve receptors is reversible and insects recover fully, 13 and there is generally no increased mortality due to low-level chronic exposure.
Indeed, a number of studies have found that exposure to low doses of imidacloprid resulted in foragers being more active and carrying more pollen! 14 Some plants secrete nicotine or caffeine in their nectar; recent research 15 suggests that bees prefer a bit of stimulant "buzz" and are able to accurately self dose--avoiding syrup spiked to toxic levels.
Bottom line: Any number of scientists have diligently tried to find any sorts of sublethal effects of neonics on bees, but have failed to demonstrate adverse effects at the colony level at doses produced by seed treatments.
Effect Upon Brood
The surprising thing here is that bee larvae appear to be essentially immune to the effects of neonics! In fact no one's been able to come up with LD50's because you simply can't dissolve enough of the insecticide in syrup to cause 50% of the larvae to die! 16, 17
However, there could be indirect effects, should the nurse bees--the main consumers of pollen in the hive--be affected by neonics residues. It is plausible that the nurses may exhibit reduced brood feeding. Hatjina 18 found in a lab study that nurse bees fed field-realistic doses of imidacloprid had reduced hypopharyngeal glands (that produce jelly).
On the other hand, perhaps nurses amped up on stimulants work harder--Lu 19 found that field-realistic doses of imidacloprid actually increased broodrearing, and that even extremely high doses had no significant effect upon brood area.
Bottom line: if there were an effect on brood, we would expect to see it in field studies. Such studies do not show negative effects at realistic doses.
Vine Crops--Squashes And Melons
Colonies fare poorly on vine crops (cucurbits) unless they have alternate forage (pers obs). Exposure to pesticides likely exacerbates this problem. Two recent studies found that foliar, soil, or irrigation-applied imidacloprid may result in residues in squash or pumpkin nectar and pollen to levels at which some behavioral effects on bees may occur.
Dively 20 found that seed treatment of pumpkins was safe for bees, but that if neonics are applied close to bloom (as by chemigation or foliar application) that they may contaminate the pollen to the extent that one might expect some effects on the "pollen hogs" in the colony, that is, newly emerged workers and drones, or nurse bees.
Stoner 21 found that at allowed label rates for squash, neonic residues in nectar or pollen could push into the low range of observable behavioral effects. Such effects would likely only be serious to honey bees should lack of alternative forage be available. However, this would be different for the specialized native squash bees: "squash bees are specialists on Cucurbita, feeding their larvae exclusively on Cucurbita pollen, and also build their nests in soil, often directly beneath squash and pumpkin vines, so they could have much more exposure to the soil-applied insecticides used on these crops." 22
Sunflowers
Beekeepers in France emphatically blamed Gaucho seed treatment of sunflowers for colony losses. Bonmatin 23 (clearly on a mission against imidacloprid) found that sunflowers could recover imidacloprid from the soil following crops treated the previous year, and that the plants concentrated the residues in the flower head tissue (although he did not analyze nectar). Even so, he did not find residues that should have caused intoxication, even with seed treated at a much higher rate than on the U.S. label.
In Argentina, Stadler 24 placed hives in the center of large fields of flowering sunflowers from seed treated again at a higher rate than the U.S. label, and confirmed that at least 20% of the pollen in the combs was sunflower, and that the colonies had stored sunflower honey. They could not detect residues of imidacloprid in the pollen, and found that the colonies in the treated field actually performed better than in the untreated! They then moved the hives to natural pasture, and checked them again after 7 months, and found no differences between the groups.
So I don't understand the videos I've seen of trembling or lethargic bees on sunflower blossoms in France. If any U.S. beekeepers have had trouble with bees on seed-treated sunflowers, I'd like to hear!
Buildup In Soil
In some clay soils residues of the neonicotinoids bond tightly to soil particles and may degrade slowly. However, the question is whether the roots of subsequently planted crops are able to absorb them (a Bayer rep pointed out to me that if they did, the farmer wouldn't need to pay for seed treatment the next year). Data from canola fields in Canada (Fig. 2), in which treated seed has been planted year after year, do not support that residues escalate in the bloom, and a study is currently being run in California.
Figure 2. Some of Canadian beekeeper Cory Bacon's hives working canola this July. Lab studies aside, Canadian bees appear to do quite well on seed-treated canola year after year, and I don't hear the beekeepers complaining.
Native Pollinators
There are many other insects that feed on nectar and pollen. Native bees (Fig. 3) would be especially susceptible to systemic insecticides, since they do not fly far to forage, their larvae consume pollen directly, and due to their solitary nature, if the behavior of any female bee is disrupted, she may be unable to leave offspring. However, should native bee larvae have as high a tolerance of neonicotinoids as do honey bee larvae, the concern for larvae may be unfounded.
Figure 3. A sweat bee, Agapostemon virescens, on chicory flowering alongside an Indiana corn field. It is likely that solitary bees, such as this species, would be more negatively affected by neonicotinoids than would a honey bee colony. Photo by Larry Garrett, ID thanks to Dr. Robbin Thorpe.
Solitary native bees are an excellent bioindicator of whether systemic insecticides are causing problems, since they do not have a "reserve" as does a honey bee colony. As far as I can tell from the research, the decline in native bee populations appears to be mostly from habitat loss due to wall-to-wall tillage, not to mention spraying with old-school pesticides. There is scant evidence that field-relevant doses of neonics harm native pollinators, but this is an area that cries for additional research. Two good species to investigate would be our native squash and sunflower bees, since both forage predominately on the nectar and pollen of those plants, and since neonicotinoids are applied to both those crops.
Other Species Of Life
There is legitimate concern about the effects of seed treatments upon earthworms. Dittbrenner 25 found that some species moved less soil in response to imidacloprid. Other researchers 26 have found that some predatory species of insects or spiders may be negatively affected in treated fields, likely due to the suppression of aphid populations-seed treatment only suppresses aphids while plants are young. As plants grow, the insecticide becomes too diluted to affect either sap-sucking insects or (ideally) pollen- or nectar-feeding insects.
The seed treatments appear to be more environmentally friendly to birds (who learn to avoid the seeds) and mammals than the insecticides that they replace
Water Pollution
I've got a background in aquatic biology, and I agree with Dr. Henk Tennekes that levels of imidacloprid in surface waters in areas of heavy applications on non food crops (such as in the Netherlands) are of concern for aquatic ecosystems. Jody Johnson 27 found 7-30 ppb in some urban/suburban water, and up to 130 ppb in nursery puddles, and low levels in some streams. Neonics are relatively nontoxic to fish, but could affect the populations of the invertebrates upon which they feed.
Landscape/Ornamental Uses
Dr. Vera Krischik 28 has pointed out the potential dangers of landscape or ornamental uses of imidacloprid due to the possibility of extremely high doses making it into the nectar. Residues that would not be allowed in field crops are possible with landscape and nursery applications, and there are reports of bees dying from nectar from treated nursery plants. I concur with Dr. Krishik's concerns.
Tree Injections
In order to kill certain tree pests (lerp psyllids on eucalypts, borers in elm or ash) imidacloprid is registered for root or tree treatment. There is reason for concern about some of these registrations, as there is unpublished data of scary high concentrations in nectar.
Foliar Applications
Clearly the best uses for neonicotinoids are for seed application or soil drench. Foliar applications open a new can of worms, due to irregularity of application, translocation to bloom or extrafloral nectaries, or to adjacent flowering weeds. Foliar applications of neonicotinoids can clearly cause bee kills, and are much more subject to vagaries in application timing and other details than are seed treatments.
The registered uses as foliar applications should be safe for bees if label directions are followed exactly, but I simply haven't seen enough data to make an assessment. Beekeepers should file incident reports if there are problems.
Simple Overuse
Dr. Jim Frazier points out that the unrotated use of the same seed treatments is contrary to good pesticide resistance management. Already we are seeing calls to expand the refuge plantings of non Bt corn; 29 it would likely be wise to do the same with neonic treatments. My concern is that if the pests develop resistance, then farmers will have to use additional sprays.
The Absence Of Any "Smoking Gun"
If neonics were actually causing colony mortality, it should be child's play to demonstrate--just feed a colony syrup or pollen spiked with the insecticide and see how long it takes to kill it. The fact is, that try as they might, no research team has ever been able to induce colony mortality by exposing the bees to field-relevant doses of any neonicotinoid (although one can get a significant kill from corn planting dust). Nor has any investigation ever been able to link neonic residues in the hive to colony mortality. Every claim that neonics are causing serious bee mortality is unsupported supposition, not backed by any concrete evidence.
The Ignoring Of Negative Findings
What is interesting about the neonics and honey bees is that the adverse effects that one may see when testing individual bees in the lab don't necessarily translate into effects at the colony level in the field. I've spoken with several researchers who have tried to demonstrate harm to colonies by feeding them large amounts of imidacloprid, and found that it is hard to see any effect. 30
Such "negative findings" are rarely published--after all, who, other than the registrant or the EPA, would be interested in studies in which investigators expose bees to the chemical, and find that nothing happens? So the majority of such findings would only be published by the registrant, and of course no one trusts their research (damned if they do, damned if they don't)!
Reviews Of The Evidence
There has been a mountain of research done on the neonics, but most folk don't have time to review it all (even if they could get their hands on the papers), so they must depend upon a trusted other to do so. Please don't take my word for it-here are some (mostly) recent reviews; most are free downloads:
Reviews With A Pro Neonic Bias:
I find that documents coming from the chemical industry typically have a reassuring slant, but invariably get their facts straight (it would be foolish for them to get caught in a lie).
Maus, C, G Cure, R Schmuck (2003) Safety of imidacloprid seed dressings to honey bees: a comprehensive overview and compilation of the current state of knowledge. Written by Bayer scientists, but the facts are sound. http://www.bulletinofinsectology.org/pdfarticles/vol56-2003-051-057maus.pdf
Reviews With An Anti Neonic Bias:
Anti-neonic reviewers tend to cherry pick out several questionable studies, embellish the implications, and ignore on-the-ground beekeeper experience.
Small Blue Marble. Free downloads of a number of neonic papers. http://smallbluemarble.org.uk/research/
Pilatic, H (2012) Pesticides and Honey Bees: State of the Science. Decent summaries of many studies. http://www.panna.org/sites/default/files/Bees&Pesticides_SOS_FINAL_May2012.pdf
Relatively Objective Reviews:
Xerces Society (who advocate on behalf of native pollinators)-Are Neonicotinoids Killing Bees? http://www.xerces.org/neonicotinoids-and-bees/]--did not find any strong evidence that neonics are harming pollinators, but recommend caution with use and further study.
AFSSA (2010) Weakening, collapse and mortality of bee colonies The French Food Safety Agency conducted a thorough review of all suspected causes of colony mortality in Europe. They arrived at the politically unpopular finding that "The investigations and field work conducted to date do not lead to any conclusion that pesticides are a major cause of die-off of bee colonies in France." http://www.uoguelph.ca/canpolin/Publications/AFSSA%20Report%20SANT-Ra-MortaliteAbeillesEN.pdf
The European Food Safety Authority in their Statement on the findings in recent studies investigating sub-lethal effects in bees of some neonicotinoids in consideration of the uses currently authorised in Europe http://www.efsa.europa.eu/fr/efsajournal/pub/2752.htm, concluded that "Further data would be necessary before drawing a definite conclusion on the behavioural effects regarding sub-lethal exposure of foragers exposed to actual doses of neonicotinoids."
Blacquiere, et al (2012) Neonicotinoids in bees: a review on concentrations, side-effects and risk assessment http://www.gesundebiene.at/wp-content/uploads/2012/02/Neonicotinoide-in-bees.pdf This is a very thorough review of 15 year's worth of research (over 100 studies).
Cresswell (2011) A meta-analysis of experiments testing the effects of a neonicotinoid insecticide (imidacloprid) on honey bees. http://www.springerlink.com/content/j7v320r55510tr54/fulltext.pdf in reviewing 14 studies, estimated that "dietary imidacloprid at field-realistic levels in nectar will have no lethal effects, but will reduce expected performance in honey bees by between 6 and 20%."
Creswell, Desneux, and vanEngelsdorp (2012) Dietary traces of neonicotinoid pesticides as a cause of population declines in honey bees: an evaluation by Hill's epidemiological criteria. (Note the coauthor Dennis vanEngelsdprp, who has studied CCD as closely as anyone) "We conclude that dietary neonicotinoids cannot be implicated in honey bee declines, but this position is provisional because important gaps remain in current knowledge. We therefore identify avenues for further investigations to resolve this longstanding uncertainty."
Of course, all researchers cover their butts and qualify their statements by suggesting that additional research needs to be done. These insecticides have been on the market for about a decade, and we are still learning about them. We definitely want to learn more about their effects upon other non target species, interactions with parasites, synergies with other pesticides, and sublethal behavioral effects.
I would prefer that you read the studies yourself, and then form your own opinions, but in reality I don't expect you to read the hundreds of studies that I've read. It's likely that most of you won't even bother to read the reviews above!
Summary: The consensus opinion of the comprehensive reviews above, as well as of the vast majority of bee researchers that I've spoken with, mirrors Blacquiere's conclusion: "Many lethal and sublethal effects of neonicotinoid insecticides on bees have been described in laboratory studies, however, no effects were observed in field studies with field-realistic dosages."
The Elephant In The Living Room
Let's just put all scientific speculation aside, and look at the obvious--the survival and productivity of colonies actually exposed to neonics-treated crops. Not only is there no compelling evidence to date that exposure to seed-treated crops is causing harm to bees, but there are plenty of examples to the contrary, such as the thriving bee operations in the Corn Belt.
Neonicotinoid seed treatments actually appear to be living up to expectation as reduced-risk insecticides. When skeptical researchers have tested actual pollen and nectar from seed-treated crops, they invariably confirm that any neonicotinoid residues are indeed quite low. Bonmatin 32 sampled imidacloprid levels in corn pollen (Fig. 4) for three years running in France--they averaged 2.1 ppb. But contaminated pollen only made up about half of the pollen trapped at the entrances, so he revised his overall colony exposure via pollen to 0.6 ppb--a level at which no harmful effects have ever been observed.
Over the past two seasons Henderson and Bromenshenk (in press) sampled trapped nectar and/or pollen from hives in canola fields in Canada and corn across the Midwest; 95% contained less than 2.5 ppb of clothianidin residues.
Figure 3. A sweat bee, Agapostemon virescens, on chicory flowering alongside an Indiana corn field. It is likely that solitary bees, such as this species, would be more negatively affected by neonicotinoids than would a honey bee colony. Photo by Larry Garrett, ID thanks to Dr. Robbin Thorpe.
Colonies subsisting on corn pollen alone may indeed go downhill, but that would be due to its lack of certain amino acids. They do not appear to suffer from going into winter with a portion of their beebread consisting of pollen from seed-treated corn. No study (and there have been several) has been able to demonstrate that colonies suffer from foraging on seed-treated corn pollen, and some suggest that it was actually of benefit to them. 33
On the Canadian prairie, colonies build up and survive fine on a diet of canola nectar and pollen from treated fields. If neonicotinoid seed treatments were indeed causing the sort of colony mortality that some claim, the Midwestern and Canadian beekeepers should notice!
The Good, The Bad, And The Ugly
My personal assessment of our state of knowledge on the neonics:
The Good
Neonics are unquestionably reduced-risk insecticides as far as humans and wildlife are concerned, and their use as seed treatments appears to be an environmentally-friendlier way to put the pesticide exactly where it is needed.
Bees and other pollinators appear to be able to thrive on the pollen and nectar of seed-treated plants.
The Bad
There are clearly documented sublethal behavioral effects, but they do not appear to affect bees at field-relevant doses, and appear to be greatly mitigated at the colony level.
Misapplication by homeowners and nurseries can result in unacceptably high residues in nectar or pollen, as can chemigation (as in vine crops).
There is the possibility of residue buildup in soil, which should be monitored.
Landscape and ornamental use can result in runoff into aquatic ecosystems, as documented by Henk Tennkes.
I suggest that beekeepers work closely with regulators on these issues.
The Ugly
Foliar (spray) applications are less well studied than seed treatments, and have greater potential for inadvertent impact on pollinators. Applications to flowering (or soon to be flowering) plants could cause serious bee mortality, and should be carefully regulated.
Injections of, or root application to, nectar-producing trees. For the sake of pollinators these applications must be closely investigated and monitored.
Planting dust from sowing of corn. Although significant planting dust kills are rare, they are ugly. This issue is a bleeding wound to the beekeeping community, and needs to be addressed by the EPA and the registrants. Beekeepers should not be forced to suffer mortality to their livestock due to unregulated pneumatic planter dust. France and Germany have models that we can follow. Beekeepers rightfully feel strongly that the registrants should step forward and compensate beekeepers for their losses until the issue is resolved.
Conclusion
There is no conclusion. Neonics have only been on the market for about a decade, and we are learning how best to use and regulate them. There is plenty of current research and monitoring being done, and the world's main regulatory agencies are currently carefully reviewing their registrations.
Separating Fact From Fiction
Up 'til now this article has been my best shot at an objective review of the scientific data and on-the-ground assessments of the neonicotinoid insecticides. Now I am going to shift from statement of fact to my own personal opinions.
I don't want to hammer on the anti-neonic crowd, nor do I want to sound condescending. One can indeed make a circumstantial case against the neonics, and I feel for beekeepers who have watched their hives fall apart--especially from pesticide issues. What I found, however, is that if one really does their homework, that the case against the neonics largely falls apart.
What bothers me is when advocates embellish the facts to suit their case. I choke on the amount of mis- or disinformation in many of their publications. For example, a recent issue of Britain's The Beekeepers Quarterly 34 informs us that:
"in California [neonics] were applied to the entire almond crop for the last decade--which is why American bees collapsed so dramatically"
How easy it would have been to solve CCD if only that statement had any veracity! In truth, neonics were not used to any extent on almonds, a fact easy to check since California pesticide use reports are freely available. I find this sort of tossing about misinformation to be unethical.
The facts are that that when I checked the use reports for 2003, 2006, 2009, and 2010, there were zero neonic applications in the first two years, and only 96 and 1070 lbs of imidacloprid applied in 2009 and 2010 respectively (58 applications in 2010, and one app. of thiamethoxam of 0.17 lbs). To put those figures into perspective, about 20 million pounds of some 350 different pesticides are applied to almonds each season, predominately fungicides, which the growers spray liberally over the bees and bloom during wet springs. Yet colonies generally come out of almonds looking great!
It's true that Bayer withdrew the registration for imidacloprid for almonds, but rather than being an admission of a problem, 35 it simply wasn't worth it for Bayer to perform additional supportive studies for a product that not only wasn't being used, but had gone off patent and would have been sold by copycat manufacturers using Bayer's data (Dr. David Fischer, pers comm).
The problem with misinformation is that well-meaning folk then hop on the bandwagon to push their legislators to do something about an imagined problem. The more that I investigate pesticide issues, the more I find that policy has been driven by the politics of misinformation and fear, rather than by objective analysis of risks vs. benefits. I quoted the introduction to this article from a very readable book (a free download which I highly recommend) called "Scared to Death." 36 The author gives examples in which well-meaning advocacy groups have fomented enough public pressure to force the withdrawal of this or that chemical from the market, despite a lack of evidence that the chemical was in truth harmful!
Caution: If you are a lifelong environmentalist, reading a decidedly pro-chemical book such as this will take you out of your comfort zone, and may force you to reevaluate your established views. However, it is impossible to dismiss the author's analysis, since he does a pretty good job of backing up his claims with facts!
Overstepping The Bounds
I strongly support the pesticide watchdog groups, and frequently refer to their websites for information. However, I feel that they sometimes fall into Abraham Maslow's trap of: "If the only tool you have is a hammer, you tend to treat everything as if it were a nail." Some of these groups would have us believe that every health problem that humans or bees have can be blamed upon pesticides, a fear that I bought into in my younger days. But reality is not that simple.
For example, in researching the DPR database, I came across the figures for total pesticide use per county in California. 37 Aha, I thought, here's a chance to nail a correlation between pesticide exposure and cancer! So I ran down a map for incidence of cancer by county to compare. 38 To my utter surprise, Fresno and Kern, agricultural counties using 30 and 25 million pounds of pesticides, respectively, in 2010 had lower cancer rates than did the pristine Northern California coastal counties such as Humboldt and Mendocino (0.03 and 1 million pounds). That bastion of environmental activism and organic everything, Marin county (0.06 million lbs), was in the highest tier of cancer incidence! Astoundingly, all six of the Calif counties with the highest pesticide usage were in the lowest tiers of cancer rates. Go figure!
The neonicotinoids (generally lumped together with GMO's) have currently been pumped up to be a straw man that is responsible for the demise of the honey bee, and some advocacy groups are pulling out all stops in order to take them down. A problem happens when advocacy groups shift from merely informing our regulatory agencies, to the starting of public campaigns (that ignore actual evidence) to push lawmakers to overstep the regulators and ban a certain chemical anyway. This can result in unintended consequences to both humans and bees.
I have a vested interest in pesticides that are safer for humans, and the neonics fit that bill. In the case of bees, should seed treatment with clothianidin be banned, as PANNA is pushing, it's not like farmers are all going to suddenly go organic--they will simply substitute other insecticides, which will then pollute the environment (and likely cause bee mortality) to a much greater degree-even some "organic" pesticides are more harmful to bees or other beneficials than some synthetics. 39, 40
Not only that, but when emotion trumps science, what are farmers and the Plant Protection Product industry supposed to do? It takes millions of dollars to bring a new product to market--including the newer generation "biopesticides" and reduced-risk pesticides. Why should industry invest if their hard work all goes up in smoke as the result of an irrationally fearful public campaign?
Practical application: my concern is that the beekeeping community should be cautious about allowing itself to be used as a poster child for the "neonicotinoids are the cause of CCD and the extinction of the bee" NGO's. Some of these same advocates could well be campaigning next year against the natural toxins, or grains of GMO pollen, that are found in some honeys!
The EPA is actually doing a decent job. I've read their risk assessments for the neonics. They ask the right questions, and base their decisions on scientific evidence, not anecdote and emotion. I feel that when anti-chemical advocates or beekeepers bypass the system, that our society and the environment may suffer. The current focus on the neonicotinoids has drawn attention away from the incontrovertible damage caused to colonies every year by spray applications of other pesticides, as well as from important bee research which is finally elucidating the biological causes of colony mortality worldwide. To me, this misdirection of focus is a problem.
Folks, all regulatory agencies worldwide are fully aware of the questions regarding the neonicotinoid insecticides. The EPA is stuck between a hostile congress and farm lobby on one side, and the NGO advocacy groups and beekeepers on the other, and must stick to scientific evidence. There are plenty of watchdogs making sure that EPA does its job.
Let's Redirect Our Energy
Instead of putting unwarranted lobbying effort against the single insecticide clothianidin, the bee industry would better benefit by going after (as Darren Cox says) "the low-hanging fruit"--the all-too-common bee kills due to spray applications of other pesticides. This is a labeling, educational, and enforcement issue.
The EPA needs to better clarify its label requirements to prevent applicators from spraying onto flowering crops or allowing pesticide drift onto impact adjacent areas.
The EPA needs to reassess the impact of fungicides, surfactants, other adjuvants, or tank mixes upon bees.
Growers and applicators need to be better educated as to how to protect their crops without harming pollinators. Sometimes simply changing the timing of spraying can protect bees.
EPA needs to push state agencies to cooperate with (rather than discourage) beekeepers when they suffer damages.
State agencies need to take the lead in actually enforcing pesticide laws when violations occur.
The EPA has brought beekeepers to the regulatory table, and we are currently being well represented by the National Honey Bee Advisory Board, and by Darren Cox at the Pesticide Program Dialogue Committee. I'm greatly encouraged that the NHBAB currently includes beekeeper/growers--who see both sides of the issue of necessary plant protection vs. "acceptable damage" to bees. The commercial beekeepers are clearly letting the EPA know of the extent of their losses due to pesticides.
I want to also be clear that we should all be appreciative of the hard work done by the NGO's (overzealous or not) and especially by those beekeepers who, at considerable personal expense, donate their time toward the benefit of our industry by lobbying the regulators to pay attention to our very real issues.
Last Minute Update:
As I was getting ready to send this article off to press, the EPA denied the recent petition requesting emergency suspension of clothianidin based on imminent hazard, stating in its response:
"Based on the data, literature, and incidents cited in the petition and otherwise available to the Office of Pesticide Programs, the EPA does not find there currently is evidence adequate to demonstrate an imminent and substantial likelihood of serious harm occurring to bees and other pollinators from the use of clothianidin." 41
You can read the technical supporting documents yourself. 42 I do not for a moment doubt the earnestness of the petitioners, but I found that the EPA interpreted the research exactly as I have, and concur that there was simply not enough evidence (to date) that clothianidin poses a major threat to bees, beekeeping, or pollinators in general.
References
1 Entine, J (2011) Scared Death: How Chemophobia Threatens Public Health. http://www.acsh.org/include/docFormat_list.asp?docRecNo=1133&docType=0
2 July ABJ
3 Credit to Entine (2010) op. cit.
4 Tomizawa, M and JE Casida (2009) Molecular recognition of neonicotinoid insecticides: the determinants of life or death. Acc. Chem. Res. 42(2): 260-269.
5 Pimentel, D. 2001. Environmental effects of pesticides on public health, birds and other organisms. Rachel Carson and the Conservation Movement: Past Present and Future. Conference presented 10-12 August 2001, Shepherdstown, W.V. http://rachels-carson-of-today.blogspot.com/2011/02/environmental-effects-of-pesticides-on.html
6 Munkvold, G (2006) Seed Treatment http://www.extension.iastate.edu/Publications/CS16.pdf
7 Decourtye and Devillers (2010) Ecotoxicity of Neonicotinoid Insecticides to Bees. In, Insect Nicotinic Acetylcholine Receptors, Advances in Experimental Medicine and Biology 683: 85-95, DOI: 10.1007/978-1-4419-6445-8_8.
8 Ramakrishnan, R (1999) Imidacloprid-enhanced Reticulitermes flavipes (Kollar) (Isoptera: Rhinotermitidae) susceptibility to the entomopathogen Metarhizium anisopliae (Metsch.) Sorokin. J. Econ. Entomol 92:1125-1132.
9 Peters, J M (1967). Factors affecting caffeine toxicity: a review of the literature. The Journal of Clinical Pharmacology and the Journal of New Drugs (7): 131-141
10 Suchail, S, et al (2004a) Metabolism of imidacloprid in Apis mellifera. Pest Manag Sci 60:291-296
11 Suchail, S, et al (2004b) In vivo distribution and metabolisation of 14C-imidacloprid in different compartments of Apis mellifera L. Pest Manag Sci 60(11):1056-62 (2004b).
12 Tennekes HA. The significance of the Druckrey-Kupfmuller equation for risk assessment-the toxicity of neonicotinoid insecticides to arthropods is reinforced by exposure time. Toxicology 276(1):1-4.
13 Dr. John Casida, pers comm
14 Faucon, J-P, et al (2005) Experimental study on the toxicity of imidacloprid given in syrup to honey bee (Apis mellifera) colonies. Pest Manag Sci 61:111-125.
15 Are bees addicted to caffeine and nicotine?.ScienceDaily. Retrieved February 8, 2011, from http://www.sciencedaily.com/releases/2010/02/100210101504.htm
16 Lodesani, M, et al (2009) Effects of coated maize seed on honey bees: Effects on the brood. http://www.cra-api.it/online/immagini/Apenet_2009_eng.pdf
17 Lodesani, Marco, pers comm
18 Hatjina, F and T Dogaroglu (2010) Imidacloprid effect on honey bees under laboratory conditions using hoarding cages. http://www.coloss.org/publications/proceedings_workshop_bologna_2010
19 Lu,C, KM Warchol, RA Callahan (2012) In situ replication of honey bee colony collapse disorder. Bulletin of Insectology 65 (1): 99-106.
20 Dively, GP, Kamel A (2012) Insecticide residues in pollen and nectar of a cucurbit crop and their potential exposure to pollinators. J Agric Food Chem. 60: 4449-4456.
21 Stoner KA and BD Eitzer (2012) movement of soil-applied imidacloprid and thiamethoxam into nectar and pollen of squash (Cucurbita pepo). PLoS ONE 7(6): e39114. doi:10.1371/journal.pone.0039114
22 ibid
23 Bonmatin, JM, et al (2005) Quantification of imidacloprid uptake in maize crops. J. Agr. Food Chem. 53: 5336-5341.
24 Stadler T, et al (2003) Long-term toxicity assessment of imidacloprid to evaluate side effects on honey bees exposed to treated sunflower in Argentina, Bull Insect 2003; 56:77-81.
25 Dittbrenner, N, et al (2011) Assessment of short and long-term effects of imidacloprid on the burrowing behaviour of two earthworm species (Aporrectodea caliginosa and Lumbricus terrestris) by using 2D and 3D post-exposure techniques. Chemosphere 84(10): 1349-1355.
26 Albajes R, Lopez C, Pons X (2003) Predatory fauna in cornfields and response to imidacloprid seed treatment. J Econ Entomol. 96(6):1805-13.
27 Jody Johnson (2011 ABRC)
28 Krischik,VA, AI Landmark, and GE. Heimpel (2007) Soil-Applied Imidacloprid Is Translocated to Nectar and Kills Nectar-Feeding Anagyrus pseudococci (Girault) (Hymenoptera: Encyrtidae). Environ. Entomol. 36(5): 1238-1245.
29 http://www.sciencedaily.com/releases/2012/06/120605102846.htm)-it
30 Dively, GP, et al (2010) Sublethal and synergistic effects of pesticides http://agresearch.umd.edu/recs/WREC/files/2010Programs/EASSubletha%20Effects2010.pdf
31 Creswell, Desneux, and vanEngelsdorp (2012) Dietary traces of neonicotinoid pesticides as a cause of population declines in honey bees: an evaluation by Hill's epidemiological criteria. Pest Management Science 68(6): 819-827
32 Bonmatin (2005) Op. cit.
33 Nguyen BK, et al (2009) Does imidacloprid seed-treated maize have an impact on honey bee mortality? J Econ Entomol 102:616-623.
34 The Beekeepers Quarterly June 2012 (U.K.) Neonicotinoids--Our toxic countryside http://www.boerenlandvogels.nl/sites/default/files/BKQ%20108%20-%20Neonicotinoid%20Pesticides_0.pdf
35 http://www.panna.org/sites/default/files/BayerPullImidacloprid.pdf
36 Entine, op. cit.
37 http://www.cdpr.ca.gov/docs/pur/pur10rep/comrpt10.pdf
38 http://www.chcf.org/~/media/MEDIA%20LIBRARY%20Files/PDF/C/PDF%20CancerInCalifornia12.pdf
39 Bahlai, CA, et al (2010) Choosing organic pesticides over synthetic pesticides may not effectively mitigate environmental risk in soybeans. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0011250
40 http://www.organicfarming101.com/organic-pesticides/
41 Response to petition http://www.regulations.gov/#!documentDetail;D=EPA-HQ-OPP-2012-0334-0006
42 Technical supporting documents http://www.regulations.gov/#!documentDetail;D=EPA-HQ-OPP-2012-0334-0012
Category: Pesticide Issues
Tags: insecticides, neonicotinoids | neonicotinoids Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/neonicotinoids/ |
Nosema Ceranae and Honey Production in Healthy Colonies
Nosema Ceranae And Honey Production In Healthy Colonies
Randy Oliver and Brion Dunbar
ScientificBeekeeping.com
First Published in ABJ in November 2012
There is considerable scientific and practical debate about the degree of impact that Nosema ceranae infection has upon the honey bee colony. It is reasonable to assume that there would be noticeable impairment, since infection by its cousin, Nosema apis, is well documented to adversely affect bee metabolism, protein levels, longevity, and most noticeably, honey production [1]. Studies on the new parasite have found similar metabolic harm [2], [3]. And Dr. Frank Eischen's data from Louisiana [4] suggests that infection by N. ceranae also suppresses honey yields. In this study, we wished to see whether infection by Nosema ceranae was related to poor honey production in colonies of roughly the same strength, as opposed to colonies simply weakened in strength by nosema infection.
One of the problems with trying to document any correlation between N. ceranae and colony production is that that the typical method of monitoring the parasite consists of determining the average spore count from a small sample of bees. This method is demonstrably unreliable, depending upon factors such as from where in the hive the sample is taken, the time of day, the presence in the sample of a single highly-infected bee, or the number of bees sampled [5]. Furthermore, mean spore counts may not correlate well with the actual degree of infection [6].
To overcome the problems inherent with mean spore counts, I've been revisiting Dr. G.F. White's original method of assessing the degree of nosema infection in the colony by squashing bee guts one at a time [7]. In my first study, I took samples from the two strongest and two weakest colonies in several apiaries in December, and compared the percentage of bees showing infection (Fig. 1).
Figure 1. Distribution of nosema prevalence in the weakest and strongest hives in my apiaries in early December, based upon 10-bee samples taken from under the lid or outside combs. In none of the strong hives were more than 1 bee out of 10 infected; whereas the majority of the weak hives scored at least 1 or more infected bees out of 10, and 40% scored 2 or more positives. Chart reprinted from Sick Bees 15.
There was a clear relationship in December between colony strength and the proportion of infected bees in a hive. By February, nosema prevalence in some dwindling colonies had risen to 8-10 bees out of 10! By changing my assessment method to gut squashes rather than mean spore counts, for the first time I could see a relationship between infection by Nosema ceranae and poor colony performance!
Skip forward to spring. My hives returned from almonds looking great, whereupon I split and requeened them all. The splits grew rapidly during the best spring in years, and gained weight on the early flows in April. But then during our main flow in June, things came to a screeching halt-- despite looking strong and healthy, most hives did not even make adequate winter stores. The normal variation in colony-to-colony honey production was arrestingly apparent--a number of hungry colonies pulled early honey down out of the second brood chamber, yet others cried for additional supers, and filled them!
I couldn't help but suspect that the poor producers might be suffering from a nosema infection (there are no overt symptoms of infection by N. ceranae). Intrigued by my findings above, I decided to see if the same held true for honey production-that is, whether I could detect a difference in infection levels between the best and worst producing healthy colonies in each yard.
Methods
With the assistance of beekeeper Brion Dunbar, I took samples from 10 apiaries on June 15 and 16, as the main honey flow was ending. Each apiary had been started from nucs in early April, mostly with sister queens (different for each yard). In each apiary we identified the two colonies that had produced the most honey, and the two that had produced the least, inspecting each colony to exclude those showing any signs of disease, queen problems, or lack of cluster size (not surprisingly, we excluded a number of nonproductive colonies for the above reasons). In other words, we wanted to compare only strong, apparently healthy colonies to determine whether their differences in honey production were due solely to the degree of nosema infection.
We took bee samples from under the lid or from an outside comb. Brion took on the Herculean task of individually squashing and viewing the gut contents of 10 bees from each hive (for a total of 410 bees), scoring each bee as being either positive or negative for nosema infection.
Results
The results surprised us--there was no striking difference in the prevalence of infected bees between the productive and nonproductive hives! On the average, 7% of the sampled bees were infected in the productive colonies, compared to 10.5% in the nonproductive (not statistically significant). The distribution of the degree of infection was similar for both groups of hives (Fig. 2), with one notable exception--an apparently badly-infected colony in the nonproductive group.
Figure 2. Distribution of nosema prevalence at the end of the honey flow in June. Although a larger percentage (55%) of the productive hives scored negative for nosema infection (as opposed to 38% of the nonproductive), that relationship did not necessarily hold for lightly infected colonies. Overall, both groups had similar distributions of infection prevalence.
Discussion
It is easy to understand how colonies weakened in population due to nosema infection would produce less honey. We suspected that even in strong colonies, nosema, due to its metabolic drag on the bees, would suppress honey production. So in this study we compared the prevalence of infection between apparently healthy colonies at the extreme ends of weight gain in each yard (most productive vs. least productive).
Since we had earlier found a marked difference in nosema infection between strong and weak hives the previous fall, we fully expected to find more nosema in the nonproductive hives. To our surprise, there was no striking trend in that direction. Such a relationship might have been more evident had we sampled more hives, or taken more bees in each sample.
It's likely that by excluding any sick or weak colonies that we also omitted any badly-infected hives from analysis-in our sporadic sampling of weak hives in the operation (data not shown) we often found nosema to be prevalent. Note that of the 41 colonies selected, in only 3 were more than 20% of the bees in the samples infected. Returning to Dr. White's detailed studies on Nosema apis, he [8] concluded:
As a rule colonies which in the spring of the year show less than 10 per cent Nosema-infected bees gain in strength and the losses are not detected. This is often true also in cases where the infection is somewhat greater than 10 per cent. When the number of infected bees approaches 50 per cent the colonies become noticeably weakened and in many cases death takes place.
So perhaps colonies can still be productive despite having up to 20% of their bees infected by Nosema cerana, so long as they remain strong. But that may be the exception- keep in mind that 16 of the 20 productive colonies had less than that rate of infection, and only 1 had more than 20% infected. On the other hand, in the nonproductive hives, 13 of 21 had at least 10% of the bees infected. So these data suggest that the "tip point" at which nosema noticeably affects honey production occurs when more than about 10-20% of the bees are infected.
Nosema ceranae was certainly present in my operation in June--we found infected bees in over half the colonies, productive or nonproductive. Keep in mind that our samples of only 10 bees would certainly underestimate whether infection was present--it's likely that every single colony in my operation contained at least a few infected bees. But by early August, nosema was hard to find when I sampled for it, despite the fact that I had not applied any treatments. This relative disappearance of nosema in late summer appears to be common [9].
In conclusion, it did not appear that infection by nosema was the main cause for the differences in honey production between my strong colonies--other factors must have been involved. It also appears that if a colony is able to maintain its strength despite being infected with nosema at a low level, then it can still make honey. And finally, our results perhaps support Dr. White's conclusion that colonies are less likely to be productive when more than 10% of the bees are infected by nosema.
Acknowledgements
Thanks to Brion Dunbar for completing the tedious task of squashing and scoring bees. And thanks to the donors to ScientificBeekeeping.com for supporting this sort of practical research.
References
[1] Fries, I (1993) Nosema apis - a parasite in the honey bee colony. Bee World 74 (1): 5-19
[2] Mayack, C and D Naug (2010) Parasitic infection leads to decline in hemolymph sugar levels in honeybee foragers. Journal of Insect Physiology 56(11):1572-1575
[3] https://scientificbeekeeping.com/sick-bees-part-17-nosema-the-smoldering-epidemic/
[4] Eischen, FA, et al (2011) Impact of nutrition, Varroa destructor and Nosema ceranae on colonies in southern Louisiana. Proceedings of the American Bee Research Conference 2011
[5] https://scientificbeekeeping.com/sick-bees-part-16-the-quick-squash-method/
[6] Traver, BE and RD Fell (2011) Prevalence and infection intensity of nosema in honey bee (Apis mellifera L.) colonies in Virginia. Journal of Invertebrate Pathology 107(1):43-49.
[7] https://scientificbeekeeping.com/sick-bees-part-15-an-improved-method-for-nosema-sampling/
[8] White, GF (1919) Nosema-Disease. USDA Bulletin No. 780. A free download from Google Books.
[9] Rennich, K, et al (2012) 2011-2012 National Honey Bee Pests and Diseases Survey Report. http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
Category: Colony Health - Diseases, Viruses, CCD
Tags: honey production, nosema ceranae | nosema ceranae Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/nosema-ceranae-2/ |
Sick Bees - Part 18E: Colony Collapse Revisited - Genetically Modified Plants
First published in: ABJ December 2012
Genetically Modified Plants
What Is Genetic Modification?
There's Nothing New About Transgenics
GMOs
An Odd Series of Connections
The Vilifying of Monsanto
What Are They Up To?
Practicality Overrides Principle
Hold the Hate Mail
The Changing Face of Agriculture
Bt Crops
Roundup Ready
Direct Effects of Roundup Use
Indirect Effects of Roundup Use
The Future of Roundup
Reality Check
Looking Ahead: The Chemical Treadmill & Pest Resistance
Additional Discussion
The Back Story on Plant Breeding and GM Crops
The Profit Motive
Enter GM Crops
The Second "Green Revolution"
Cautions About GM
Perspectives on GM
So What's The Problem?
Acknowledgements
References
Sick Bees - Part 18E:
Colony Collapse Revisited - Genetically Modified Plants
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in Dec 2012
Genetically modified (or GM) plants have attracted a large amount of media attention in recent years and continue to do so. Despite this, the general public remains largely unaware of what a GM plant actually is or what advantages and disadvantages the technology has to offer, particularly with regard to the range of applications for which they can be used [1].
The above quote is certainly an understatement! Genetically Modified Organisms (GMO's) are a highly contentious topic these days, and blamed by some for the demise of bees. In researching the subject, I found the public discussion to be highly polarized--plant breeders and farmers are largely enthusiastic (with appropriate reservations) about the benefits of genetic engineering, whereas health and environmental advocacy groups tend to be fearful of the new technology [2]. I will largely save my review of the history and pros and cons of GM crops for my website, and focus this article upon how GMO's relate to honey bee health.
What Is Genetic Modification?
The knowledge of genetics was not applied to plant breeding until the 1920's; up 'til then breeders would blindly cross promising cultivars and hope for the best. With today's genetic engineering, breeders can now take a gene from one plant (or animal, fungus, or bacterium) and splice it into the DNA of another plant. If they get it just right, the new gene can confer resistance to frost, drought, pests, salinity, or disease. Or it could make the crop more nutritious, more flavorful, etc. Such genetically modified crops are also called "transgenic," "recombinant," "genetically engineered," or "bioengineered."
There's Nothing New About Transgenics
There is nothing new about transgenic organisms, in fact you (yes you) are one. Viruses regularly swap genes among unrelated organisms via a process called "horizontal gene transfer" [3]. For example, the gene which is responsible for the formation of the mammalian placenta was not originally a mammal gene--it was inserted into our distant ancestors by a virus. If a gene introduced by a virus confers a fitness advantage to the recipient, then that gene may eventually be propagated throughout that species' population. Until recently, we didn't even know that this process has occurred throughout the evolution of life, and didn't know or care whether a crop was "naturally" transgenic!
GMO's
Both the scientific community and industry have done a terrible job at explaining genetic engineering to a distrustful public. There are clearly potential issues with genetic engineering, but they are being carefully addressed by independent scientists [4] and regulatory agencies, especially in Europe:
From the first generation of GM crops, two main areas of concern have emerged, namely risk to the environment and risk to human health.... Although it is now commonplace for the press to adopt 'health campaigns', the information they publish is often unreliable and unrepresentative of the available scientific evidence [5].
Jeffrey Smith, in his book "Seeds of Deception" [6] details a number of legitimate issues and early missteps in bioengineering, as well as pointing out the substantial political influence firms such as Monsanto have upon researchers, regulators, and legislators. We should be cautious to take their assurances with a grain of salt. On the other hand, I've checked the claims of other anti-GMO crusaders for factual accuracy, and found that many simply don't hold water. For example, two headlined studies of late, one on rats fed GE corn and Roundup herbicide, and another on the purported increased use of herbicides due to GE crops simply do not stand up to objective scrutiny [7]. It bothers me that the public is being misled by myths and exaggeration from both sides.
From my point of view, GE holds incredible promise and should be pursued in earnest, yet must also be very carefully monitored and regulated. In any case, GE crops have been widely adopted in U.S. agriculture (Table 1), and thus are now a part of beekeeping.
Table 1. The genetically engineered traits available to farmers have evolved rapidly as technology improves and as such crops become more widely adopted. Table from http://www.census.gov/compendia/statab/2012/tables/12s0834.pdf.
An Odd Series Of Connections
In 1972, the dean of biological sciences at my university hired me to set up a "world class insectary" (which I did). I raised mass quantities of insects for hormone extraction, in the hope that we might develop a new generation of eco-friendly insecticides [8]. Several years later I was shocked when Monsanto-a widely-despised chemical company with a sordid history- then hired him to create "a world-class molecular biology company" (which he apparently did). In 2002, Monsanto was spun off as an independent agricultural company.
Jump forward to 2010, when I had the good fortune to work with an Israeli startup--Beeologics--and witnessed the efficacy of their eco-friendly dsRNA antiviral product for honey bees. But to bring the product to market, they needed more backing. To my utter astonishment, they recently sold themselves to Monsanto!
The Vilifying Of Monsanto
These days one can simply mention the name "Monsanto" in many circles, and immediately hear a kneejerk chorus of hisses and boos. Sure, it had been easy for me to enjoy the camaraderie of riding the anti-Monsanto bandwagon; but I realized that that I shouldn't allow that sort of fun to substitute for the responsibility of doing my homework and getting to the actual facts of the matter! When I did so, I found that some of Monsanto's actions did indeed deserve opprobrium; but that much of the criticism directed at the current company is undeserved (Monsanto suffers from an ingenerate inability to practice effective PR). Concurrent with the purchase of Beeologics, Monsanto hired well-respected apiarist (and columnist) Jerry Hayes to head up a new honey bee health division, and appointed some prominent beekeepers (not me) to its advisory board. It dismays me that some beekeepers then immediately jump to the erroneous conclusion that Jerry has sold his soul to the Devil--nothing could be further from the truth!
What Are They Up To?
Some beekeepers imaginatively feared that Monsanto was about to create a GM bee or was up to some other nefarious plot. But in reality, Monsanto's vision of its future direction is anything but evil--I suggest that you peruse their website for your own edification [9], [10]. Of course I was curious as to why they had purchased Beeologics, since the market for bee medicine is far too tiny to draw the interest of a giant corporation. But one needn't be some sort of psychic in order to figure out a corporation's plans--all you need do is to read its recent patents, which are a virtual crystal ball for seeing ten years into the future. So I searched out any patents containing the words "Monsanto" and "RNAi."
To my great relief, I found that Monsanto was not up to some evil plot--far from it! I suggest you read two of the patents yourself [11]:
Chemical pesticidal agents are not selective and exert their effects on non-target fauna as well...Some chemical pesticidal agents have been shown to accumulate in food, and to exhibit adverse effects on workers that manufacture and apply such chemical agents. Thus there has been a long felt need for methods for controlling or eradicating... pest infestation on or in plants, i.e., methods which are selective, environmentally inert, non-persistent, biodegradable, and that fit well into pest resistance management schemes. Plant biotechnology provides a means to control pest infestations by providing plants that express one or more pest control agents. Recombinant pest control agents have generally been reported to be proteins selectively toxic to a target pest that are expressed by the cells of a recombinant plant.
What the patents tell us is that Monsanto clearly sees that the public is sick of pesticides. Genetic RNAi technology would allow plant breeders to develop crop cultivars that control insect pests in the same manner that the plants naturally control viruses. All that the breeder need do would be to identify a unique target protein in a particular pest, and then splice a gene into the plant to produce a "blocking" dsRNA molecule that would prevent the pest from building that specific protein. The beauty is that dsRNA molecules are already naturally found in plant tissues, the blocking molecule would be entirely specific for that pest alone, completely nontoxic to humans or other non target species, and be rapidly biodegradable. It would be a win all around (except for the pest)--crop protection, no toxic pesticides, and a sustainable farming technology (as well as a market for Monsanto's products, since they would need to continually develop slightly different cultivars in order to avoid pest resistance). Who'd have guessed that Monsanto would be leading the way toward developing eco-friendly pest control? Life is full of surprises!
Practicality Overrides Principle
Some folk make GM crops out to be some sort of abomination of nature, and shun them with religious fervor. I'm not sure that this is the best course for environmentalists to take, and that perhaps, in the face of an expanding human population and a warming climate, we should leave all the possible plant breeding solutions on the table. The organic farming community wholeheartedly endorses the biotechnology of "marker assisted selection" [12], yet arbitrarily draws the line at the directed insertion of desirable genes. This may sound like heresy, but as an environmentalist, I suggest that GE holds great promise for developing more nutritious plants that don't require pesticides, fertilizer, or irrigation--all of which would be wins for organic farming.
From a biological standpoint, I simply don't see GM crops as being any more inherently dangerous than conventionally bred crops. Our domestic plants today are often far from "natural"--you wouldn't recognize the ancestors of many. Be aware that even conventionally bred cultivars of several crops (beans, potatoes, celery, etc.) often turn out to be too toxic for humans.
This is not by any means a fluff piece for Monsanto or agribusiness. Farming is not what it used to be. In the U.S., 85% of farm sales are produced by less than 10% of farms, which hold 44% of farm acreage [13]. A mere six companies collectively control around half of the proprietary seed market, and three quarters of the global agrochemical market [14]. I abhor such corporate domination; neither do I see today's high-input agricultural practices as being either sustainable or ecologically wise.
That said, human demands upon the Earth's finite ecosystem are growing. There are only about 4.5 acres of biologically productive land on the surface of the Earth available for each current human inhabitant. Depending upon the culture's lifestyle, we use anywhere from 25 acres (U.S.) to as little as 1 acre (Bangladesh) to feed and clothe each person. Unfortunately for the bee (and many other species), due to human population growth there are over 200,000 additional human mouths to feed every single day--each requiring the conversion of another couple of acres of natural habitat into farmland!
It doesn't take a mathematician to figure out that if we wish to conserve natural ecosystems that we need to get more yield out of existing cropland! And one of the best ways to do that is to breed crops that are more productive and pest-resistant. The plant scientists in the corporate labs are making huge strides in developing such cultivars, both by GM and conventional breeding. If they manage to file a patent [15], so what?--other breeders can easily "steal" the germplasm away from the patented genes, and in any case, the patents expire after 20 years!
Monsanto has seen the writing on the wall--farmers and consumers are demanding not only more food production, but also more eco-friendly agricultural practices. Monsanto research is heading in that direction with their conventional breeding programs, the development of "biological" insecticides [16], and the goal of producing pesticide-free dsRNA crops. Add to that that the company could actually bring to market dsRNA medications against bee viruses, nosema, and perhaps varroa. All would be huge wins for the honey bee and beekeepers!
Hold The Hate Mail
Full disclosure: so despite my innate aversion to corporate dominance and corporate agriculture, I feel that we beekeepers should work with Monsanto to develop products for the beekeeping industry, as well as bee-friendly cultivars of crop plants, and have thus personally decided to be a cooperator in their initial bee research trial. Is this some sort of Faustian bargain? I don't know, but as a condition of my cooperation, I asked, and Monsanto agreed, to allow me to share the data collected with the beekeeping community--which could be a big win for us, since Monsanto has some of the best analytic labs in the world! I feel that it is far better to have Monsanto working on the side of beekeepers, rather than perhaps against us. At this point, I'd like to leave the GM debate behind, and address the facts of the matter as to any relationship between GM crops and CCD.
The Changing Face Of Agriculture
Genetic engineering has clearly changed the face of agriculture in the U.S. (Fig. 1).
Figure 1. These three crops account for over half of all U.S. acreage planted to principal crops, and all are worked to some extent by bees. Data from http://www.ers.usda.gov/data-products/adoption-of-genetically-engineered-crops-in-the-us.aspx
As can be seen from the figure above, any bees near corn, soy, or cotton are going to be exposed to pollen and nectar from GM plants, as well as to indirect effects due to the technology. So could GM crops be the cause of CCD?
Bt Crops
Biological plausibility: the insecticidal Bt toxins in GM corn and cotton pollen could harm adult or larval bees.
Organic farmers have long used the spores of the bacterium Bacillus thuringiensis (Bt) to kill caterpillars. Bt spores germinate in the caterpillar gut, and the bacterium produces insecticidal crystalline proteins (Cry proteins) that bind to specific receptors on the insect intestinal wall. Since different insect species have different receptors on their gut cells, different strains of Bt have evolved to specifically kill various caterpillars, beetles, mosquitoes, etc. [17]. The proteins are so species specific that wax moths can be controlled on combs by Bt aizawai, which produces Cry proteins that are toxic to moth larvae, but not to bees.
Molecular biologists tweak these Cry proteins to make them even more species specific, and then insert them into plant DNA, so that the plant then produces the proteins itself, thus making its tissues toxic to the target species. In order to delay the inevitable evolution of Cry-resistant pests, growers plant a percentage of "refuge" crop not containing the Cry genes. Even so, any particular Cry gene will only be effective for some number of years until resistant pests show up.
People have expressed concern about a poisonous substance being introduced into plant tissues, and to them I highly recommend the paper "Misconceptions about the Causes of Cancer" [18]. The reality is that plant tissues are naturally awash in poisonous substances. Plants have needed to repel herbivores throughout their evolution, and since plants can't run, hide, or bite back, they do it chemically. Many of our most popular fruits, nuts, grains, and vegetables (and especially herbs and spices) contain powerful phytotoxins. Their wild ancestors required cooking or leaching before the plant was edible to humans. Plant breeders systematically select for cultivars with lower levels of (the often strongly flavored) toxins.
Plants that are naturally resistant to pests contain more phytotoxins, often produced in response to damage from insects. For example, the sprouts of wheat, corn, and rye produce potent mutagens (enjoy that cup of wheatgrass juice!) [19]. And some plants naturally contain symbiotic bacteria and fungi in their tissues, which produce non-plant chemicals [20]. There is absolutely nothing biologically novel about insecticidal toxins in plant tissues.
The toxicity (or lack thereof) of Cry proteins to non-target organisms, especially upon two "charismatic" species--the honey bee and the monarch butterfly--has been well studied [21], [22], [23]. A recent and very well-designed experiment on the effect of GM Bt corn pollen upon the growth and survival of honey bee larvae was recently performed by a team of independently-funded German researchers [24]. They added pollen from four different sources to a standard semi-artificial larval diet.
Results: surprisingly, the larvae fed the pollen from the "stacked" GM corn containing a combination of three different Cry proteins exhibited a higher survival rate (100%), than those fed non-GM corn pollen! To me, a big plus for this study was that they also included a positive control of pollen from a wild plant said to be harmful to bees--only about 30% of those larvae survived! This finding confirmed that even some natural pollens are quite toxic, and that we should compare any toxicity trials of pesticides with those of the natural phytotoxins in nature.
Analysis: CCD and colony mortality occur even in the absence of GM Bt crops; feeding GM Bt pollen to adult bees or larvae does not cause observable adverse effects.
Verdict on Bt crops: The specific Bt cry proteins used in GM crops were intentionally chosen to not cause harm to bees. There is no evidence to date that they do. On the other hand, Bt crops require less use of insecticides that are clearly toxic to bees [25].
Roundup Ready
Monsanto's pitch is that Roundup Ready®️ (RR) crops allow farmers to practice weed-free "no till" farming, which saves both topsoil and money. The catch is that farmers must then douse their fields with Monsanto's flagship product, Roundup (ensuring sales of that herbicide--a great marketing strategy). Bayer CropScience has followed suit by introducing crops resistant to its Liberty herbicide, which has a different mode of action.
Herbicide-resistant crops do indeed address several major environmental problems:
No till farming does in fact require less labor and reduces soil compaction.
Farmers get greater production due to less competition from weeds.
No till also reduces the amount of petrochemical fuel involved in tillage.
No till greatly reduces soil erosion, which has long been a major environmental concern.
No till may help to sequester carbon in the soil, and to rebuild soil.
So what's not to love about Roundup Ready? There are a few main complaints--(1) the massive spraying of the active ingredient, glyphosate, for which there is questionable evidence that it may be an endocrine disruptor [26], (2) claims of intimidation by Monsanto of farmers who choose not to plant RR seed, and (3) the environmental impact and sustainability of the sort of weed-free monoculture possible with RR crops.
So how do Roundup and RR crops relate to honey bees?
Direct Effects Of Roundup Use
Biological plausibility: either the active ingredient (glyphosate), or the adjuvants could cause bee toxicity.
The EPA has thoroughly reviewed the research and found glyphosate to be practically nontoxic to bees (and humans). They have found the same for Roundup's adjuvant polyoxyethylene-alkylamine. However, some beekeepers tell me that they see increased bee mortality following the spraying of glyphosate (Fig. 3), but are not sure whether it was a generic product, or perhaps contained additional ingredients (surfactants, fungicides, or insecticides) added to the tank mix.
Figure 3. A farmer spraying glyphosate herbicide over Roundup Ready corn seedlings. Photo courtesy of beekeeper Larry Garrett.
Analysis: there is no strong evidence that the spraying of Roundup or generic glyphosate herbicide is directly causing significant bee mortality. However, Drs. Jim and Maryann Frazier have legitimate concerns about the effect of some adjuvants--especially the organosilicones [27], [28].
Indirect Effects Of Roundup Use
Biological plausibility: the elimination of weeds reduces bee forage.
The success of Roundup Ready technology has allowed farmers to largely eliminate weeds from their fields (at least until the inevitable resistant weeds take over). But they don't stop there--nowadays they practice "clean farming" and use herbicides to burn off every weed along the fencerows and in the ditches--the very places that bees formerly had their best foraging. This elimination of flowering weeds severely reduces the amount of available of bee forage, plus kills off the host plants of native pollinators (such as monarch butterflies) and beneficial insects.
European honey bees evolved in Europe (hence the name), and are adapted to the nutrition provided by Old World flowering plants. Many of the weeds in North America are old friends of the honey bee. On the other hand, honey bees were never exposed to corn, soybeans, sunflowers, or squashes until recently; neither corn nor sunflowers supply complete amino acid profiles in their respective pollens. Until the advent of Roundup Ready, the weeds in an around crops provided alternative nectar and pollen sources for bees; today there is often nary a bee-nutritious weed to be seen in or around a field of corn or soybeans (Fig. 4).
Figure 4. I took this photo of a no-till herbicide-resistant corn field, prior to the shading canopy of the crop closing over. Note the total lack of any sort of bee forage (or any species of anything other than corn). The soil surface is a far cry from the original densely vegetated prairie sod. Prior to RR, there was more weedy forage for bees, and especially from the traditional weed-controlling crop rotation into legumes or pasture.
Update: there's a great deal of debate about the safely of Roundup (the formulated product with it's surfactants) and its active ingredient, glyphosate. From http://npic.orst.edu/factsheets/archive/glyphotech.html
"In plants, glyphosate disrupts the shikimic acid pathway through inhibition of the enzyme 5-enolpyruvylshikimate-3-phosphate (EPSP) synthase. The resulting deficiency in EPSP production leads to reductions in aromatic amino acids that are vital for protein synthesis and plant growth.
As far as the claims that glyphosate causes cancer (notably Non-Hodgkin's Lymphoma), I agree with the regulatory agencies that the case against glyphosate is very weak. As far as glyphosate being an endocrine disruptor, I'll leave it to the researchers and regulatory agencies to figure it out. As I type these words, I've actually got caged bees to which I'm feeding glyphosate (at a field-realistic dose) for a trial, and not seeing increased mortality. But some research indicates that it may be harmful to the gut microbiota. This sort of research takes time, and eventually we'll figure out just how safe or harmful glyphosate is to bees, humans, or the environment.
But nothing in nature is simple. Eliminating the competition of weeds and insects may allow plants to hold back from the production of natural toxins. And a surprising piece of research found corn kernels from plants sprayed with either of two different herbicides actually contain more of the healthful carotenoids [30]!
The Future Of Roundup
It took Monsanto several years to genetically engineer Roundup-resistant crops, yet took farmers only slightly longer to inadvertently produce Roundup-resistant weeds by the conventional breeding technique of applying a strong selective pressure-the continuous application of Roundup!
Weed management scientists consider glyphosate to be a once-in-a-100-year discovery--it works on 140 species of weeds, and is relatively environmentally friendly. However, its overuse has led to the creation of several "driver weeds" that could soon lead to its redundancy in corn, soy, and cotton acreage [31]. This will drive farmers to turn to other herbicides (which will also in time fail). We can only hope that someday they will be forced back into practicing crop rotation into legumes and pasture.
Reality Check
In order to clarify cause and effect, I often seek out extreme cases. Such would be the situation in the Corn Belt, where I could compare the USDA's hive and honey data from the old days to those under today's intense planting of GM crops (Fig. 5)!
Figure 5. The most intense planting of GM crops is in Iowa and Illinois (the dark green areas of the map above). U.S. farmers planted nearly 100 million acres of corn this year, and 76 million of soy. That is enough acreage to cover the entire state of Texas with GM crops!. Source: http://www.nass.usda.gov/Charts_and_Maps/Crops_County/pdf/CR-PL10-RGBChor.pdf
So I went through the tedious process of downloading and transcribing the NASS agricultural census figures for Iowa. I entered the amount of corn acreage, the total number of colonies in the state, and what I consider to be the best measure of colony health--honey yield per hive (which of course is largely weather dependent, but should show any trends). I plotted the data below (Fig. 6):
Figure 6. Bee and corn data from Iowa, and the dates of introduction of corn pest control technologies. The dotted line is median honey yield per colony. No factor appears to have affected honey production, but colony numbers have decreased since the arrival of varroa. Gaps are missing data. Source NASS.
Note: for non beekeepers, varroa is a parasitic mite that arrived in the U.S. around 1990 and quickly became, and still remains, the Number One problem in bee health-far more than any other factor.
Over the years, corn acreage increased by 18%. Other than the prodigious crop of 1988, honey production has averaged around 67 lbs per hive. The thing that stands out is the plot of number of colonies. Hive numbers jumped up in the late 1980's, likely due to federal honey price support payments, which peaked in 1988, and were cut off in 1994 [[i]]. Colony numbers peaked in 1990, the same year that varroa arrived in Ohio, and went down from there, leveling off to about half the number of hives present in the 1970's.
I fully expected honey yields to decrease concurrent with the adoption of Roundup Ready varieties, but they didn't! Colonies still produce as much honey today as they did in the past, but this might be partially due to having fewer bees working the same amount of land, or to increased soybean nectar (which saved a number of Midwestern beekeepers from disaster during this year's droughts).
Perhaps even more surprising is the fact that in a state covered in corn and soy, colony productivity did not appear to be affected by the introductions of either Bt or Roundup Ready corn, nor by the universal use of neonicotinoid seed treatments (between corn and soy, on over roughly two thirds of the entire state land area). Note that honey yields actually increased for a few years following the introduction of clothianidin seed treatment!
Tellingly, hive numbers started to decrease after the arrival of varroa, and plummeted in the late 1990's as fluvalinate failed as a miticide, and many beekeepers simply threw up their hands and quit the business.
Verdict on herbicide tolerant crops: from a nutritional standpoint, the increased use of herbicides, and the associated weed free "clean farming" has certainly not helped the bees in corn/soy areas, but it is hard to make a case for them causing colony collapse.
Verdict on GM crops in general: Allow me to quote from the USDA:
...there is no correlation between where GM crops are planted and the pattern of CCD incidents. Also, GM crops have been widely planted since the late 1990s, but CCD did not appear until 2006. In addition, CCD has been reported in countries that do not allow GM crops to be planted, such as
Switzerland [33].
Looking Ahead: The Chemical Treadmill & Pest Resistance
It is interesting to observe the evolution of agriculture from the perspective of a biologist. Simple systems in nature are inherently less stable than complex systems. The current agricultural model in the U.S. exemplifies simplicity to the extreme--plant a single species into bare soil year after year, killing any competitive weeds or insects with pesticides (either sprayed, systemic, or engineered into the plants), and attempt to maintain fertility by adding energy-costly fertilizer. From a biological perspective, such a strategy is little more than an intense selective breeding program for the most resistant pests, and doomed to escalating chemical and energy inputs until the system collapses under its own weight.
I'm anything but a salesman for either Bt nor RR crops. Both are mere short-term solutions--resistant bugs and weeds are already starting to spread. I also have questions about the benefits of herbicide-intense no till planting [34], and hope that farmers return to alternative methods of weed control [35]. Luckily, the system will likely be self correcting, eventually forcing humanity to practice more sustainable methods of farming the land. However, I suggest that those methods may well include the wise use of biotechnology.
Additional Discussion
The Back Story On Plant Breeding And GM Crops
Traditionally, farmers simply replanted with the seeds from the most desirable individual plants year after year; this is the simplest form of "selective breeding." For example, all the various cole crops (cabbage, kale, broccoli, cauliflower, kohlrabi, Brussels sprouts) were developed by intentionally selecting for unusual forms of the species (resulting from random recombination of the natural allelic diversity, spontaneous mutants, or natural hybrids). This sort of selective breeding tends to result in a diverse assembly of locally-adapted cultivars. In Oaxaca, Mexico- the birthplace of corn-some 150 traditional varieties of maize are grown without pesticides or herbicides, thereby maintaining an invaluable reservoir of genetically-diversity "germplasm," which breeders can then cross and backcross in order to develop new cultivars (e.g., for pest or drought resistance).
In the early years of the U.S., seeds from desirable cultivars were distributed to farmers by the government, and plant breeding was performed at universities and at the USDA [36]. But since every strain breeds true, a farmer could save the seed and replant, leaving little opportunity for seed companies to make a buck. So in 1883, they formed the American Seed Trade Association and began to lobby for the cessation of the government programs.
The Profit Motive
In the early part of the 20th century, the companies began to promote hybrids-- crosses of two (or more) different strains or species that exhibited some sort of "hybrid vigor"--offering greater production, tastier fruit, or some other desirable characteristic. Hybrids were a godsend to the companies, since they are often sterile or don't breed true, meaning that farmers needed to purchase (rather than save) seed each season.
The seed lobby eventually shifted public funding away from the free distribution of selected seedstocks to instead encouraging the USDA and universities to develop inbred parental lines and breeding stock that the seed trade could then use to create proprietary hybrid varieties. By 1960, farmers planted less than 5% of corn from saved seed; and less than 10% of soybeans by 2001. As on-farm familiarity with the saving of seed was forgotten, farmers became willing consumers of produced seed.
Enter GM Crops
Then in 1980, the Supreme Court decided that seed companies could patent new varieties if they contained distinct and novel genetic markers. This meant that farmers (in some countries) could now be required to sign licensing agreements to allow them to use the patented seed each season [37] (there is a hodge-podge of international patent laws in this regard [38]).
The Second "Green Revolution"
The first "green revolution" was based upon fertilizer, pesticides, and hybrid seed (and also resulted in forcing farmers onto "agricultural treadmills"-making them less self sufficient and sustainable, and more reliant upon purchased seed, pesticide and fertilizer use, and upon borrowed money).
In 1950 the Secretary of Agriculture Ezra Benson said to farmers, "Get big or get out." His 1970s successor, Earl Butts, repeated that message, and exhorted farmers to "plant fence row to fence row" and to "adapt or die." Politicians who understood that a well-fed electorate is a happy electorate promoted policies that resulted in the destruction of the small family farm. Our policy of price supports and favorable treatment of agribusiness has changed the face of the American farm and the composition of the American diet [39].
Today's "second green revolution" is based upon technological advances in plant genetics (including GM) and the (at least partial) replacement of nasty pesticides with "biologicals." As an environmentalist, I find the new revolution to be more promising for ecological sustainability, but it is not without its downside--the current consolidation of agribusiness. As I mentioned before, farms, seed companies, and chemical companies are all being bought up by a few main players. Philip Howard details this consolidation in a free download [40], from which I quote:
This consolidation is associated with a number of impacts that constrain the opportunities for renewable agriculture. Some of these include declining rates of saving and replanting seeds, as firms successfully convince a growing percentage of farmers to purchase their products year after year; a shift in both public and private research toward the most profitable proprietary crops and varieties, but away from the improvement of varieties that farmers can easily replant; and a reduction in seed diversity, as remaining firms eliminate less profitable lines from newly acquired subsidiaries.
He then speaks of the concept of the "treadmill":
For the majority of farmers, however, the result is that they must constantly increase yields in order to simply maintain the same revenue. [Monsanto's sales pitch is that economic success in farming is driven by yield per acre [41]. Those that are unable to keep up with this treadmill will "fall off," or exit farming altogether. Their land ends up being "cannibalized" by remaining farmers who seek to increase scale of production as another means of keeping up with the treadmill, leading to the increasing centralization of agriculture. Farmers who have managed to stay in business have adapted to this process, and are typically on the leading edge of the adoption of new technologies. As a result, they have a high degree of confidence in science and technological innovations.
However, this problem has nothing to do with GMO's, but is rather due to the public's unknowing acceptance of the practice. Capitalism inevitably leads to consolidation unless consumers stop supporting corporate agribusiness with their pocketbooks and their votes, and start demanding that their government enforce antitrust efforts and better support small farmers.
But we are allowing economics and politics to distract us from the topic at hand--the technology of genetic engineering in plant breeding.
Cautions About GM
The most vocal critic of genetic modification is Jeffrey Smith, fear-mongering author of Seeds of Deception, producer of the film Genetic Roulette, and executive director of the inappropriately-named Institute for Responsible Technology. Smith is a gifted and effective communicator, as well as being a practitioner of "yogic flying" [42]. I will be the first to say that Smith's anti-GMO claims [43] would scare the pants off of anyone, and make for compelling story! The problem is that he plays loose with the facts--most of his claims simply do not stand up to any sort of scientific scrutiny. I suggest that for an objective analysis of the facts, that you visit AcademicsReviewed.org, a website that tests popular claims against peer-reviewed science. They address each of Smith's alarming "facts" one by one [44]. It is a thrilling ride to open the two web pages side by side, first being shocked by Smith's wild and scary claims, and then reading the factual rebuttal to each! The thing that most bothers me about Smith's writing is that he treats GM cultivars generically, rather than specifically addressing the merits or concerns for them individually. This makes little sense, since any conventional crop has cultivars that cause human allergy or contain excessive levels of natural toxins, yet no one calls for the testing of each of them!
Perspectives On GM Crops
As you may have guessed by now, to me, the GM debate should not be about being pro or con, rather it should be about the intelligent discussion of reconciling its promise with its problems. The GE genie is out of the bottle, and I can't see that anyone is going to put it back in-so we might as well work with it! So let's cut through the hype and hysteria, the fears and judgments, and try to objectively look at the facts of the matter:
From a plant breeder standpoint, genetic engineering holds incredible promise for the development of crops that could be tremendously beneficial to humans or the environment. For example, "Transgenic cotton has reduced the need for conventional insecticides used against lepidopteran [pests] an average in the USA about 59.4% [and] Texas 74.7%...an average number of pesticide applications in conventional cotton has fallen from 4.3 in 1995 to 2.1 in the USA... with benefits to human health and the environment" [45].
GM is only a part of plant breeding--most advances continue to be in conventional breeding, now assisted by "marker assisted selection," which is embraced by environmentalists [46].
However, someone needs to pay for the research, and the taxpayer is not doing it! For a thoughtful discussion of the benefits of gene patents, see [47].
Novel genetic markers can be patented, and a licensing fee can be charged, despite the fact that they are not GM!
From a consumer standpoint, advanced breeding techniques can result in cheaper and more nutritious food, and less environmental impact from farming.
Consumers have erroneously been led to believe that GM crops are dangerous to their health, and call for application of the precautionary principle. My gosh, please read "Misconceptions about the causes of cancer" [48]. Few foods are entirely "safe"! And "safety" can never be proven--it can only be disproven. And no studies have ever disproven the safety of GM crops, nor have doctors noticed anyone ever getting sick from them, despite our eating them for 15 years!
In truth, some scientists argue that plants produced by classical breeding methods should undergo the same safety testing regime as genetically modified plants. There have been plenty of instances where plants bred using classical techniques have been unsuitable for human consumption, causing toxicity or allergic reactions.
Those that speak of applying the "precautionary principle" should read Jon Entine's trenchant analysis of the fallacy of overapplication of that principle [49]. In truth, our regulators (EPA and FDA) vigorously apply the precautionary principle in the form "reasonable certainty of no harm."
The benefits of seed biotechnology cannot be realized without good seed germplasm to start with. So a few large seed companies started buying up their competitors to acquire the most productive and desirable varieties.
The downside of the above practice is that by 2008, 85% of GM maize patents and 70% of non-maize GM plant patents in the U.S. were owned by the top three seed companies: Monsanto, DuPont, and Syngenta [50]. Note that economists figure that when four firms control 40% of a market, it is no longer competitive; in the case of GE crops, the top four seed firms control 56% of the global proprietary seed market!
On the flip side, these profits are an incentive for the large corporations to invest in innovative plant breeding research--Monsanto spends about $2 million a day on this. This is important to keep in mind in an increasingly hungry world.
On the dark side, Monsanto's nearly $12 billion in annual sales allows the company to lobby regulators, influence universities, and spin the news. These are standard business practices for any large corporation, but hardly make Monsanto uniquely evil.
Be aware that patented genes are of use only if inserted into high-producing cultivars-which are developed by conventional breeding (which constitutes nearly half of Monsanto's plant breeding budget). These desirable cultivars have no patent protection. Monsanto uses a non GE technology called SMART = Selection with Markers and Advanced Reproductive Technologies. SMART technology is warmly embraced by environmental groups [51].
Adding a genetic marker allows a company to identify its proprietary strains, like putting a nametag on a dog. But clever breeders can back engineer the desirable germplasm out from patent protection.
And remember that patents expire after 20 years. The patents for Roundup Ready soybeans expire in 2014--at which time farmers, universities, and seed companies will then be free to propagate and sell the variety [52]. Patents are granted in order to spur innovation; by filing for patent protection, a company must make its discoveries public knowledge. This is a good thing.
Monsanto invests 44% of its R&D on conventional (as opposed to GM breeding).
Monsanto has also given rights to some of their patented crops to poorer countries, and recently donated a database of some 4000 genetic markers from cotton to Texas A&M [53]. The university plant breeders are excited in that the information will assist them in their conventional (non-GM) breeding of cotton, to the benefit of the environment [54 ].
From the farmer's standpoint, he has the choice of purchasing GE varieties that may be more productive, reduce insecticide use, or reduce tillage costs [55]. Keep in mind that there is nothing keeping him from purchasing "conventional" non-GM seed--it is available (I checked, and it sells at about half the cost of GM seed). In our free enterprise system there is nothing to keep non-GM seed companies from selling an alternative product if there is a demand. Farmers who are unimpressed by GM varieties freely switch back to conventional seed.
From an agricultural standpoint, the widespread adoption of a few favored crop varieties (GM or not) can result in the irreplaceable loss of crop genetic diversity--this is of great concern to plant breeders. If you haven't yet seen the graphic of our loss of crop genetic diversity from National Geographic magazine, you should! [56]. Luckily, this does not appear to be occurring yet with maize in Oaxaca [57], but there is a legitimate concern that economics will force traditional farmers out of business, leading to the loss of heirloom varieties. However, this is not a GM issue, but rather an effect of consolidation.
From a sustainability standpoint, there is nothing to prevent constant breeding innovation to keep pace with pest evolution. Genetically engineered crops can play a role in sustainable farming as our agricultural practices begin to shift to more ecologically sustainable methods.
One should keep in mind how the simple splicing of a virus gene into the papaya saved the Hawaiian papaya growers from the ravages of ringspot virus--the GE papaya is the mainstay of the industry, and by virtue of keeping the virus in check actually allows nearby organic papayas to thrive. Yet ecoterrorists recently hacked down thousands of GM trees [58]. It's interesting to read the history of "Golden Rice" [59] to see how the anti-GMO lobby is specifically scared that the success of such a lifesaving crop might open the door for acceptance of other GM plants!
Update Jan 2013
News item: Leading Environmental Activist's Blunt Confession: I Was Completely Wrong To Oppose GMOs. Blog in Slate Magazine
"If you fear genetically modified food, you may have Mark Lynas to thank. By his own reckoning, British environmentalist helped spur the anti-GMO movement in the mid-'90s, arguing as recently at 2008 that big corporations' selfish greed would threaten the health of both people and the Earth. Thanks to the efforts of Lynas and people like him, governments around the world--especially in Western Europe, Asia, and Africa--have hobbled GM research, and NGOs like Greenpeace have spurned donations of genetically modified foods.
But Lynas has changed his mind--and he's not being quiet about it. On Thursday at the Oxford Farming Conference, Lynas delivered a blunt address: He got GMOs wrong."
Anyone opposed to GMO's should read Mr. Lynas' well thought out address: http://www.marklynas.org/2013/01/lecture-to-oxford-farming-conference-3-january-2013/
Update May 2014
I've compiled a list of recent worthwhile reading on the "other side" of the GMO debate at https://scientificbeekeeping.com/gmo-updates/
So What's The Problem?
The problem is that anti-GMO advocacy groups are determined to put a stop to all GE technology. They targeted California with Prop 37, which applied only to packaged foods and produce. A more cynical take on Prop 37 was that it was all about marketing: "If your produce is no different in terms of taste, safety and nutrition from a competitor, and costs more, apparently the only marketing option is to create a negative image of your competitor's product" [60].
If Prop 37 had been successful, the promoters would then have targeted restaurants, the meat and dairy industry, and the beverage industry. I personally feel that this is an extreme position, what with the human population growing hungrier every day, and climate change threatening agriculture worldwide with heat, drought, pestilence, and salinity problems. Not only that, but GM crops hold promise for cheap omega-3 fatty acids (so that we don't have to harvest fish for them), cost-effective biofuels, and less expensive pharmaceuticals.
A good blog on the problem with the anti-GMO fear campaign can be found at [61], from which I quote:
It would be bad enough if something like the Seralini study simply contributed to the unnecessary angst amongst consumers around the world. It also has very real political, economic and practical effects. For instance brand conscious food companies have used their leverage to prevent the development of GMO versions of potatoes, bananas, coffee and other crops because they fear controversy. Apple growers worried about the market response are opposing the introduction of a non-browning apple even though it was developed by one of their own fruit companies. French activists destroyed a government-run field trial of a virus-resistant root stock which could have made it possible to produce good wine on sites that have become useless because of contamination with sting nematodes and the virus they vector. California voters have the potential to pass a seriously flawed "GMO labeling" initiative next month that could only serve the purposes of the lawyers and "natural products" marketers who created it. More importantly, European and Japanese importers of wheat essentially blackmailed the North American wheat producers into blocking biotech wheat development because those companies were nervous about consumer response in countries where GMO angst is so high. This has delayed by decades not only specific desirable trait development, but also what might have been an enormous private investment in a crop that is critically important for feeding a lot more people than just those in those rich countries. There is a huge cost of "precaution" based on poor science.
I believe that people should be well informed before taking a stance on important issues. I'd like to suggest one last excellent blog by an independent U.C. Berkeley evolutionary biologist and medical researcher:"How Bt Corn and Roundup Ready Soy Work - And Why They Should Not Scare You [62].
Acknowledgements
As always, thanks to my friend and collaborator in research Peter Loring Borst, and to anyone who still reads my articles after finding out that I've collaborated with Monsanto!
References
[1] Key S, et al (2008) Genetically modified plants and human health. J R Soc Med.101(6):290-298. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2408621/
[2] For example: Antoniou, M, et al (2012) GMO myths and truths.
(Broken Link!) http://earthopensource.org/files/pdfs/GMO_Myths_and_Truths/GMO_Myths_and_Truths_1.3.pdf
[3] Chiba S, et al. (2011) Widespread endogenization of genome sequences of non-retroviral RNA viruses into plant genomes. PLoS Pathog 7(7): e1002146.
[4] Domingo, JL and JG Bordonaba (2011) A literature review on the safety assessment of genetically modified plants. Environment International 37: 734-742.
[5] Key (2008) op. cit.
[6] Smith, JM (2003) Seeds of Deception. Yes! Books
[7] Seralini, GE, et al (2012) Long term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize. Food and Chemical Toxicology (2012) http://foodpoisoningbulletin.com/wp-content/uploads/Toxicity-of-Roundup-Ready-Maize.pdf;
Reviews
http://www.forbes.com/sites/henrymiller/2012/09/25/scientists-smell-a-rat-in-fraudulent-genetic-engineering-study/2/
http://www.efsa.europa.eu/en/faqs/faqseralini.htm#9, http://www.emilywillinghamphd.com/2012/09/was-it-gmos-or-bpa-that-did-in-those.html,
(Broken Link!) http://www.ask-force.org/web/Seralini/Anonymous-Rat-List-Spaying-2003.pdfs, http://storify.com/vJayByrne/was-seralini-gmo-study-designed-to-generate-negati;
Benbrook, CM (2012) Impacts of genetically engineered crops on pesticide use in the U.S. -- the first sixteen years. Environmental Sciences Europe 24:24 http://www.enveurope.com/content/pdf/2190-4715-24-24.pdf,
Review http://weedcontrolfreaks.com/2012/10/do-genetically-engineered-crops-really-increase-herbicide-use/#more-432
[8] http://journals.tubitak.gov.tr/agriculture/issues/tar-04-28-6/tar-28-6-1-0309-5.pdf
[9] http://www.monsanto.com/whoweare/Pages/monsanto-history.aspx
[10] http://www.businessweek.com/stories/2010-01-10/monsanto-v-dot-food-inc-dot-over-how-to-feed-the-world
[11] Methods for genetic control of plant pest infestation and compositions thereof
http://www.freepatentsonline.com/8088976.html
http://www.freepatentsonline.com/7943819.html
[12] http://www.greenpeace.org/australia/PageFiles/348427/smart-breeding.pdf
[13] 2007 figures http://www.census.gov/compendia/statab/2012/tables/12s0835.pdf
[14] ETC Group (2008) Who owns nature? Corporate power and the final frontier in the commodification of life. http://www.etcgroup.org/sites/www.etcgroup.org/files/publication/707/01/etc_won_report_final_color.pdf
[15] Blakeney, M (2011) Trends in intellectual property rights relating to genetic resources for food and agriculture. http://www.fao.org/docrep/meeting/022/mb684e.pdf This document covers the hodge-podge of international patent laws regarding plants and animals.
[16] http://www.monsanto.com/products/Pages/biodirect-ag-biologicals.aspx
[17] History of Bt http://www.bt.ucsd.edu/bt_history.html
Mode of action http://www.bt.ucsd.edu/how_bt_work.html
[18] Gold 2002 Misconceptions about the causes of cancer http://potency.berkeley.edu/pdfs/Gold_Misconceptions.pdf A "MUST READ"!
[19] Buchmann CA, et al (2007) Dihydroxy-7-methoxy-1,4-benzoxazin-3-one (DIMBOA) and 2,4-dihydroxy-1,4-benzoxazin-3-one (DIBOA), two naturally occurring benzoxazinones contained in sprouts of Gramineae are potent aneugens in human-derived liver cells (HepG2). Cancer Lett. 246 (1-2):290-9.
[20] http://en.wikipedia.org/wiki/Endophyte
[21] Duan JJ, et al (2008) A meta-analysis of effects of Bt crops on honey bees (Hymenoptera: Apidae). PLoS ONE 3(1): e1415.
[22] Center for Environmental Risk Assessment (2011) A review of the environmental safety of the Cry1Ab protein. http://cera-gmc.org/docs/cera_publications/cry1ab_en.pdf
[23] Han, P, et al (2012) Does transgenic Cry1Ac + CpTI cotton pollen affect hypopharyngeal gland development and midgut proteolytic enzyme activity in the honey bee Apis mellifera L. (Hymenoptera, Apidae)? Ecotoxicology. 2012 Aug 7. [Epub ahead of print]
[24] Hendriksma HP, et al (2011) Testing pollen of single and stacked insect-resistant bt-maize on in vitro reared honey bee larvae. PLoS ONE 6(12): e28174.
[25] Benbrook, CM (2012) op. cit.
[26] Reviewed in http://www.sourcewatch.org/index.php/Glyphosate
[27] Mullin, C.A., J.L. Frazier, M.T. Frazier & T.J. Ciarlo - A primer on pesticide formulation 'inerts' and honey bees. http://www.extension.org/pages/58650/proceedings-of-the-american-bee-research-conference-2011
[28] Ciarlo TJ, CA Mullin, JL Frazier, DR Schmehl (2012) Learning impairment in honey bees caused by agricultural spray adjuvants. PLoS ONE 7(7): e40848.
[29] Johal, GS and DM Huber (2009) Glyphosate effects on diseases of plants. Europ. J. Agronomy 31: 144-152. http://www.organicconsumers.org/documents/huber-glyphosates-2009.pdf
Huber, DM (2010) Ag chemical and crop nutrient interactions - current update. http://www.calciumproducts.com/dealer_resources/Huber.pdf
Reviewed in (Broken Link!) http://www.weeds.iastate.edu/mgmt/2010/glyMndisease.pdf
[30] Kopsell et al. (2009) increase in nutritionally important sweet corn kernel carotenoids following mesotrione and atrazine applications. Journal of Agricultural and Food Chemistry 090619124509017 DOI: 10.1021/jf9013313
[31] Laws, F (2010) http://cornandsoybeandigest.com/issues/will-glyphosate-fall-wayside-resistance-grows
[32] http://www.nationalaglawcenter.org/assets/crs/RS20759.pdf
[33] http://www.ars.usda.gov/is/AR/archive/jul12/July2012.pdf
[34] http://www.misereor.org/fileadmin/redaktion/MISEREOR_no%20till.pdf
[35] http://www.acresusa.com/toolbox/reprints/Organic%20weed%20control_aug02.pdf
[36] http://www.seedalliance.org/Seed_News/SeminisMonsanto/
[37] (Broken Link!) http://earthopensource.org/files/pdfs/GMO_Myths_and_Truths/GMO_Myths_and_Truths_1.3a.pdf
[38] Blakeney, M (2011) Trends in intellectual property rights relating to genetic resources for food and agriculture. http://www.fao.org/docrep/meeting/022/mb684e.pdf This document covers the debate involved in international patent law regarding plants and animals.
[39] Philpott, T (2008) A reflection on the lasting legacy of 1970s USDA Secretary Earl Butz. http://grist.org/article/the-butz-stops-here/; but for a contrary view by an actual corn farmer, read Hurst, B (2010) No Butz About It. (Broken Link!) http://www.american.com/archive/2010/july/no-butz-about-it
[40] Howard, Philip H. 2009. Visualizing consolidation in the global seed industry: 1996-2008. Sustainability, 1(4), 1266-1287. http://www.mdpi.com/2071-1050/1/4/1266/pdf
[41] http://www.monsanto.com/investors/Documents/Whistle%20Stop%20Tour%20VI%20-%20Aug%202012/WST-Fraley_RD_Update.pdf
[42] http://academicsreview.org/reviewed-individuals/jeffrey-smith/
[43] http://responsibletechnology.org/docs/145.pdf
[44] http://academicsreview.org/reviewed-content/genetic-roulette/
[45] Greenberg, S, et al (2012) Economic and Environmental Impact Transgenically Modified Cotton Comparative with Synthetic Chemicals for Insect Control. Journal of Agricultural Science and Technology B 2 750-757.
[46] Greenpeace (2009) Smart Breeding. Marker-Assisted Selection: A non-invasive biotechnology alternative to genetic engineering of plant varieties. http://www.greenpeace.org/australia/PageFiles/348427/smart-breeding.pdf
[47] http://www.genengnews.com/gen-articles/in-defense-of-gene-patenting/2052/
[48] Gold 2002 Misconceptions about the causes of cancer http://potency.berkeley.edu/pdfs/Gold_Misconceptions.pdf
[49] Entine, J (2010) Crop Chemophobia: Will Precaution Kill the Green Revolution? http://www.jonentine.com/pdf/CROPCHEMOPHOBIApre-orderform.pdf
[50] Howard, Philip H. 2009. Visualizing consolidation in the global seed industry: 1996-2008. Sustainability, 1(4), 1266-1287. http://www.mdpi.com/2071-1050/1/4/1266/pdf
[51] http://www.greenpeace.org/australia/PageFiles/348427/smart-breeding.pdf
[52] http://www.monsanto.com/newsviews/Pages/roundup-ready-patent-expiration.aspx;
[53] http://www.cotton247.com/article/3401/monsanto-donates-marker-technology
[54] http://www.youtube.com/watch?v=dcZyFH_eITQ
[55] http://www.biofortified.org/2012/05/the-frustrating-lot-of-the-american-sweet-corn-grower/#more-8670
[56] http://ngm.nationalgeographic.com/2011/07/food-ark/food-variety-graphic If you didn't see this graphic in National Geographic, you should!
[57] (Broken Link!) http://researchnews.osu.edu/archive/mexmaize.htm
[58] http://www.huffingtonpost.com/2011/08/20/genetically-modified-papayas-attacked_n_932152.html
[59] http://en.wikipedia.org/wiki/Golden_rice
[60] http://westernfarmpress.com/blog/proposition-37-gone-probably-not-forgotten?
[61] http://appliedmythology.blogspot.com/2012/10/can-damage-from-agenda-driven-junk.html?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+AppliedMythology+%28Applied+Mythology%29
[62] http://www.science20.com/michael_eisen/how_bt_corn_and_roundup_ready_soy_work_and_why_they_should_not_scare_you
Category: Colony Health - Diseases, Viruses, CCD
Tags: collapse, colony, genetically, gm crops, gmo, modified, plants, sick bees | plants Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/plants/ |
Understanding Colony Buildup and Decline: Part 5 - Egglaying, Adult Survivorship, and Modeling Colony Growth
First published in: American Bee Journal, June 2015
Understanding Colony Buildup and Decline - Part 5
Egglaying, Adult Survivorship, And Modeling Colony Growth
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in June 2015
CONTENTS
Some Questions Begging For Answers
Survivorship Of The Workers
A Simplified Mathematical Model
Question: Why Does The Population Stop Growing After 10 Weeks?
Population Top Out
Playing Catch Up
Next
Acknowledgements
Citations and Footnotes
I could wax poetic about the wonder of the honey bee superorganism, but when it comes to making management decisions, it is more informative to use a reductionist approach to understand why to do what. In the case of colony buildup, this means studying the math of recruitment vs. attrition. So let's do the math!
I left off during the linear growth phase of the colony (following the spring turnover) with several unanswered questions:
Some Questions Begging For Answers
To what extent does a queen's pace of egglaying vary over the course of a season?
Why does it seem to take only 6-10 weeks to reach maximum colony population?
What determines the maximum size to which a colony will grow?
Why can weak colonies sometimes catch up with those that got a head start?
And why does the population stop growing after 10 weeks?
So let's see if we can find answers to each of these questions in turn:
Question: To what extent does a queen's pace of egglaying vary over the course of a season?
In order to answer this question, we'd need regular measurements of the amount of sealed brood in a number of colonies over the course of the season. And again, Lloyd Harris' data provides us with that information. I plotted out his measurements for established colonies in their second year, five of which had been requeened the previous July, and three of which had queens in their second year (Fig. 1).
Figure 1. Average rates of egglaying [[i]] for 8 different queens in overwintered colonies over each 12-day time period in the spring of 1977 in Manitoba. In these two groups of hives, the queens tended to rapidly ramp up their egglaying as the colonies expanded their broodnests in April and May, tending to peak in mid May, and then settle back down a bit afterward.
[i] Specifically, the amount of sealed brood, which underestimates the actual rate of egglaying.
In answer to our question, Harris' queens hit peak egglaying early in the season (young queens exhibiting the higher rates), and then tended to level off at a lower rate (although still at nearly an egg a minute, 24 hrs a day). The hiccups in brood production appeared to be related to crowding of the broodnests during nectar flows (and then bursts of egglaying as the cells were cleared). The swarm impulse didn't occur until July.
Practical application: as far as management for maximum egg production, there are four main things that the beekeeper can do: (1) protect the hive from cold, (2) keep young queens, (3) manage the broodnests to avoid restriction of the queen's ability to find a place to lay (this could involve reversing the supers, or rearranging or adding drawn comb), and (4) feeding during times of dearth or poor weather.
Scientific Notes:
Scientists typically present the results of their studies as mean (average) values for each test group, but means alone may mean little. When you look at graphs showing means (averages), be sure to look at the error bars (usually the standard error of the mean--SEM) which is an indication of how much variation there was relative to the size of the group. If the error bars are large relative to the differences in means between the test groups, then the reader may want to ask what was the cause of that variability.
The human brain is far better at detecting patterns in pictures rather than in columns of numbers. For this reason, my readers may notice that I tend to favor showing raw data in graphical form for each individual colony, in order to let you use their own eyes to see the degree of variation from colony to colony, yet at the same time to look for patterns or trends.
Another frequently misunderstood term is "significance," which the lay reader may confuse with meaning "substantial" or "meaningful." This is often not the case. A scientist can't say that there was any difference between the results from two test groups unless it was "significantly different" from that which would be expected to occur due to random variation--this is called statistical significance. But statistical significance may not have much practical application.
As a hypothetical example, imagine a study in which a researcher treated 1000 hives with a test substance (also running 1000 control hives). Imagine that the result was that the test substance appeared to increase mean honey production in the test group by 1 ounce per hive. Due to the large "n" (number of hives), that result might allow the researcher to state that "feeding the product significantly increased honey production." But few beekeepers would get too excited about a product that increased per-hive productivity by only an ounce--in this case the results might be significant statistically, but insignificant practically.
On another subject, in this series I'm drawing heavily upon Lloyd Harris' exemplary data set. But one must be cautious about extrapolating general principles based upon a single data set. Keeping this in mind, I've compared Harris' data to that of many others, both historical and recent, and feel that it is indeed representative.
Now that we have good estimates for the range of rates of egglaying, we can calculate the total recruitment of new workers over any period of time. For example, simple math shows that at the rate of say 1200 eggs per day, a colony's total recruitment over 6 - 10 weeks will result in an additional 60,400 - 84,000 workers. But from this we must then subtract the attrition of aged or worn out workers. In order to calculate this, we must understand the expected survivorship of those workers.
Survivorship Of The Workers
As recently pointed out by my friend Peter Borst [2], beekeepers have long speculated about how long a worker honey bee lives, but it wasn't until the advent of good marking paints that this question began to be answered with hard data.
Worker survivorship is well reviewed by Woyke [3], who found that:
Workers' lives appear to be shortened by the amount of broodrearing that they do.
An intense honey flow can also shorten their lives.
Measured mean worker lifespans (by various researchers) varied from 16.6 to 37.6 days, perhaps averaging (during the productive season) about 30 days.
Woyke also noted that despite high brood production, under unfavorable conditions colonies may not reach populations exceeding 30,000 bees.
This information is useful, but we need to know more than the simple estimate of average worker longevity. What we really need to know is the day-by-day rate of attrition of any cohort of bees at various times of the year. Few researchers have dedicated serious time to finding the answer to this question. One of the best data sets is that of Sakagami and Fukuda [4] (Fig. 2).
Figure 2. Worker bee survivorship of Italian-type bees in Japan, after Sakagami (1968). The main honey flow (clover) occurs in June, and appeared to shorten the lives of workers due to increased foraging.
Let's now compare the above to Lloyd Harris' even more extensive data from Manitoba a decade later (Fig. 3):
Figure 3. Worker bee survivorship of Italian-type bees in Manitoba, after Harris [[i]; raw data courtesy the author]. Note how remarkably similar were the survivorship curves for Italian-type workers during June in either Japan or Manitoba. Harris found this survivorship curve to be consistent from April through August.
[i] Harris, JL (2010) The effect of requeening in late July on honey bee colony development on the Northern Great Plains of North America after removal from an indoor winter storage facility. Journal of Apicultural Research and Bee World 49(2): 159-169.
These data sets strongly suggest that worker survivorship is relatively constant over the course of the summer. So we now know how much attrition to subtract from recruitment. Let's go back to the math!
A Simplified Mathematical Model
Question: Why does it seem to take a colony only 6-10 weeks to reach maximum population?
Question: And then why does the population seem to stop growing after 10 weeks?
In order to attempt to answer the above questions, I created the simple Excel spreadsheet shown in Table 1. In the yellow cells, I can enter the initial starting population of adult bees, and also the number of adults emerging per day (I used the term "eggs per day" since it better reflects the influence of the queen [6]). And then, applying Harris' percentages of surviving bees at each 12-day time point (thanks to Lloyd for sharing his original data), I had the spreadsheet calculate the number of bees in each 12-day age cohort still expected to be alive at each future time point. Then I simply added each column in order to obtain the total colony population at each time point.
10,000 Starting population of adult bees
1000 Eggs per day 12 days previous
12,000 Amt sealed brood 12 days previous
Day 0 12 24 36 48 60 72 84 96
0 10,000 9,523 7,574 4,756 2,219 562 47 1 0
12 12,000 11,424 9,204 5,700 2,664 672 56 1
24 12,000 11,424 9,204 5,700 2,664 672 56
36 12,000 11,424 9,204 5,700 2,664 672
48 12,000 11,424 9,204 5,700 2,664
60 12,000 11,424 9,204 5,700
72 12,000 11,424 9,204
84 12,000 11,424
96 12,000
Total 10,000 21,535 31,022 37,420 40,595 41,614 41,783 41,806 41,818
Table 1. Calculation of colony buildup over time based upon the queen's egglaying rate and Lloyd Harris' adult survivability curve. Illustrated is an example for a colony starting at 10,000 bees, with a queen laying 1000 eggs per day. Note that at about 60 days the birth rate and death rate reach equilibrium, and the colony essentially stops growing.
What struck me when I created this spreadsheet is that the rate of recruitment and the rate of attrition consistently reach equilibrium at about 60 days after the broodnest is fully established. Think about it- assuming that the queen's rate of egglaying remains constant, but that the adult population continues to grow, then at some point the daily rate of attrition of the increasing adult population will match the daily rate of recruitment. At that point, the birth rate and the death rate reach equilibrium, and will remain so until either the birth rate or death rate changes.
But wait, you say, what about the influence of the starting population? Of course, a colony with a larger initial broodnest (such as a strong overwintered hive) gets a jump start, and can grow to its maximum in about 6 weeks (42 days). But the interesting thing is that after 10 weeks (70 days) of normal attrition, there are only a negligible amount of bees remaining from any initial adult population, meaning that the size of any starting population is irrelevant by that time.
Practical application: Surprise, surprise--the colony reaches maximum population at about 60 days after the broodnest is fully established--in agreement with the common beekeeper experience that it takes about 6 weeks for an overwintered colony to build up, or 10 weeks for a package. Those rules of thumb are based upon simple arithmetic.
Population Top Out
Question: What determines the maximum size to which a colony will grow?
I then used my spreadsheet to calculate the ultimate equilibrium population reached at various rates of egglaying (Fig. 4):
Figure 4. I arbitrarily started each colony at 10,000 bees [[i]], with sealed brood emerging at the indicated rates of egglaying. Keep in mind that by 60 days, normal attrition would have caused the initial 10,000 adult bees to have dwindled to less than 600, thus having little influence on the overall colony population. Note that, at any egglaying rate, colonies reach an equilibrium maximum population at about 60 days after brood begins to emerge at the rate of the queen's laying capacity.
[i] The size of the starting population makes no difference.
Conclusion: based upon Lloyd's survivorship curve, which appears to be quite consistent from mid spring through late summer, a healthy, well fed colony will rapidly grow in about 60 days to its maximum size, which will be roughly 42x its daily recruitment (number of workers emerging per day). E.g., at an egglaying rate of 1000 per day, a colony will reach equilibrium at about 42,000 bees (which is consistent with measurements by a number of researchers).
Practical application: Poor nutrition or brood disease will reduce the percentage of the queen's eggs that make it to adulthood, and nosema or extremely heavy foraging will reduce adult survivorship. Either factor will reduce the ultimate equilibrium size of the colony's population (or prevent it from building altogether).
Playing Catch Up
Question: Then why can weak colonies sometimes catch up with those that got a head start?
Again and again I've seen some of the dinks that I leave behind when I move my strong colonies to almond pollination in early February, grow so rapidly in strength that they've caught up with the strong colonies by the time I bring them home several weeks later. And Russian or Carniolan bees, which overwinter with much smaller clusters than my Italians, often manage to explode their populations to match those of the Italians in time for the honey flow. But if population growth is linear, how can a weak colony catch up with a strong colony?
I'm hardly the first to ponder on this; Jeffree published a graph of the buildups of three colonies in Scotland in 1947 to illustrate the point [8](Fig. 5).
Figure 5. The year 1947 was exceptionally good for bees in Aberdeen, but not all colonies fared equally well. Note how all three colonies declined in late winter, pulled off successful spring turnovers, and grew linearly to their respective maximum strengths. However, only Colony D reached full strength in time to effectively take advantage of the main flow--producing 229 lbs of surplus honey. After Jeffrey [[i]].
[i] Jeffrey, EP (1959) Op cit, Figure 3.
Colony D came through the winter with a decent cluster size, pulled off a successful spring turnover in May, and reached a modest 30,000 bees (about 16 frames) in time to produce 229 lbs of surplus from the main honey flow. Colony E started tiny, yet still pulled off a successful spring turnover, catching up with D about 5 weeks later, and made 132 lbs (having missed hitting full strength in time for the main flow). On the other hand, poor little Colony F (690 individual bees at its low point) struggled with its spring turnover, and was unable to grow large enough to take advantage of the main honey flow (making only 28 lbs), but still reached an acceptable size for wintering by the end of the season.
So how the heck was Colony E able to catch up with D? The answer can again be explained by the math in Table 1 and by looking at the growth curves in Fig. 4. Once a colony establishes a broodnest large enough for a queen to hit her laying capacity, it indeed grows at a linear rate, but then slows way down at about 48 days. That slowdown causes colonies with head starts to lose their lead, allowing colonies s lagging slightly behind to catch up. Secondly, if a late-starting queen lays even 100 more eggs per day than an early starter, her colony will gain nearly 4000 bees more than the early starter over the next 48 days.
But lastly, if the colony is unable to complete a strong spring turnover early enough, it really misses the boat, and will be unable to grow strong in time for the main flow. Thus, colonies coming out of winter fairly strong at first spring pollen will generally have a leg up on weaker ones. But as anyone who has watched a hive of Russian bees explode in strength can confirm, some races of bees are adapted to later springs, and more rapid buildup.
Practical application: timing is everything. Unless the colony synchronizes its buildup to reach peak at the beginning of the main flow, it won't be able to take full advantage of that honey flow. Our goal as beekeepers is to manage our colonies for such synchronization. If they are strong too early, they may swarm; and if too late, won't be able to produce a surplus.
I'm acutely aware of this issue this season, since our local flora is flowering 2-4 weeks earlier than usual. We have a management plan based upon splitting our hives shortly after they return from almonds and have grown to the size that they are thinking of swarming. But this season, the forage that we depend upon for the buildup of our splits had already finished flowering before the colonies were ready to split. And now we're facing the likelihood of an early main flow, followed by an abnormally long summer drought. We've been busting our butts trying to keep up.
Next
Causes of hiccups in colony buildup.
Acknowledgements
I again wish to express my gratitude to Lloyd Harris for sharing his data set. And of course to Peter Borst for his assistance in literature research. And there is no way that I could justify taking the time to research and write these articles without the generous donations by beekeepers to ScientificBeekeeping.com.
Citations And Footnotes
[1] Specifically, the amount of sealed brood, which underestimates the actual rate of egglaying.
[2] Borst, PL (2013) How long does a honey bee live? ABJ 153(3): 241-244.
[3] Woyke, J (1984) Correlations and interactions between population, length of worker life and honey production by honeybees in a temperate region. J. of Apic. Res. 23(3): 148-156.
[4] Sakagami, SF & H Fukuda (1968) Life tables for worker honeybees. Res. Popul, Ecol. X: 127-139.
[5] Harris, JL (2010) The effect of requeening in late July on honey bee colony development on the Northern Great Plains of North America after removal from an indoor winter storage facility. Journal of Apicultural Research and Bee World 49(2): 159-169.
[6] Actual worker survival from egg to larva is around 90% in unstressed colonies, so these figures actually underestimate the numbers of eggs laid by the queen. Fukuda, H. and Sakagami, S.F. 1968. Worker brood survival in honeybees. Res. Popul. Ecol. 10: 31-39.
[7] The size of the starting population makes no difference.
[8] Jeffree, EP (1959) The size of honey-bee colonies throughout the year and the best size to winter. A lecture given to the Central Association of Bee-Keepers
[9] Jeffrey, EP (1959) Op cit, Figure 3.
Category: Bee Behavior and Biology
Tags: adult survivorship, colony buildup, colony decline, colony growth, egglaying | colony growth Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/colony-growth/ |
Understanding Colony Buildup and Decline: Part 5 - Egglaying, Adult Survivorship, and Modeling Colony Growth
First published in: American Bee Journal, June 2015
Understanding Colony Buildup and Decline - Part 5
Egglaying, Adult Survivorship, And Modeling Colony Growth
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in June 2015
CONTENTS
Some Questions Begging For Answers
Survivorship Of The Workers
A Simplified Mathematical Model
Question: Why Does The Population Stop Growing After 10 Weeks?
Population Top Out
Playing Catch Up
Next
Acknowledgements
Citations and Footnotes
I could wax poetic about the wonder of the honey bee superorganism, but when it comes to making management decisions, it is more informative to use a reductionist approach to understand why to do what. In the case of colony buildup, this means studying the math of recruitment vs. attrition. So let's do the math!
I left off during the linear growth phase of the colony (following the spring turnover) with several unanswered questions:
Some Questions Begging For Answers
To what extent does a queen's pace of egglaying vary over the course of a season?
Why does it seem to take only 6-10 weeks to reach maximum colony population?
What determines the maximum size to which a colony will grow?
Why can weak colonies sometimes catch up with those that got a head start?
And why does the population stop growing after 10 weeks?
So let's see if we can find answers to each of these questions in turn:
Question: To what extent does a queen's pace of egglaying vary over the course of a season?
In order to answer this question, we'd need regular measurements of the amount of sealed brood in a number of colonies over the course of the season. And again, Lloyd Harris' data provides us with that information. I plotted out his measurements for established colonies in their second year, five of which had been requeened the previous July, and three of which had queens in their second year (Fig. 1).
Figure 1. Average rates of egglaying [[i]] for 8 different queens in overwintered colonies over each 12-day time period in the spring of 1977 in Manitoba. In these two groups of hives, the queens tended to rapidly ramp up their egglaying as the colonies expanded their broodnests in April and May, tending to peak in mid May, and then settle back down a bit afterward.
[i] Specifically, the amount of sealed brood, which underestimates the actual rate of egglaying.
In answer to our question, Harris' queens hit peak egglaying early in the season (young queens exhibiting the higher rates), and then tended to level off at a lower rate (although still at nearly an egg a minute, 24 hrs a day). The hiccups in brood production appeared to be related to crowding of the broodnests during nectar flows (and then bursts of egglaying as the cells were cleared). The swarm impulse didn't occur until July.
Practical application: as far as management for maximum egg production, there are four main things that the beekeeper can do: (1) protect the hive from cold, (2) keep young queens, (3) manage the broodnests to avoid restriction of the queen's ability to find a place to lay (this could involve reversing the supers, or rearranging or adding drawn comb), and (4) feeding during times of dearth or poor weather.
Scientific Notes:
Scientists typically present the results of their studies as mean (average) values for each test group, but means alone may mean little. When you look at graphs showing means (averages), be sure to look at the error bars (usually the standard error of the mean--SEM) which is an indication of how much variation there was relative to the size of the group. If the error bars are large relative to the differences in means between the test groups, then the reader may want to ask what was the cause of that variability.
The human brain is far better at detecting patterns in pictures rather than in columns of numbers. For this reason, my readers may notice that I tend to favor showing raw data in graphical form for each individual colony, in order to let you use their own eyes to see the degree of variation from colony to colony, yet at the same time to look for patterns or trends.
Another frequently misunderstood term is "significance," which the lay reader may confuse with meaning "substantial" or "meaningful." This is often not the case. A scientist can't say that there was any difference between the results from two test groups unless it was "significantly different" from that which would be expected to occur due to random variation--this is called statistical significance. But statistical significance may not have much practical application.
As a hypothetical example, imagine a study in which a researcher treated 1000 hives with a test substance (also running 1000 control hives). Imagine that the result was that the test substance appeared to increase mean honey production in the test group by 1 ounce per hive. Due to the large "n" (number of hives), that result might allow the researcher to state that "feeding the product significantly increased honey production." But few beekeepers would get too excited about a product that increased per-hive productivity by only an ounce--in this case the results might be significant statistically, but insignificant practically.
On another subject, in this series I'm drawing heavily upon Lloyd Harris' exemplary data set. But one must be cautious about extrapolating general principles based upon a single data set. Keeping this in mind, I've compared Harris' data to that of many others, both historical and recent, and feel that it is indeed representative.
Now that we have good estimates for the range of rates of egglaying, we can calculate the total recruitment of new workers over any period of time. For example, simple math shows that at the rate of say 1200 eggs per day, a colony's total recruitment over 6 - 10 weeks will result in an additional 60,400 - 84,000 workers. But from this we must then subtract the attrition of aged or worn out workers. In order to calculate this, we must understand the expected survivorship of those workers.
Survivorship Of The Workers
As recently pointed out by my friend Peter Borst [2], beekeepers have long speculated about how long a worker honey bee lives, but it wasn't until the advent of good marking paints that this question began to be answered with hard data.
Worker survivorship is well reviewed by Woyke [3], who found that:
Workers' lives appear to be shortened by the amount of broodrearing that they do.
An intense honey flow can also shorten their lives.
Measured mean worker lifespans (by various researchers) varied from 16.6 to 37.6 days, perhaps averaging (during the productive season) about 30 days.
Woyke also noted that despite high brood production, under unfavorable conditions colonies may not reach populations exceeding 30,000 bees.
This information is useful, but we need to know more than the simple estimate of average worker longevity. What we really need to know is the day-by-day rate of attrition of any cohort of bees at various times of the year. Few researchers have dedicated serious time to finding the answer to this question. One of the best data sets is that of Sakagami and Fukuda [4] (Fig. 2).
Figure 2. Worker bee survivorship of Italian-type bees in Japan, after Sakagami (1968). The main honey flow (clover) occurs in June, and appeared to shorten the lives of workers due to increased foraging.
Let's now compare the above to Lloyd Harris' even more extensive data from Manitoba a decade later (Fig. 3):
Figure 3. Worker bee survivorship of Italian-type bees in Manitoba, after Harris [[i]; raw data courtesy the author]. Note how remarkably similar were the survivorship curves for Italian-type workers during June in either Japan or Manitoba. Harris found this survivorship curve to be consistent from April through August.
[i] Harris, JL (2010) The effect of requeening in late July on honey bee colony development on the Northern Great Plains of North America after removal from an indoor winter storage facility. Journal of Apicultural Research and Bee World 49(2): 159-169.
These data sets strongly suggest that worker survivorship is relatively constant over the course of the summer. So we now know how much attrition to subtract from recruitment. Let's go back to the math!
A Simplified Mathematical Model
Question: Why does it seem to take a colony only 6-10 weeks to reach maximum population?
Question: And then why does the population seem to stop growing after 10 weeks?
In order to attempt to answer the above questions, I created the simple Excel spreadsheet shown in Table 1. In the yellow cells, I can enter the initial starting population of adult bees, and also the number of adults emerging per day (I used the term "eggs per day" since it better reflects the influence of the queen [6]). And then, applying Harris' percentages of surviving bees at each 12-day time point (thanks to Lloyd for sharing his original data), I had the spreadsheet calculate the number of bees in each 12-day age cohort still expected to be alive at each future time point. Then I simply added each column in order to obtain the total colony population at each time point.
10,000 Starting population of adult bees
1000 Eggs per day 12 days previous
12,000 Amt sealed brood 12 days previous
Day 0 12 24 36 48 60 72 84 96
0 10,000 9,523 7,574 4,756 2,219 562 47 1 0
12 12,000 11,424 9,204 5,700 2,664 672 56 1
24 12,000 11,424 9,204 5,700 2,664 672 56
36 12,000 11,424 9,204 5,700 2,664 672
48 12,000 11,424 9,204 5,700 2,664
60 12,000 11,424 9,204 5,700
72 12,000 11,424 9,204
84 12,000 11,424
96 12,000
Total 10,000 21,535 31,022 37,420 40,595 41,614 41,783 41,806 41,818
Table 1. Calculation of colony buildup over time based upon the queen's egglaying rate and Lloyd Harris' adult survivability curve. Illustrated is an example for a colony starting at 10,000 bees, with a queen laying 1000 eggs per day. Note that at about 60 days the birth rate and death rate reach equilibrium, and the colony essentially stops growing.
What struck me when I created this spreadsheet is that the rate of recruitment and the rate of attrition consistently reach equilibrium at about 60 days after the broodnest is fully established. Think about it- assuming that the queen's rate of egglaying remains constant, but that the adult population continues to grow, then at some point the daily rate of attrition of the increasing adult population will match the daily rate of recruitment. At that point, the birth rate and the death rate reach equilibrium, and will remain so until either the birth rate or death rate changes.
But wait, you say, what about the influence of the starting population? Of course, a colony with a larger initial broodnest (such as a strong overwintered hive) gets a jump start, and can grow to its maximum in about 6 weeks (42 days). But the interesting thing is that after 10 weeks (70 days) of normal attrition, there are only a negligible amount of bees remaining from any initial adult population, meaning that the size of any starting population is irrelevant by that time.
Practical application: Surprise, surprise--the colony reaches maximum population at about 60 days after the broodnest is fully established--in agreement with the common beekeeper experience that it takes about 6 weeks for an overwintered colony to build up, or 10 weeks for a package. Those rules of thumb are based upon simple arithmetic.
Population Top Out
Question: What determines the maximum size to which a colony will grow?
I then used my spreadsheet to calculate the ultimate equilibrium population reached at various rates of egglaying (Fig. 4):
Figure 4. I arbitrarily started each colony at 10,000 bees [[i]], with sealed brood emerging at the indicated rates of egglaying. Keep in mind that by 60 days, normal attrition would have caused the initial 10,000 adult bees to have dwindled to less than 600, thus having little influence on the overall colony population. Note that, at any egglaying rate, colonies reach an equilibrium maximum population at about 60 days after brood begins to emerge at the rate of the queen's laying capacity.
[i] The size of the starting population makes no difference.
Conclusion: based upon Lloyd's survivorship curve, which appears to be quite consistent from mid spring through late summer, a healthy, well fed colony will rapidly grow in about 60 days to its maximum size, which will be roughly 42x its daily recruitment (number of workers emerging per day). E.g., at an egglaying rate of 1000 per day, a colony will reach equilibrium at about 42,000 bees (which is consistent with measurements by a number of researchers).
Practical application: Poor nutrition or brood disease will reduce the percentage of the queen's eggs that make it to adulthood, and nosema or extremely heavy foraging will reduce adult survivorship. Either factor will reduce the ultimate equilibrium size of the colony's population (or prevent it from building altogether).
Playing Catch Up
Question: Then why can weak colonies sometimes catch up with those that got a head start?
Again and again I've seen some of the dinks that I leave behind when I move my strong colonies to almond pollination in early February, grow so rapidly in strength that they've caught up with the strong colonies by the time I bring them home several weeks later. And Russian or Carniolan bees, which overwinter with much smaller clusters than my Italians, often manage to explode their populations to match those of the Italians in time for the honey flow. But if population growth is linear, how can a weak colony catch up with a strong colony?
I'm hardly the first to ponder on this; Jeffree published a graph of the buildups of three colonies in Scotland in 1947 to illustrate the point [8](Fig. 5).
Figure 5. The year 1947 was exceptionally good for bees in Aberdeen, but not all colonies fared equally well. Note how all three colonies declined in late winter, pulled off successful spring turnovers, and grew linearly to their respective maximum strengths. However, only Colony D reached full strength in time to effectively take advantage of the main flow--producing 229 lbs of surplus honey. After Jeffrey [[i]].
[i] Jeffrey, EP (1959) Op cit, Figure 3.
Colony D came through the winter with a decent cluster size, pulled off a successful spring turnover in May, and reached a modest 30,000 bees (about 16 frames) in time to produce 229 lbs of surplus from the main honey flow. Colony E started tiny, yet still pulled off a successful spring turnover, catching up with D about 5 weeks later, and made 132 lbs (having missed hitting full strength in time for the main flow). On the other hand, poor little Colony F (690 individual bees at its low point) struggled with its spring turnover, and was unable to grow large enough to take advantage of the main honey flow (making only 28 lbs), but still reached an acceptable size for wintering by the end of the season.
So how the heck was Colony E able to catch up with D? The answer can again be explained by the math in Table 1 and by looking at the growth curves in Fig. 4. Once a colony establishes a broodnest large enough for a queen to hit her laying capacity, it indeed grows at a linear rate, but then slows way down at about 48 days. That slowdown causes colonies with head starts to lose their lead, allowing colonies s lagging slightly behind to catch up. Secondly, if a late-starting queen lays even 100 more eggs per day than an early starter, her colony will gain nearly 4000 bees more than the early starter over the next 48 days.
But lastly, if the colony is unable to complete a strong spring turnover early enough, it really misses the boat, and will be unable to grow strong in time for the main flow. Thus, colonies coming out of winter fairly strong at first spring pollen will generally have a leg up on weaker ones. But as anyone who has watched a hive of Russian bees explode in strength can confirm, some races of bees are adapted to later springs, and more rapid buildup.
Practical application: timing is everything. Unless the colony synchronizes its buildup to reach peak at the beginning of the main flow, it won't be able to take full advantage of that honey flow. Our goal as beekeepers is to manage our colonies for such synchronization. If they are strong too early, they may swarm; and if too late, won't be able to produce a surplus.
I'm acutely aware of this issue this season, since our local flora is flowering 2-4 weeks earlier than usual. We have a management plan based upon splitting our hives shortly after they return from almonds and have grown to the size that they are thinking of swarming. But this season, the forage that we depend upon for the buildup of our splits had already finished flowering before the colonies were ready to split. And now we're facing the likelihood of an early main flow, followed by an abnormally long summer drought. We've been busting our butts trying to keep up.
Next
Causes of hiccups in colony buildup.
Acknowledgements
I again wish to express my gratitude to Lloyd Harris for sharing his data set. And of course to Peter Borst for his assistance in literature research. And there is no way that I could justify taking the time to research and write these articles without the generous donations by beekeepers to ScientificBeekeeping.com.
Citations And Footnotes
[1] Specifically, the amount of sealed brood, which underestimates the actual rate of egglaying.
[2] Borst, PL (2013) How long does a honey bee live? ABJ 153(3): 241-244.
[3] Woyke, J (1984) Correlations and interactions between population, length of worker life and honey production by honeybees in a temperate region. J. of Apic. Res. 23(3): 148-156.
[4] Sakagami, SF & H Fukuda (1968) Life tables for worker honeybees. Res. Popul, Ecol. X: 127-139.
[5] Harris, JL (2010) The effect of requeening in late July on honey bee colony development on the Northern Great Plains of North America after removal from an indoor winter storage facility. Journal of Apicultural Research and Bee World 49(2): 159-169.
[6] Actual worker survival from egg to larva is around 90% in unstressed colonies, so these figures actually underestimate the numbers of eggs laid by the queen. Fukuda, H. and Sakagami, S.F. 1968. Worker brood survival in honeybees. Res. Popul. Ecol. 10: 31-39.
[7] The size of the starting population makes no difference.
[8] Jeffree, EP (1959) The size of honey-bee colonies throughout the year and the best size to winter. A lecture given to the Central Association of Bee-Keepers
[9] Jeffrey, EP (1959) Op cit, Figure 3.
Category: Bee Behavior and Biology
Tags: adult survivorship, colony buildup, colony decline, colony growth, egglaying | egglaying Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/egglaying/ |
Understanding Colony Buildup and Decline: Part 5 - Egglaying, Adult Survivorship, and Modeling Colony Growth
First published in: American Bee Journal, June 2015
Understanding Colony Buildup and Decline - Part 5
Egglaying, Adult Survivorship, And Modeling Colony Growth
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in June 2015
CONTENTS
Some Questions Begging For Answers
Survivorship Of The Workers
A Simplified Mathematical Model
Question: Why Does The Population Stop Growing After 10 Weeks?
Population Top Out
Playing Catch Up
Next
Acknowledgements
Citations and Footnotes
I could wax poetic about the wonder of the honey bee superorganism, but when it comes to making management decisions, it is more informative to use a reductionist approach to understand why to do what. In the case of colony buildup, this means studying the math of recruitment vs. attrition. So let's do the math!
I left off during the linear growth phase of the colony (following the spring turnover) with several unanswered questions:
Some Questions Begging For Answers
To what extent does a queen's pace of egglaying vary over the course of a season?
Why does it seem to take only 6-10 weeks to reach maximum colony population?
What determines the maximum size to which a colony will grow?
Why can weak colonies sometimes catch up with those that got a head start?
And why does the population stop growing after 10 weeks?
So let's see if we can find answers to each of these questions in turn:
Question: To what extent does a queen's pace of egglaying vary over the course of a season?
In order to answer this question, we'd need regular measurements of the amount of sealed brood in a number of colonies over the course of the season. And again, Lloyd Harris' data provides us with that information. I plotted out his measurements for established colonies in their second year, five of which had been requeened the previous July, and three of which had queens in their second year (Fig. 1).
Figure 1. Average rates of egglaying [[i]] for 8 different queens in overwintered colonies over each 12-day time period in the spring of 1977 in Manitoba. In these two groups of hives, the queens tended to rapidly ramp up their egglaying as the colonies expanded their broodnests in April and May, tending to peak in mid May, and then settle back down a bit afterward.
[i] Specifically, the amount of sealed brood, which underestimates the actual rate of egglaying.
In answer to our question, Harris' queens hit peak egglaying early in the season (young queens exhibiting the higher rates), and then tended to level off at a lower rate (although still at nearly an egg a minute, 24 hrs a day). The hiccups in brood production appeared to be related to crowding of the broodnests during nectar flows (and then bursts of egglaying as the cells were cleared). The swarm impulse didn't occur until July.
Practical application: as far as management for maximum egg production, there are four main things that the beekeeper can do: (1) protect the hive from cold, (2) keep young queens, (3) manage the broodnests to avoid restriction of the queen's ability to find a place to lay (this could involve reversing the supers, or rearranging or adding drawn comb), and (4) feeding during times of dearth or poor weather.
Scientific Notes:
Scientists typically present the results of their studies as mean (average) values for each test group, but means alone may mean little. When you look at graphs showing means (averages), be sure to look at the error bars (usually the standard error of the mean--SEM) which is an indication of how much variation there was relative to the size of the group. If the error bars are large relative to the differences in means between the test groups, then the reader may want to ask what was the cause of that variability.
The human brain is far better at detecting patterns in pictures rather than in columns of numbers. For this reason, my readers may notice that I tend to favor showing raw data in graphical form for each individual colony, in order to let you use their own eyes to see the degree of variation from colony to colony, yet at the same time to look for patterns or trends.
Another frequently misunderstood term is "significance," which the lay reader may confuse with meaning "substantial" or "meaningful." This is often not the case. A scientist can't say that there was any difference between the results from two test groups unless it was "significantly different" from that which would be expected to occur due to random variation--this is called statistical significance. But statistical significance may not have much practical application.
As a hypothetical example, imagine a study in which a researcher treated 1000 hives with a test substance (also running 1000 control hives). Imagine that the result was that the test substance appeared to increase mean honey production in the test group by 1 ounce per hive. Due to the large "n" (number of hives), that result might allow the researcher to state that "feeding the product significantly increased honey production." But few beekeepers would get too excited about a product that increased per-hive productivity by only an ounce--in this case the results might be significant statistically, but insignificant practically.
On another subject, in this series I'm drawing heavily upon Lloyd Harris' exemplary data set. But one must be cautious about extrapolating general principles based upon a single data set. Keeping this in mind, I've compared Harris' data to that of many others, both historical and recent, and feel that it is indeed representative.
Now that we have good estimates for the range of rates of egglaying, we can calculate the total recruitment of new workers over any period of time. For example, simple math shows that at the rate of say 1200 eggs per day, a colony's total recruitment over 6 - 10 weeks will result in an additional 60,400 - 84,000 workers. But from this we must then subtract the attrition of aged or worn out workers. In order to calculate this, we must understand the expected survivorship of those workers.
Survivorship Of The Workers
As recently pointed out by my friend Peter Borst [2], beekeepers have long speculated about how long a worker honey bee lives, but it wasn't until the advent of good marking paints that this question began to be answered with hard data.
Worker survivorship is well reviewed by Woyke [3], who found that:
Workers' lives appear to be shortened by the amount of broodrearing that they do.
An intense honey flow can also shorten their lives.
Measured mean worker lifespans (by various researchers) varied from 16.6 to 37.6 days, perhaps averaging (during the productive season) about 30 days.
Woyke also noted that despite high brood production, under unfavorable conditions colonies may not reach populations exceeding 30,000 bees.
This information is useful, but we need to know more than the simple estimate of average worker longevity. What we really need to know is the day-by-day rate of attrition of any cohort of bees at various times of the year. Few researchers have dedicated serious time to finding the answer to this question. One of the best data sets is that of Sakagami and Fukuda [4] (Fig. 2).
Figure 2. Worker bee survivorship of Italian-type bees in Japan, after Sakagami (1968). The main honey flow (clover) occurs in June, and appeared to shorten the lives of workers due to increased foraging.
Let's now compare the above to Lloyd Harris' even more extensive data from Manitoba a decade later (Fig. 3):
Figure 3. Worker bee survivorship of Italian-type bees in Manitoba, after Harris [[i]; raw data courtesy the author]. Note how remarkably similar were the survivorship curves for Italian-type workers during June in either Japan or Manitoba. Harris found this survivorship curve to be consistent from April through August.
[i] Harris, JL (2010) The effect of requeening in late July on honey bee colony development on the Northern Great Plains of North America after removal from an indoor winter storage facility. Journal of Apicultural Research and Bee World 49(2): 159-169.
These data sets strongly suggest that worker survivorship is relatively constant over the course of the summer. So we now know how much attrition to subtract from recruitment. Let's go back to the math!
A Simplified Mathematical Model
Question: Why does it seem to take a colony only 6-10 weeks to reach maximum population?
Question: And then why does the population seem to stop growing after 10 weeks?
In order to attempt to answer the above questions, I created the simple Excel spreadsheet shown in Table 1. In the yellow cells, I can enter the initial starting population of adult bees, and also the number of adults emerging per day (I used the term "eggs per day" since it better reflects the influence of the queen [6]). And then, applying Harris' percentages of surviving bees at each 12-day time point (thanks to Lloyd for sharing his original data), I had the spreadsheet calculate the number of bees in each 12-day age cohort still expected to be alive at each future time point. Then I simply added each column in order to obtain the total colony population at each time point.
10,000 Starting population of adult bees
1000 Eggs per day 12 days previous
12,000 Amt sealed brood 12 days previous
Day 0 12 24 36 48 60 72 84 96
0 10,000 9,523 7,574 4,756 2,219 562 47 1 0
12 12,000 11,424 9,204 5,700 2,664 672 56 1
24 12,000 11,424 9,204 5,700 2,664 672 56
36 12,000 11,424 9,204 5,700 2,664 672
48 12,000 11,424 9,204 5,700 2,664
60 12,000 11,424 9,204 5,700
72 12,000 11,424 9,204
84 12,000 11,424
96 12,000
Total 10,000 21,535 31,022 37,420 40,595 41,614 41,783 41,806 41,818
Table 1. Calculation of colony buildup over time based upon the queen's egglaying rate and Lloyd Harris' adult survivability curve. Illustrated is an example for a colony starting at 10,000 bees, with a queen laying 1000 eggs per day. Note that at about 60 days the birth rate and death rate reach equilibrium, and the colony essentially stops growing.
What struck me when I created this spreadsheet is that the rate of recruitment and the rate of attrition consistently reach equilibrium at about 60 days after the broodnest is fully established. Think about it- assuming that the queen's rate of egglaying remains constant, but that the adult population continues to grow, then at some point the daily rate of attrition of the increasing adult population will match the daily rate of recruitment. At that point, the birth rate and the death rate reach equilibrium, and will remain so until either the birth rate or death rate changes.
But wait, you say, what about the influence of the starting population? Of course, a colony with a larger initial broodnest (such as a strong overwintered hive) gets a jump start, and can grow to its maximum in about 6 weeks (42 days). But the interesting thing is that after 10 weeks (70 days) of normal attrition, there are only a negligible amount of bees remaining from any initial adult population, meaning that the size of any starting population is irrelevant by that time.
Practical application: Surprise, surprise--the colony reaches maximum population at about 60 days after the broodnest is fully established--in agreement with the common beekeeper experience that it takes about 6 weeks for an overwintered colony to build up, or 10 weeks for a package. Those rules of thumb are based upon simple arithmetic.
Population Top Out
Question: What determines the maximum size to which a colony will grow?
I then used my spreadsheet to calculate the ultimate equilibrium population reached at various rates of egglaying (Fig. 4):
Figure 4. I arbitrarily started each colony at 10,000 bees [[i]], with sealed brood emerging at the indicated rates of egglaying. Keep in mind that by 60 days, normal attrition would have caused the initial 10,000 adult bees to have dwindled to less than 600, thus having little influence on the overall colony population. Note that, at any egglaying rate, colonies reach an equilibrium maximum population at about 60 days after brood begins to emerge at the rate of the queen's laying capacity.
[i] The size of the starting population makes no difference.
Conclusion: based upon Lloyd's survivorship curve, which appears to be quite consistent from mid spring through late summer, a healthy, well fed colony will rapidly grow in about 60 days to its maximum size, which will be roughly 42x its daily recruitment (number of workers emerging per day). E.g., at an egglaying rate of 1000 per day, a colony will reach equilibrium at about 42,000 bees (which is consistent with measurements by a number of researchers).
Practical application: Poor nutrition or brood disease will reduce the percentage of the queen's eggs that make it to adulthood, and nosema or extremely heavy foraging will reduce adult survivorship. Either factor will reduce the ultimate equilibrium size of the colony's population (or prevent it from building altogether).
Playing Catch Up
Question: Then why can weak colonies sometimes catch up with those that got a head start?
Again and again I've seen some of the dinks that I leave behind when I move my strong colonies to almond pollination in early February, grow so rapidly in strength that they've caught up with the strong colonies by the time I bring them home several weeks later. And Russian or Carniolan bees, which overwinter with much smaller clusters than my Italians, often manage to explode their populations to match those of the Italians in time for the honey flow. But if population growth is linear, how can a weak colony catch up with a strong colony?
I'm hardly the first to ponder on this; Jeffree published a graph of the buildups of three colonies in Scotland in 1947 to illustrate the point [8](Fig. 5).
Figure 5. The year 1947 was exceptionally good for bees in Aberdeen, but not all colonies fared equally well. Note how all three colonies declined in late winter, pulled off successful spring turnovers, and grew linearly to their respective maximum strengths. However, only Colony D reached full strength in time to effectively take advantage of the main flow--producing 229 lbs of surplus honey. After Jeffrey [[i]].
[i] Jeffrey, EP (1959) Op cit, Figure 3.
Colony D came through the winter with a decent cluster size, pulled off a successful spring turnover in May, and reached a modest 30,000 bees (about 16 frames) in time to produce 229 lbs of surplus from the main honey flow. Colony E started tiny, yet still pulled off a successful spring turnover, catching up with D about 5 weeks later, and made 132 lbs (having missed hitting full strength in time for the main flow). On the other hand, poor little Colony F (690 individual bees at its low point) struggled with its spring turnover, and was unable to grow large enough to take advantage of the main honey flow (making only 28 lbs), but still reached an acceptable size for wintering by the end of the season.
So how the heck was Colony E able to catch up with D? The answer can again be explained by the math in Table 1 and by looking at the growth curves in Fig. 4. Once a colony establishes a broodnest large enough for a queen to hit her laying capacity, it indeed grows at a linear rate, but then slows way down at about 48 days. That slowdown causes colonies with head starts to lose their lead, allowing colonies s lagging slightly behind to catch up. Secondly, if a late-starting queen lays even 100 more eggs per day than an early starter, her colony will gain nearly 4000 bees more than the early starter over the next 48 days.
But lastly, if the colony is unable to complete a strong spring turnover early enough, it really misses the boat, and will be unable to grow strong in time for the main flow. Thus, colonies coming out of winter fairly strong at first spring pollen will generally have a leg up on weaker ones. But as anyone who has watched a hive of Russian bees explode in strength can confirm, some races of bees are adapted to later springs, and more rapid buildup.
Practical application: timing is everything. Unless the colony synchronizes its buildup to reach peak at the beginning of the main flow, it won't be able to take full advantage of that honey flow. Our goal as beekeepers is to manage our colonies for such synchronization. If they are strong too early, they may swarm; and if too late, won't be able to produce a surplus.
I'm acutely aware of this issue this season, since our local flora is flowering 2-4 weeks earlier than usual. We have a management plan based upon splitting our hives shortly after they return from almonds and have grown to the size that they are thinking of swarming. But this season, the forage that we depend upon for the buildup of our splits had already finished flowering before the colonies were ready to split. And now we're facing the likelihood of an early main flow, followed by an abnormally long summer drought. We've been busting our butts trying to keep up.
Next
Causes of hiccups in colony buildup.
Acknowledgements
I again wish to express my gratitude to Lloyd Harris for sharing his data set. And of course to Peter Borst for his assistance in literature research. And there is no way that I could justify taking the time to research and write these articles without the generous donations by beekeepers to ScientificBeekeeping.com.
Citations And Footnotes
[1] Specifically, the amount of sealed brood, which underestimates the actual rate of egglaying.
[2] Borst, PL (2013) How long does a honey bee live? ABJ 153(3): 241-244.
[3] Woyke, J (1984) Correlations and interactions between population, length of worker life and honey production by honeybees in a temperate region. J. of Apic. Res. 23(3): 148-156.
[4] Sakagami, SF & H Fukuda (1968) Life tables for worker honeybees. Res. Popul, Ecol. X: 127-139.
[5] Harris, JL (2010) The effect of requeening in late July on honey bee colony development on the Northern Great Plains of North America after removal from an indoor winter storage facility. Journal of Apicultural Research and Bee World 49(2): 159-169.
[6] Actual worker survival from egg to larva is around 90% in unstressed colonies, so these figures actually underestimate the numbers of eggs laid by the queen. Fukuda, H. and Sakagami, S.F. 1968. Worker brood survival in honeybees. Res. Popul. Ecol. 10: 31-39.
[7] The size of the starting population makes no difference.
[8] Jeffree, EP (1959) The size of honey-bee colonies throughout the year and the best size to winter. A lecture given to the Central Association of Bee-Keepers
[9] Jeffrey, EP (1959) Op cit, Figure 3.
Category: Bee Behavior and Biology
Tags: adult survivorship, colony buildup, colony decline, colony growth, egglaying | colony decline Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/colony-decline/ |
Understanding Colony Buildup and Decline: Part 5 - Egglaying, Adult Survivorship, and Modeling Colony Growth
First published in: American Bee Journal, June 2015
Understanding Colony Buildup and Decline - Part 5
Egglaying, Adult Survivorship, And Modeling Colony Growth
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in June 2015
CONTENTS
Some Questions Begging For Answers
Survivorship Of The Workers
A Simplified Mathematical Model
Question: Why Does The Population Stop Growing After 10 Weeks?
Population Top Out
Playing Catch Up
Next
Acknowledgements
Citations and Footnotes
I could wax poetic about the wonder of the honey bee superorganism, but when it comes to making management decisions, it is more informative to use a reductionist approach to understand why to do what. In the case of colony buildup, this means studying the math of recruitment vs. attrition. So let's do the math!
I left off during the linear growth phase of the colony (following the spring turnover) with several unanswered questions:
Some Questions Begging For Answers
To what extent does a queen's pace of egglaying vary over the course of a season?
Why does it seem to take only 6-10 weeks to reach maximum colony population?
What determines the maximum size to which a colony will grow?
Why can weak colonies sometimes catch up with those that got a head start?
And why does the population stop growing after 10 weeks?
So let's see if we can find answers to each of these questions in turn:
Question: To what extent does a queen's pace of egglaying vary over the course of a season?
In order to answer this question, we'd need regular measurements of the amount of sealed brood in a number of colonies over the course of the season. And again, Lloyd Harris' data provides us with that information. I plotted out his measurements for established colonies in their second year, five of which had been requeened the previous July, and three of which had queens in their second year (Fig. 1).
Figure 1. Average rates of egglaying [[i]] for 8 different queens in overwintered colonies over each 12-day time period in the spring of 1977 in Manitoba. In these two groups of hives, the queens tended to rapidly ramp up their egglaying as the colonies expanded their broodnests in April and May, tending to peak in mid May, and then settle back down a bit afterward.
[i] Specifically, the amount of sealed brood, which underestimates the actual rate of egglaying.
In answer to our question, Harris' queens hit peak egglaying early in the season (young queens exhibiting the higher rates), and then tended to level off at a lower rate (although still at nearly an egg a minute, 24 hrs a day). The hiccups in brood production appeared to be related to crowding of the broodnests during nectar flows (and then bursts of egglaying as the cells were cleared). The swarm impulse didn't occur until July.
Practical application: as far as management for maximum egg production, there are four main things that the beekeeper can do: (1) protect the hive from cold, (2) keep young queens, (3) manage the broodnests to avoid restriction of the queen's ability to find a place to lay (this could involve reversing the supers, or rearranging or adding drawn comb), and (4) feeding during times of dearth or poor weather.
Scientific Notes:
Scientists typically present the results of their studies as mean (average) values for each test group, but means alone may mean little. When you look at graphs showing means (averages), be sure to look at the error bars (usually the standard error of the mean--SEM) which is an indication of how much variation there was relative to the size of the group. If the error bars are large relative to the differences in means between the test groups, then the reader may want to ask what was the cause of that variability.
The human brain is far better at detecting patterns in pictures rather than in columns of numbers. For this reason, my readers may notice that I tend to favor showing raw data in graphical form for each individual colony, in order to let you use their own eyes to see the degree of variation from colony to colony, yet at the same time to look for patterns or trends.
Another frequently misunderstood term is "significance," which the lay reader may confuse with meaning "substantial" or "meaningful." This is often not the case. A scientist can't say that there was any difference between the results from two test groups unless it was "significantly different" from that which would be expected to occur due to random variation--this is called statistical significance. But statistical significance may not have much practical application.
As a hypothetical example, imagine a study in which a researcher treated 1000 hives with a test substance (also running 1000 control hives). Imagine that the result was that the test substance appeared to increase mean honey production in the test group by 1 ounce per hive. Due to the large "n" (number of hives), that result might allow the researcher to state that "feeding the product significantly increased honey production." But few beekeepers would get too excited about a product that increased per-hive productivity by only an ounce--in this case the results might be significant statistically, but insignificant practically.
On another subject, in this series I'm drawing heavily upon Lloyd Harris' exemplary data set. But one must be cautious about extrapolating general principles based upon a single data set. Keeping this in mind, I've compared Harris' data to that of many others, both historical and recent, and feel that it is indeed representative.
Now that we have good estimates for the range of rates of egglaying, we can calculate the total recruitment of new workers over any period of time. For example, simple math shows that at the rate of say 1200 eggs per day, a colony's total recruitment over 6 - 10 weeks will result in an additional 60,400 - 84,000 workers. But from this we must then subtract the attrition of aged or worn out workers. In order to calculate this, we must understand the expected survivorship of those workers.
Survivorship Of The Workers
As recently pointed out by my friend Peter Borst [2], beekeepers have long speculated about how long a worker honey bee lives, but it wasn't until the advent of good marking paints that this question began to be answered with hard data.
Worker survivorship is well reviewed by Woyke [3], who found that:
Workers' lives appear to be shortened by the amount of broodrearing that they do.
An intense honey flow can also shorten their lives.
Measured mean worker lifespans (by various researchers) varied from 16.6 to 37.6 days, perhaps averaging (during the productive season) about 30 days.
Woyke also noted that despite high brood production, under unfavorable conditions colonies may not reach populations exceeding 30,000 bees.
This information is useful, but we need to know more than the simple estimate of average worker longevity. What we really need to know is the day-by-day rate of attrition of any cohort of bees at various times of the year. Few researchers have dedicated serious time to finding the answer to this question. One of the best data sets is that of Sakagami and Fukuda [4] (Fig. 2).
Figure 2. Worker bee survivorship of Italian-type bees in Japan, after Sakagami (1968). The main honey flow (clover) occurs in June, and appeared to shorten the lives of workers due to increased foraging.
Let's now compare the above to Lloyd Harris' even more extensive data from Manitoba a decade later (Fig. 3):
Figure 3. Worker bee survivorship of Italian-type bees in Manitoba, after Harris [[i]; raw data courtesy the author]. Note how remarkably similar were the survivorship curves for Italian-type workers during June in either Japan or Manitoba. Harris found this survivorship curve to be consistent from April through August.
[i] Harris, JL (2010) The effect of requeening in late July on honey bee colony development on the Northern Great Plains of North America after removal from an indoor winter storage facility. Journal of Apicultural Research and Bee World 49(2): 159-169.
These data sets strongly suggest that worker survivorship is relatively constant over the course of the summer. So we now know how much attrition to subtract from recruitment. Let's go back to the math!
A Simplified Mathematical Model
Question: Why does it seem to take a colony only 6-10 weeks to reach maximum population?
Question: And then why does the population seem to stop growing after 10 weeks?
In order to attempt to answer the above questions, I created the simple Excel spreadsheet shown in Table 1. In the yellow cells, I can enter the initial starting population of adult bees, and also the number of adults emerging per day (I used the term "eggs per day" since it better reflects the influence of the queen [6]). And then, applying Harris' percentages of surviving bees at each 12-day time point (thanks to Lloyd for sharing his original data), I had the spreadsheet calculate the number of bees in each 12-day age cohort still expected to be alive at each future time point. Then I simply added each column in order to obtain the total colony population at each time point.
10,000 Starting population of adult bees
1000 Eggs per day 12 days previous
12,000 Amt sealed brood 12 days previous
Day 0 12 24 36 48 60 72 84 96
0 10,000 9,523 7,574 4,756 2,219 562 47 1 0
12 12,000 11,424 9,204 5,700 2,664 672 56 1
24 12,000 11,424 9,204 5,700 2,664 672 56
36 12,000 11,424 9,204 5,700 2,664 672
48 12,000 11,424 9,204 5,700 2,664
60 12,000 11,424 9,204 5,700
72 12,000 11,424 9,204
84 12,000 11,424
96 12,000
Total 10,000 21,535 31,022 37,420 40,595 41,614 41,783 41,806 41,818
Table 1. Calculation of colony buildup over time based upon the queen's egglaying rate and Lloyd Harris' adult survivability curve. Illustrated is an example for a colony starting at 10,000 bees, with a queen laying 1000 eggs per day. Note that at about 60 days the birth rate and death rate reach equilibrium, and the colony essentially stops growing.
What struck me when I created this spreadsheet is that the rate of recruitment and the rate of attrition consistently reach equilibrium at about 60 days after the broodnest is fully established. Think about it- assuming that the queen's rate of egglaying remains constant, but that the adult population continues to grow, then at some point the daily rate of attrition of the increasing adult population will match the daily rate of recruitment. At that point, the birth rate and the death rate reach equilibrium, and will remain so until either the birth rate or death rate changes.
But wait, you say, what about the influence of the starting population? Of course, a colony with a larger initial broodnest (such as a strong overwintered hive) gets a jump start, and can grow to its maximum in about 6 weeks (42 days). But the interesting thing is that after 10 weeks (70 days) of normal attrition, there are only a negligible amount of bees remaining from any initial adult population, meaning that the size of any starting population is irrelevant by that time.
Practical application: Surprise, surprise--the colony reaches maximum population at about 60 days after the broodnest is fully established--in agreement with the common beekeeper experience that it takes about 6 weeks for an overwintered colony to build up, or 10 weeks for a package. Those rules of thumb are based upon simple arithmetic.
Population Top Out
Question: What determines the maximum size to which a colony will grow?
I then used my spreadsheet to calculate the ultimate equilibrium population reached at various rates of egglaying (Fig. 4):
Figure 4. I arbitrarily started each colony at 10,000 bees [[i]], with sealed brood emerging at the indicated rates of egglaying. Keep in mind that by 60 days, normal attrition would have caused the initial 10,000 adult bees to have dwindled to less than 600, thus having little influence on the overall colony population. Note that, at any egglaying rate, colonies reach an equilibrium maximum population at about 60 days after brood begins to emerge at the rate of the queen's laying capacity.
[i] The size of the starting population makes no difference.
Conclusion: based upon Lloyd's survivorship curve, which appears to be quite consistent from mid spring through late summer, a healthy, well fed colony will rapidly grow in about 60 days to its maximum size, which will be roughly 42x its daily recruitment (number of workers emerging per day). E.g., at an egglaying rate of 1000 per day, a colony will reach equilibrium at about 42,000 bees (which is consistent with measurements by a number of researchers).
Practical application: Poor nutrition or brood disease will reduce the percentage of the queen's eggs that make it to adulthood, and nosema or extremely heavy foraging will reduce adult survivorship. Either factor will reduce the ultimate equilibrium size of the colony's population (or prevent it from building altogether).
Playing Catch Up
Question: Then why can weak colonies sometimes catch up with those that got a head start?
Again and again I've seen some of the dinks that I leave behind when I move my strong colonies to almond pollination in early February, grow so rapidly in strength that they've caught up with the strong colonies by the time I bring them home several weeks later. And Russian or Carniolan bees, which overwinter with much smaller clusters than my Italians, often manage to explode their populations to match those of the Italians in time for the honey flow. But if population growth is linear, how can a weak colony catch up with a strong colony?
I'm hardly the first to ponder on this; Jeffree published a graph of the buildups of three colonies in Scotland in 1947 to illustrate the point [8](Fig. 5).
Figure 5. The year 1947 was exceptionally good for bees in Aberdeen, but not all colonies fared equally well. Note how all three colonies declined in late winter, pulled off successful spring turnovers, and grew linearly to their respective maximum strengths. However, only Colony D reached full strength in time to effectively take advantage of the main flow--producing 229 lbs of surplus honey. After Jeffrey [[i]].
[i] Jeffrey, EP (1959) Op cit, Figure 3.
Colony D came through the winter with a decent cluster size, pulled off a successful spring turnover in May, and reached a modest 30,000 bees (about 16 frames) in time to produce 229 lbs of surplus from the main honey flow. Colony E started tiny, yet still pulled off a successful spring turnover, catching up with D about 5 weeks later, and made 132 lbs (having missed hitting full strength in time for the main flow). On the other hand, poor little Colony F (690 individual bees at its low point) struggled with its spring turnover, and was unable to grow large enough to take advantage of the main honey flow (making only 28 lbs), but still reached an acceptable size for wintering by the end of the season.
So how the heck was Colony E able to catch up with D? The answer can again be explained by the math in Table 1 and by looking at the growth curves in Fig. 4. Once a colony establishes a broodnest large enough for a queen to hit her laying capacity, it indeed grows at a linear rate, but then slows way down at about 48 days. That slowdown causes colonies with head starts to lose their lead, allowing colonies s lagging slightly behind to catch up. Secondly, if a late-starting queen lays even 100 more eggs per day than an early starter, her colony will gain nearly 4000 bees more than the early starter over the next 48 days.
But lastly, if the colony is unable to complete a strong spring turnover early enough, it really misses the boat, and will be unable to grow strong in time for the main flow. Thus, colonies coming out of winter fairly strong at first spring pollen will generally have a leg up on weaker ones. But as anyone who has watched a hive of Russian bees explode in strength can confirm, some races of bees are adapted to later springs, and more rapid buildup.
Practical application: timing is everything. Unless the colony synchronizes its buildup to reach peak at the beginning of the main flow, it won't be able to take full advantage of that honey flow. Our goal as beekeepers is to manage our colonies for such synchronization. If they are strong too early, they may swarm; and if too late, won't be able to produce a surplus.
I'm acutely aware of this issue this season, since our local flora is flowering 2-4 weeks earlier than usual. We have a management plan based upon splitting our hives shortly after they return from almonds and have grown to the size that they are thinking of swarming. But this season, the forage that we depend upon for the buildup of our splits had already finished flowering before the colonies were ready to split. And now we're facing the likelihood of an early main flow, followed by an abnormally long summer drought. We've been busting our butts trying to keep up.
Next
Causes of hiccups in colony buildup.
Acknowledgements
I again wish to express my gratitude to Lloyd Harris for sharing his data set. And of course to Peter Borst for his assistance in literature research. And there is no way that I could justify taking the time to research and write these articles without the generous donations by beekeepers to ScientificBeekeeping.com.
Citations And Footnotes
[1] Specifically, the amount of sealed brood, which underestimates the actual rate of egglaying.
[2] Borst, PL (2013) How long does a honey bee live? ABJ 153(3): 241-244.
[3] Woyke, J (1984) Correlations and interactions between population, length of worker life and honey production by honeybees in a temperate region. J. of Apic. Res. 23(3): 148-156.
[4] Sakagami, SF & H Fukuda (1968) Life tables for worker honeybees. Res. Popul, Ecol. X: 127-139.
[5] Harris, JL (2010) The effect of requeening in late July on honey bee colony development on the Northern Great Plains of North America after removal from an indoor winter storage facility. Journal of Apicultural Research and Bee World 49(2): 159-169.
[6] Actual worker survival from egg to larva is around 90% in unstressed colonies, so these figures actually underestimate the numbers of eggs laid by the queen. Fukuda, H. and Sakagami, S.F. 1968. Worker brood survival in honeybees. Res. Popul. Ecol. 10: 31-39.
[7] The size of the starting population makes no difference.
[8] Jeffree, EP (1959) The size of honey-bee colonies throughout the year and the best size to winter. A lecture given to the Central Association of Bee-Keepers
[9] Jeffrey, EP (1959) Op cit, Figure 3.
Category: Bee Behavior and Biology
Tags: adult survivorship, colony buildup, colony decline, colony growth, egglaying | colony buildup Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/colony-buildup/ |
Understanding Colony Buildup and Decline: Part 6 - Hiccups in Colony Linear Buildup
First published in: American Bee Journal, July 2015
Understanding Colony Buildup and Decline - Part 6
Hiccups In Colony Linear Buildup
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in July 2015
CONTENTS
Return To Playing Catch Up
Real World Hiccups
The Effect Of Cold Weather
The Effect Of Rainy Weather
Spring Starvation
From Too Little To Too Much
Brood Survivorship
Adult Survivorship
Take Home Message
Acknowledgements
Citations and Footnotes
Under ideal conditions, colonies grow in a linear manner once the broodnest is well established. But ideal conditions don't always occur in the real world. By being aware of factors that may reduce the rate of colony buildup, the beekeeper may be able to intervene and get the colony back on track.
Return To Playing Catch Up
Creating a mathematical model for colony buildup and decline is not a mere academic exercise-it has great practical application. When you attempt to create a mathematical model, you quickly find out which critical elements you don't fully understand.
Practical application: in my own case, my newfound understanding of exactly why weak colonies are able to catch up in size with stronger colonies helps me to better grasp why springtime splits have the potential to grow as large as established colonies. Ideally, I want to split my colonies small enough to keep them from swarming, but large enough that they can build to optimal honey-producing strength.
But when I was faced with my sons' questions as to what is the ideal amount of brood and adult bees to put into each split, I realized that I couldn't honestly answer with certainty. So I spent considerable time in creating a spreadsheet to calculate the growth of nucs dependent upon those variables (as well as temperature and quality of the queen). I'm currently testing that model by carefully tracking the individual buildup of nucs in a test group specifically created with different measured amounts of brood and bees. I'll let you know when I get the results.
Real World Hiccups
I find the modeling of colony growth under ideal conditions to be mathematically elegant. But of course in the real world, conditions are often less than ideal. Any number of transient phenomena can handicap colony growth, or thwart it altogether. So let's take another look at the hiccups in growth exhibited by Harris' colonies in my colorful chart of colony demographics (Fig. 1):
Figure 1. Note the three instances (in mid May, early and late July) in which broodrearing was curtailed, leading to hiccups in the expected linear growth of the colonies [[i]]. I've indicated on this graph the timing of a spring cold snap, as well as the main honeyflow.
[i] These hiccups in egglaying are broken out by individual queen in Fig. 1 of my previous article
So what caused those sudden reductions in egglaying?
The Effect Of Cold Weather
I searched the weather history for Manitoba during the period of time during which Harris collected his data. It appears that the first dip in egglaying occurred during a cold snap in early May, right during the critical "spring turnover." The cold weather would have precluded foraging for pollen, and the freezing nighttime temperatures (15degF) would have forced the tiny clusters (averaging only about 7000 adult bees--less than 4 frame's worth) to contract tightly--thus limiting the amount of comb suitable for broodrearing.
Practical application: cold nighttime temperatures are a major limiting factor for the buildup of small colonies, since they must go into tight cluster, which severely limits both the size of the broodnest, as well as the number of bees available for nursing duties (since the majority must be engaged in forming a heat-generating "insulating shell").
The Effect Of Rainy Weather
April showers may bring May flowers, but even a single day of rainy weather may have a profound effect upon a growing colony. In a meticulous and intriguing study from the lab of Austrian bee researcher Karl Crailsheim [2], a rain machine was used to prevent the bees in an observation hive from foraging for only a single day at time, while keeping the inside temperature constant. What they found was that:
During rainy periods nurses spent less than half as much time nursing brood as they did during sunny periods. Our experiment suggests that the activity of the nurses is linked to the influx of food and its passage from bee to bee. Nurses receive food more often and over a longer period on days with good weather conditions than on days with bad weather conditions... It seems that the flow of nectar diminishes after only one night and causes the decline in nursing activity even on the first day with bad weather conditions and the following night.
Wow, even a single day of rain cuts nursing visits to brood by half! The researches didn't make observations on what happened during longer storms, but I have. After about three days of rainy weather, a rapidly-growing colony will have completely depleted its pollen stores, and begins to go into protein deficit, forcing the nurses to start using their body reserves (in their fat bodies). And then it may get worse...
During prolonged rainy weather, a colony may shift from rapid growth to cannibalism of the brood within a matter of days. Such an unexpected disaster hit us hard a few years ago. In the photo below, we were adding second brood chambers to strong singles on a nice nectar and pollen flow in mid May, right at the beginning of our main honey flow (Figs. 2-5).
Figure 2. In mid May 2011, our colonies were rapidly building during our spring flow, and we had recently added the second brood chambers for them to move into, with the expectation that they'd be quickly filled with brood and honey. This was beekeeping at its best!
Figure 3. We were running an experiment at the time, and I happened to take a photo of a typical brood frame. Note the reserves of honey and beebread present on May 10th. A few days later the colonies were shaking nectar and whitening wax.
Figure 4. We live in the mountains, where the weather is rapidly changeable. We got hit by a surprise snowstorm on April 25. All photos were taken in the same yard.
Figure 5. Within four days, the hungry colonies had consumed all honey reserves and all pollen reserves. They then desperately started cannibalizing the brood-first the eggs, then young larvae, then older larvae. They don't normally cannibalize sealed brood, since it no longer needs to be fed, and those pupae may be the colony's only chance for survival.
We donned our cold weather gear and madly fed syrup. We were able to avert major brood cannibalism in most of our colonies, which quickly recovered when the weather turned back to warm. But those colonies that were forced to cannibalize their brood got set back so hard that they were unable to even put on winter stores during the main flow, and needed to be fed later in the season.
Practical application: someone incredulously asked me, do you really go out and feed bees during miserable weather? I answered, Well, duh, 'cuz during good weather they're able to feed themselves-that's why we are called bee keepers.
Such brood cannibalism [3], albeit less dramatic, frequently occurs in my area during the two week pollen and nectar dearth that we typically experience between the end of apple bloom and the beginning of the late spring flow. I often observe plenty of freshly-laid eggs each day, but the nurses apparently eat them up rather than trying to feed larvae when there is not enough protein coming in.
Practical application: the main determinant of the development of a busting colony for honey production is having a steady supply of pollen and nectar coming in during the period beginning 6-8 weeks before the start of the main flow. It is during this time that the feeding of pollen sub can be of great benefit during periods of inclement weather or pollen dearth (as occurs in my area immediately after the end of fruit bloom).
Spring Starvation
In my area, other than during storms or the two-week post fruit bloom dearth, there is usually plenty of nectar and pollen coming in during springtime, and we rarely need to feed our splits. But from time to time, we must perform emergency feeding of the ravenous growing colonies. In the case of the colonies in the experiment shown in the photos above, I could not get approval to break protocol and feed the hives during the storm (despite my daily entreaties). The result was that a number starved on the fourth night (Figs. 6 & 7).
Figure 6. It breaks my heart to see a vigorous young colony starve to death, as indicated by the heads buried in the cells.
Fig. 7. After 4 days of bad weather, many of the colonies in the experimental yard succumbed to starvation. It was heartbreaking and ugly-this is a view of a typical bottom board. This disaster could have been easily averted by the feeding of a few dollars worth of sugar in any form.
I've also seen similar starvation of my strongest colonies during almond bloom if the weather turns foul. Many's the time that I've dumped granulated sugar over the combs (if I didn't have syrup with me) in order to save a colony. One time, all it took was a can of soda pop poured over the immobile bees to give them enough energy to move onto some swapped frames of honey.
During intermittent nectar dearths, colonies lacking adequate honey reserves can suffer minor starvation events. Unless you are closely monitoring the yards, all that you may see is a handful of dead bees in front of the hive, and if there has been a resumption of the nectar flow since the brief dearth, you may not be able to figure out what caused the kill (Fig. 8).
Figure 8. A "minor" starvation event occurred in this outyard in late June during a brief break in nectar availability. No colonies died, but similar to this one, most had a small pile of dead bees in front (this occurred in an area far from any pesticide applications). Only by checking the age structure of the remaining brood was I able to figure out what had gone wrong, since by the time I took this photo the colonies had replenished their nectar stores.
Practical application: during these recent drought years in California, we can no longer count on our normal nectar flows. This spring has been scary--our colonies have repeatedly been on the edge of starvation, since we kept expecting the "normal" nectar flows to kick in. As I type these words, I'm starting to resign myself to the possibility that the main flow is simply not gonna happen, and that I am going to be forced to spend a fortune on sugar in order to keep my colonies alive.
It's clear that a shortage of nectar/pollen (even due to a few days of rain) can bring recruitment to a temporary halt; conversely, a surfeit can also do the same...
From Too Little To Too Much
A nice nectar and pollen flow is extremely stimulating to broodrearing. But on the other hand, too much nectar or pollen can result in the bees plugging the broodnest, filling comb that the queen would normally fill with eggs (Fig. 9).
Figure 9. A brood comb following favorable weather in almond bloom. The past few years we've had great foraging weather during almond bloom, sometimes resulting in the broodnests getting plugged out with pollen and nectar. Since the queen can't find a place in which to lay eggs, there will little recruitment of emerging workers three weeks later, and colony populations may temporarily dwindle, much to the dismay of those beekeepers needing to shake packages or make splits.
Practical application: during spring buildup, it may be necessary to either reverse the brood chambers, or to add drawn comb to the broodnest to give the queen additional room in which to lay.
Tip for beginners: excessive feeding of syrup to colonies can also cause plugging out of the broodnest, leading to swarming in the spring, or poor wintering in the fall (due to lack of broodrearing at the end of the season).
Brood Survivorship
Keep in mind that colony buildup is all about the difference between the rates of recruitment of new workers and the rate of attrition of older workers. Pathogens that affect the brood reduce the rate of recruitment. When I began beekeeping, AFB was the only brood disease that we worried about--chalkbrood had yet to reach our shores, and EFB would go away on its own once a good nectar flow resumed. Nowadays, I rarely see AFB. What I do see in spring is persistent EFB (Fig. 10), and sometimes other unidentifiable brood diseases [4].
Figure 10. European Foulbrood can bring colony buildup to a screeching halt by decreasing the rate of larval survival. The larvae in this photo are clearly symptomatic, but in many cases are difficult to detect. Unlike the EFB of yore, today's EFB may not clear up without treatment.
Although I don't see much chalkbrood any more, a few years ago I visited apiaries on the East Coast in which chalkbrood was running rampant, preventing colonies from building up. And it is not just pathogen-caused brood disease that may cause a problem. Toxic pollen (such as that of California Buckeye), nutritionally inadequate pollen, smokestack pollution, chilling of the brood due to anything that causes high adult mortality (virus, nosema, pesticides), or pesticide/miticide residues can all affect the colony similarly, in that they may reduce larval survivability.
Practical application: any factor that reduces larval survivability (such as chilling, poor nutrition, toxins, or disease) will decrease the rate of recruitment, and have a profound effect upon not only the rate of colony buildup, but unless the problem is resolved, also upon its ultimate population size.
Adult Survivorship
The rate of colony buildup is also determined by the rate of attrition of the adult bees. Ideally, springtime workers can be expected to live for an average of about 35 days. During spring buildup, adult survivorship is critical to colony success. I find that infection by either viruses or nosema can prevent a successful spring turnover due to their decreasing adult survivorship [5].
It doesn't take much of a reduction in adult survivorship to exhibit a profound effect (Fig. 11):
Figure 11. In order to create this graph, I shifted Harris' survivorship curves either longer or shorter by 5 days (roughly a 14% increase or decrease in average survivorship). Note how even a few days increase or reduction in average worker longevity has a profound effect upon colony buildup and eventual maximum population.
Practical application: any factor that negatively affects either larval or adult worker survivorship can make a huge difference in eventual colony size and honey production.
Take Home Message
Once a broodnest is established and the population has grown to the extent that the queen can hit her stride in egglaying (which takes a cluster covering at least 7 frames), the honey bee colony has the potential to grow at a linear rate of increase of nearly 2 frames of bees per week. But things don't always go well for growing colonies. As beekeepers, we can provide husbandry to minimize any breaks in the momentum of colony buildup, as well put by Jeffrey in 1959 [6]:
...in Britain colonies are ordinarily increasing in size for only about three months out of the twelve, and in late summer and throughout the long autumn, winter and early spring, numbers are steadily declining This would apparently point to two important principles in commercially successful bee-keeping: first, that the bee-keeper ought to guard carefully against any break in that swift and steady upward surge in the number of bees during April, May and June--for a break at this time cannot be fully retrieved later--and in particular it is suggested that queenless intervals should be most carefully avoided; and secondly, steps should be taken to reduce to a minimum the rate of decline during those other nine long months.
Next month: I'll continue with the swarming impulse
Acknowledgements
As always, my thanks to Lloyd Harris and Peter Borst.
Citations And Footnotes
[1] These hiccups in egglaying are broken out by individual queen in Fig. 1 of my previous article
[2] Riessberger U, & K Crailsheim (1887) Short-term effect of different weather conditions upon the behaviour of forager and nurse honey bees (Apis mellifera carnica Pollmann). Apidologie 28: 411-426. Open access.
[3] Schmickl T & K Crailsheim (2001) Cannibalism and early capping: strategy of honeybee colonies in times of experimental pollen shortages. J Comp Physiol A 187(7):541-547.
[4] For symptoms of some of the "new" brood diseases, see https://scientificbeekeeping.com/sick-bees-part-18a-colony-collaspse-revisited/
[5] See Figure 11 in Part 3 of this series.
[6] Jeffree, EP (1959) Op cit.
See also Jeffree, EP (1955) Observations on the growth and decline of honey bee colonies. Journal of Economic Entomology. 48: 732-726.
Category: Bee Behavior and Biology
Tags: adult survivorship, brood survivorship, cold weather, rainy weather, spring, starvation | adult survivorship Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/adult-survivorship/ |
Sick Bees - Part 18E: Colony Collapse Revisited - Genetically Modified Plants
First published in: ABJ December 2012
Genetically Modified Plants
What Is Genetic Modification?
There's Nothing New About Transgenics
GMOs
An Odd Series of Connections
The Vilifying of Monsanto
What Are They Up To?
Practicality Overrides Principle
Hold the Hate Mail
The Changing Face of Agriculture
Bt Crops
Roundup Ready
Direct Effects of Roundup Use
Indirect Effects of Roundup Use
The Future of Roundup
Reality Check
Looking Ahead: The Chemical Treadmill & Pest Resistance
Additional Discussion
The Back Story on Plant Breeding and GM Crops
The Profit Motive
Enter GM Crops
The Second "Green Revolution"
Cautions About GM
Perspectives on GM
So What's The Problem?
Acknowledgements
References
Sick Bees - Part 18E:
Colony Collapse Revisited - Genetically Modified Plants
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in Dec 2012
Genetically modified (or GM) plants have attracted a large amount of media attention in recent years and continue to do so. Despite this, the general public remains largely unaware of what a GM plant actually is or what advantages and disadvantages the technology has to offer, particularly with regard to the range of applications for which they can be used [1].
The above quote is certainly an understatement! Genetically Modified Organisms (GMO's) are a highly contentious topic these days, and blamed by some for the demise of bees. In researching the subject, I found the public discussion to be highly polarized--plant breeders and farmers are largely enthusiastic (with appropriate reservations) about the benefits of genetic engineering, whereas health and environmental advocacy groups tend to be fearful of the new technology [2]. I will largely save my review of the history and pros and cons of GM crops for my website, and focus this article upon how GMO's relate to honey bee health.
What Is Genetic Modification?
The knowledge of genetics was not applied to plant breeding until the 1920's; up 'til then breeders would blindly cross promising cultivars and hope for the best. With today's genetic engineering, breeders can now take a gene from one plant (or animal, fungus, or bacterium) and splice it into the DNA of another plant. If they get it just right, the new gene can confer resistance to frost, drought, pests, salinity, or disease. Or it could make the crop more nutritious, more flavorful, etc. Such genetically modified crops are also called "transgenic," "recombinant," "genetically engineered," or "bioengineered."
There's Nothing New About Transgenics
There is nothing new about transgenic organisms, in fact you (yes you) are one. Viruses regularly swap genes among unrelated organisms via a process called "horizontal gene transfer" [3]. For example, the gene which is responsible for the formation of the mammalian placenta was not originally a mammal gene--it was inserted into our distant ancestors by a virus. If a gene introduced by a virus confers a fitness advantage to the recipient, then that gene may eventually be propagated throughout that species' population. Until recently, we didn't even know that this process has occurred throughout the evolution of life, and didn't know or care whether a crop was "naturally" transgenic!
GMO's
Both the scientific community and industry have done a terrible job at explaining genetic engineering to a distrustful public. There are clearly potential issues with genetic engineering, but they are being carefully addressed by independent scientists [4] and regulatory agencies, especially in Europe:
From the first generation of GM crops, two main areas of concern have emerged, namely risk to the environment and risk to human health.... Although it is now commonplace for the press to adopt 'health campaigns', the information they publish is often unreliable and unrepresentative of the available scientific evidence [5].
Jeffrey Smith, in his book "Seeds of Deception" [6] details a number of legitimate issues and early missteps in bioengineering, as well as pointing out the substantial political influence firms such as Monsanto have upon researchers, regulators, and legislators. We should be cautious to take their assurances with a grain of salt. On the other hand, I've checked the claims of other anti-GMO crusaders for factual accuracy, and found that many simply don't hold water. For example, two headlined studies of late, one on rats fed GE corn and Roundup herbicide, and another on the purported increased use of herbicides due to GE crops simply do not stand up to objective scrutiny [7]. It bothers me that the public is being misled by myths and exaggeration from both sides.
From my point of view, GE holds incredible promise and should be pursued in earnest, yet must also be very carefully monitored and regulated. In any case, GE crops have been widely adopted in U.S. agriculture (Table 1), and thus are now a part of beekeeping.
Table 1. The genetically engineered traits available to farmers have evolved rapidly as technology improves and as such crops become more widely adopted. Table from http://www.census.gov/compendia/statab/2012/tables/12s0834.pdf.
An Odd Series Of Connections
In 1972, the dean of biological sciences at my university hired me to set up a "world class insectary" (which I did). I raised mass quantities of insects for hormone extraction, in the hope that we might develop a new generation of eco-friendly insecticides [8]. Several years later I was shocked when Monsanto-a widely-despised chemical company with a sordid history- then hired him to create "a world-class molecular biology company" (which he apparently did). In 2002, Monsanto was spun off as an independent agricultural company.
Jump forward to 2010, when I had the good fortune to work with an Israeli startup--Beeologics--and witnessed the efficacy of their eco-friendly dsRNA antiviral product for honey bees. But to bring the product to market, they needed more backing. To my utter astonishment, they recently sold themselves to Monsanto!
The Vilifying Of Monsanto
These days one can simply mention the name "Monsanto" in many circles, and immediately hear a kneejerk chorus of hisses and boos. Sure, it had been easy for me to enjoy the camaraderie of riding the anti-Monsanto bandwagon; but I realized that that I shouldn't allow that sort of fun to substitute for the responsibility of doing my homework and getting to the actual facts of the matter! When I did so, I found that some of Monsanto's actions did indeed deserve opprobrium; but that much of the criticism directed at the current company is undeserved (Monsanto suffers from an ingenerate inability to practice effective PR). Concurrent with the purchase of Beeologics, Monsanto hired well-respected apiarist (and columnist) Jerry Hayes to head up a new honey bee health division, and appointed some prominent beekeepers (not me) to its advisory board. It dismays me that some beekeepers then immediately jump to the erroneous conclusion that Jerry has sold his soul to the Devil--nothing could be further from the truth!
What Are They Up To?
Some beekeepers imaginatively feared that Monsanto was about to create a GM bee or was up to some other nefarious plot. But in reality, Monsanto's vision of its future direction is anything but evil--I suggest that you peruse their website for your own edification [9], [10]. Of course I was curious as to why they had purchased Beeologics, since the market for bee medicine is far too tiny to draw the interest of a giant corporation. But one needn't be some sort of psychic in order to figure out a corporation's plans--all you need do is to read its recent patents, which are a virtual crystal ball for seeing ten years into the future. So I searched out any patents containing the words "Monsanto" and "RNAi."
To my great relief, I found that Monsanto was not up to some evil plot--far from it! I suggest you read two of the patents yourself [11]:
Chemical pesticidal agents are not selective and exert their effects on non-target fauna as well...Some chemical pesticidal agents have been shown to accumulate in food, and to exhibit adverse effects on workers that manufacture and apply such chemical agents. Thus there has been a long felt need for methods for controlling or eradicating... pest infestation on or in plants, i.e., methods which are selective, environmentally inert, non-persistent, biodegradable, and that fit well into pest resistance management schemes. Plant biotechnology provides a means to control pest infestations by providing plants that express one or more pest control agents. Recombinant pest control agents have generally been reported to be proteins selectively toxic to a target pest that are expressed by the cells of a recombinant plant.
What the patents tell us is that Monsanto clearly sees that the public is sick of pesticides. Genetic RNAi technology would allow plant breeders to develop crop cultivars that control insect pests in the same manner that the plants naturally control viruses. All that the breeder need do would be to identify a unique target protein in a particular pest, and then splice a gene into the plant to produce a "blocking" dsRNA molecule that would prevent the pest from building that specific protein. The beauty is that dsRNA molecules are already naturally found in plant tissues, the blocking molecule would be entirely specific for that pest alone, completely nontoxic to humans or other non target species, and be rapidly biodegradable. It would be a win all around (except for the pest)--crop protection, no toxic pesticides, and a sustainable farming technology (as well as a market for Monsanto's products, since they would need to continually develop slightly different cultivars in order to avoid pest resistance). Who'd have guessed that Monsanto would be leading the way toward developing eco-friendly pest control? Life is full of surprises!
Practicality Overrides Principle
Some folk make GM crops out to be some sort of abomination of nature, and shun them with religious fervor. I'm not sure that this is the best course for environmentalists to take, and that perhaps, in the face of an expanding human population and a warming climate, we should leave all the possible plant breeding solutions on the table. The organic farming community wholeheartedly endorses the biotechnology of "marker assisted selection" [12], yet arbitrarily draws the line at the directed insertion of desirable genes. This may sound like heresy, but as an environmentalist, I suggest that GE holds great promise for developing more nutritious plants that don't require pesticides, fertilizer, or irrigation--all of which would be wins for organic farming.
From a biological standpoint, I simply don't see GM crops as being any more inherently dangerous than conventionally bred crops. Our domestic plants today are often far from "natural"--you wouldn't recognize the ancestors of many. Be aware that even conventionally bred cultivars of several crops (beans, potatoes, celery, etc.) often turn out to be too toxic for humans.
This is not by any means a fluff piece for Monsanto or agribusiness. Farming is not what it used to be. In the U.S., 85% of farm sales are produced by less than 10% of farms, which hold 44% of farm acreage [13]. A mere six companies collectively control around half of the proprietary seed market, and three quarters of the global agrochemical market [14]. I abhor such corporate domination; neither do I see today's high-input agricultural practices as being either sustainable or ecologically wise.
That said, human demands upon the Earth's finite ecosystem are growing. There are only about 4.5 acres of biologically productive land on the surface of the Earth available for each current human inhabitant. Depending upon the culture's lifestyle, we use anywhere from 25 acres (U.S.) to as little as 1 acre (Bangladesh) to feed and clothe each person. Unfortunately for the bee (and many other species), due to human population growth there are over 200,000 additional human mouths to feed every single day--each requiring the conversion of another couple of acres of natural habitat into farmland!
It doesn't take a mathematician to figure out that if we wish to conserve natural ecosystems that we need to get more yield out of existing cropland! And one of the best ways to do that is to breed crops that are more productive and pest-resistant. The plant scientists in the corporate labs are making huge strides in developing such cultivars, both by GM and conventional breeding. If they manage to file a patent [15], so what?--other breeders can easily "steal" the germplasm away from the patented genes, and in any case, the patents expire after 20 years!
Monsanto has seen the writing on the wall--farmers and consumers are demanding not only more food production, but also more eco-friendly agricultural practices. Monsanto research is heading in that direction with their conventional breeding programs, the development of "biological" insecticides [16], and the goal of producing pesticide-free dsRNA crops. Add to that that the company could actually bring to market dsRNA medications against bee viruses, nosema, and perhaps varroa. All would be huge wins for the honey bee and beekeepers!
Hold The Hate Mail
Full disclosure: so despite my innate aversion to corporate dominance and corporate agriculture, I feel that we beekeepers should work with Monsanto to develop products for the beekeeping industry, as well as bee-friendly cultivars of crop plants, and have thus personally decided to be a cooperator in their initial bee research trial. Is this some sort of Faustian bargain? I don't know, but as a condition of my cooperation, I asked, and Monsanto agreed, to allow me to share the data collected with the beekeeping community--which could be a big win for us, since Monsanto has some of the best analytic labs in the world! I feel that it is far better to have Monsanto working on the side of beekeepers, rather than perhaps against us. At this point, I'd like to leave the GM debate behind, and address the facts of the matter as to any relationship between GM crops and CCD.
The Changing Face Of Agriculture
Genetic engineering has clearly changed the face of agriculture in the U.S. (Fig. 1).
Figure 1. These three crops account for over half of all U.S. acreage planted to principal crops, and all are worked to some extent by bees. Data from http://www.ers.usda.gov/data-products/adoption-of-genetically-engineered-crops-in-the-us.aspx
As can be seen from the figure above, any bees near corn, soy, or cotton are going to be exposed to pollen and nectar from GM plants, as well as to indirect effects due to the technology. So could GM crops be the cause of CCD?
Bt Crops
Biological plausibility: the insecticidal Bt toxins in GM corn and cotton pollen could harm adult or larval bees.
Organic farmers have long used the spores of the bacterium Bacillus thuringiensis (Bt) to kill caterpillars. Bt spores germinate in the caterpillar gut, and the bacterium produces insecticidal crystalline proteins (Cry proteins) that bind to specific receptors on the insect intestinal wall. Since different insect species have different receptors on their gut cells, different strains of Bt have evolved to specifically kill various caterpillars, beetles, mosquitoes, etc. [17]. The proteins are so species specific that wax moths can be controlled on combs by Bt aizawai, which produces Cry proteins that are toxic to moth larvae, but not to bees.
Molecular biologists tweak these Cry proteins to make them even more species specific, and then insert them into plant DNA, so that the plant then produces the proteins itself, thus making its tissues toxic to the target species. In order to delay the inevitable evolution of Cry-resistant pests, growers plant a percentage of "refuge" crop not containing the Cry genes. Even so, any particular Cry gene will only be effective for some number of years until resistant pests show up.
People have expressed concern about a poisonous substance being introduced into plant tissues, and to them I highly recommend the paper "Misconceptions about the Causes of Cancer" [18]. The reality is that plant tissues are naturally awash in poisonous substances. Plants have needed to repel herbivores throughout their evolution, and since plants can't run, hide, or bite back, they do it chemically. Many of our most popular fruits, nuts, grains, and vegetables (and especially herbs and spices) contain powerful phytotoxins. Their wild ancestors required cooking or leaching before the plant was edible to humans. Plant breeders systematically select for cultivars with lower levels of (the often strongly flavored) toxins.
Plants that are naturally resistant to pests contain more phytotoxins, often produced in response to damage from insects. For example, the sprouts of wheat, corn, and rye produce potent mutagens (enjoy that cup of wheatgrass juice!) [19]. And some plants naturally contain symbiotic bacteria and fungi in their tissues, which produce non-plant chemicals [20]. There is absolutely nothing biologically novel about insecticidal toxins in plant tissues.
The toxicity (or lack thereof) of Cry proteins to non-target organisms, especially upon two "charismatic" species--the honey bee and the monarch butterfly--has been well studied [21], [22], [23]. A recent and very well-designed experiment on the effect of GM Bt corn pollen upon the growth and survival of honey bee larvae was recently performed by a team of independently-funded German researchers [24]. They added pollen from four different sources to a standard semi-artificial larval diet.
Results: surprisingly, the larvae fed the pollen from the "stacked" GM corn containing a combination of three different Cry proteins exhibited a higher survival rate (100%), than those fed non-GM corn pollen! To me, a big plus for this study was that they also included a positive control of pollen from a wild plant said to be harmful to bees--only about 30% of those larvae survived! This finding confirmed that even some natural pollens are quite toxic, and that we should compare any toxicity trials of pesticides with those of the natural phytotoxins in nature.
Analysis: CCD and colony mortality occur even in the absence of GM Bt crops; feeding GM Bt pollen to adult bees or larvae does not cause observable adverse effects.
Verdict on Bt crops: The specific Bt cry proteins used in GM crops were intentionally chosen to not cause harm to bees. There is no evidence to date that they do. On the other hand, Bt crops require less use of insecticides that are clearly toxic to bees [25].
Roundup Ready
Monsanto's pitch is that Roundup Ready®️ (RR) crops allow farmers to practice weed-free "no till" farming, which saves both topsoil and money. The catch is that farmers must then douse their fields with Monsanto's flagship product, Roundup (ensuring sales of that herbicide--a great marketing strategy). Bayer CropScience has followed suit by introducing crops resistant to its Liberty herbicide, which has a different mode of action.
Herbicide-resistant crops do indeed address several major environmental problems:
No till farming does in fact require less labor and reduces soil compaction.
Farmers get greater production due to less competition from weeds.
No till also reduces the amount of petrochemical fuel involved in tillage.
No till greatly reduces soil erosion, which has long been a major environmental concern.
No till may help to sequester carbon in the soil, and to rebuild soil.
So what's not to love about Roundup Ready? There are a few main complaints--(1) the massive spraying of the active ingredient, glyphosate, for which there is questionable evidence that it may be an endocrine disruptor [26], (2) claims of intimidation by Monsanto of farmers who choose not to plant RR seed, and (3) the environmental impact and sustainability of the sort of weed-free monoculture possible with RR crops.
So how do Roundup and RR crops relate to honey bees?
Direct Effects Of Roundup Use
Biological plausibility: either the active ingredient (glyphosate), or the adjuvants could cause bee toxicity.
The EPA has thoroughly reviewed the research and found glyphosate to be practically nontoxic to bees (and humans). They have found the same for Roundup's adjuvant polyoxyethylene-alkylamine. However, some beekeepers tell me that they see increased bee mortality following the spraying of glyphosate (Fig. 3), but are not sure whether it was a generic product, or perhaps contained additional ingredients (surfactants, fungicides, or insecticides) added to the tank mix.
Figure 3. A farmer spraying glyphosate herbicide over Roundup Ready corn seedlings. Photo courtesy of beekeeper Larry Garrett.
Analysis: there is no strong evidence that the spraying of Roundup or generic glyphosate herbicide is directly causing significant bee mortality. However, Drs. Jim and Maryann Frazier have legitimate concerns about the effect of some adjuvants--especially the organosilicones [27], [28].
Indirect Effects Of Roundup Use
Biological plausibility: the elimination of weeds reduces bee forage.
The success of Roundup Ready technology has allowed farmers to largely eliminate weeds from their fields (at least until the inevitable resistant weeds take over). But they don't stop there--nowadays they practice "clean farming" and use herbicides to burn off every weed along the fencerows and in the ditches--the very places that bees formerly had their best foraging. This elimination of flowering weeds severely reduces the amount of available of bee forage, plus kills off the host plants of native pollinators (such as monarch butterflies) and beneficial insects.
European honey bees evolved in Europe (hence the name), and are adapted to the nutrition provided by Old World flowering plants. Many of the weeds in North America are old friends of the honey bee. On the other hand, honey bees were never exposed to corn, soybeans, sunflowers, or squashes until recently; neither corn nor sunflowers supply complete amino acid profiles in their respective pollens. Until the advent of Roundup Ready, the weeds in an around crops provided alternative nectar and pollen sources for bees; today there is often nary a bee-nutritious weed to be seen in or around a field of corn or soybeans (Fig. 4).
Figure 4. I took this photo of a no-till herbicide-resistant corn field, prior to the shading canopy of the crop closing over. Note the total lack of any sort of bee forage (or any species of anything other than corn). The soil surface is a far cry from the original densely vegetated prairie sod. Prior to RR, there was more weedy forage for bees, and especially from the traditional weed-controlling crop rotation into legumes or pasture.
Update: there's a great deal of debate about the safely of Roundup (the formulated product with it's surfactants) and its active ingredient, glyphosate. From http://npic.orst.edu/factsheets/archive/glyphotech.html
"In plants, glyphosate disrupts the shikimic acid pathway through inhibition of the enzyme 5-enolpyruvylshikimate-3-phosphate (EPSP) synthase. The resulting deficiency in EPSP production leads to reductions in aromatic amino acids that are vital for protein synthesis and plant growth.
As far as the claims that glyphosate causes cancer (notably Non-Hodgkin's Lymphoma), I agree with the regulatory agencies that the case against glyphosate is very weak. As far as glyphosate being an endocrine disruptor, I'll leave it to the researchers and regulatory agencies to figure it out. As I type these words, I've actually got caged bees to which I'm feeding glyphosate (at a field-realistic dose) for a trial, and not seeing increased mortality. But some research indicates that it may be harmful to the gut microbiota. This sort of research takes time, and eventually we'll figure out just how safe or harmful glyphosate is to bees, humans, or the environment.
But nothing in nature is simple. Eliminating the competition of weeds and insects may allow plants to hold back from the production of natural toxins. And a surprising piece of research found corn kernels from plants sprayed with either of two different herbicides actually contain more of the healthful carotenoids [30]!
The Future Of Roundup
It took Monsanto several years to genetically engineer Roundup-resistant crops, yet took farmers only slightly longer to inadvertently produce Roundup-resistant weeds by the conventional breeding technique of applying a strong selective pressure-the continuous application of Roundup!
Weed management scientists consider glyphosate to be a once-in-a-100-year discovery--it works on 140 species of weeds, and is relatively environmentally friendly. However, its overuse has led to the creation of several "driver weeds" that could soon lead to its redundancy in corn, soy, and cotton acreage [31]. This will drive farmers to turn to other herbicides (which will also in time fail). We can only hope that someday they will be forced back into practicing crop rotation into legumes and pasture.
Reality Check
In order to clarify cause and effect, I often seek out extreme cases. Such would be the situation in the Corn Belt, where I could compare the USDA's hive and honey data from the old days to those under today's intense planting of GM crops (Fig. 5)!
Figure 5. The most intense planting of GM crops is in Iowa and Illinois (the dark green areas of the map above). U.S. farmers planted nearly 100 million acres of corn this year, and 76 million of soy. That is enough acreage to cover the entire state of Texas with GM crops!. Source: http://www.nass.usda.gov/Charts_and_Maps/Crops_County/pdf/CR-PL10-RGBChor.pdf
So I went through the tedious process of downloading and transcribing the NASS agricultural census figures for Iowa. I entered the amount of corn acreage, the total number of colonies in the state, and what I consider to be the best measure of colony health--honey yield per hive (which of course is largely weather dependent, but should show any trends). I plotted the data below (Fig. 6):
Figure 6. Bee and corn data from Iowa, and the dates of introduction of corn pest control technologies. The dotted line is median honey yield per colony. No factor appears to have affected honey production, but colony numbers have decreased since the arrival of varroa. Gaps are missing data. Source NASS.
Note: for non beekeepers, varroa is a parasitic mite that arrived in the U.S. around 1990 and quickly became, and still remains, the Number One problem in bee health-far more than any other factor.
Over the years, corn acreage increased by 18%. Other than the prodigious crop of 1988, honey production has averaged around 67 lbs per hive. The thing that stands out is the plot of number of colonies. Hive numbers jumped up in the late 1980's, likely due to federal honey price support payments, which peaked in 1988, and were cut off in 1994 [[i]]. Colony numbers peaked in 1990, the same year that varroa arrived in Ohio, and went down from there, leveling off to about half the number of hives present in the 1970's.
I fully expected honey yields to decrease concurrent with the adoption of Roundup Ready varieties, but they didn't! Colonies still produce as much honey today as they did in the past, but this might be partially due to having fewer bees working the same amount of land, or to increased soybean nectar (which saved a number of Midwestern beekeepers from disaster during this year's droughts).
Perhaps even more surprising is the fact that in a state covered in corn and soy, colony productivity did not appear to be affected by the introductions of either Bt or Roundup Ready corn, nor by the universal use of neonicotinoid seed treatments (between corn and soy, on over roughly two thirds of the entire state land area). Note that honey yields actually increased for a few years following the introduction of clothianidin seed treatment!
Tellingly, hive numbers started to decrease after the arrival of varroa, and plummeted in the late 1990's as fluvalinate failed as a miticide, and many beekeepers simply threw up their hands and quit the business.
Verdict on herbicide tolerant crops: from a nutritional standpoint, the increased use of herbicides, and the associated weed free "clean farming" has certainly not helped the bees in corn/soy areas, but it is hard to make a case for them causing colony collapse.
Verdict on GM crops in general: Allow me to quote from the USDA:
...there is no correlation between where GM crops are planted and the pattern of CCD incidents. Also, GM crops have been widely planted since the late 1990s, but CCD did not appear until 2006. In addition, CCD has been reported in countries that do not allow GM crops to be planted, such as
Switzerland [33].
Looking Ahead: The Chemical Treadmill & Pest Resistance
It is interesting to observe the evolution of agriculture from the perspective of a biologist. Simple systems in nature are inherently less stable than complex systems. The current agricultural model in the U.S. exemplifies simplicity to the extreme--plant a single species into bare soil year after year, killing any competitive weeds or insects with pesticides (either sprayed, systemic, or engineered into the plants), and attempt to maintain fertility by adding energy-costly fertilizer. From a biological perspective, such a strategy is little more than an intense selective breeding program for the most resistant pests, and doomed to escalating chemical and energy inputs until the system collapses under its own weight.
I'm anything but a salesman for either Bt nor RR crops. Both are mere short-term solutions--resistant bugs and weeds are already starting to spread. I also have questions about the benefits of herbicide-intense no till planting [34], and hope that farmers return to alternative methods of weed control [35]. Luckily, the system will likely be self correcting, eventually forcing humanity to practice more sustainable methods of farming the land. However, I suggest that those methods may well include the wise use of biotechnology.
Additional Discussion
The Back Story On Plant Breeding And GM Crops
Traditionally, farmers simply replanted with the seeds from the most desirable individual plants year after year; this is the simplest form of "selective breeding." For example, all the various cole crops (cabbage, kale, broccoli, cauliflower, kohlrabi, Brussels sprouts) were developed by intentionally selecting for unusual forms of the species (resulting from random recombination of the natural allelic diversity, spontaneous mutants, or natural hybrids). This sort of selective breeding tends to result in a diverse assembly of locally-adapted cultivars. In Oaxaca, Mexico- the birthplace of corn-some 150 traditional varieties of maize are grown without pesticides or herbicides, thereby maintaining an invaluable reservoir of genetically-diversity "germplasm," which breeders can then cross and backcross in order to develop new cultivars (e.g., for pest or drought resistance).
In the early years of the U.S., seeds from desirable cultivars were distributed to farmers by the government, and plant breeding was performed at universities and at the USDA [36]. But since every strain breeds true, a farmer could save the seed and replant, leaving little opportunity for seed companies to make a buck. So in 1883, they formed the American Seed Trade Association and began to lobby for the cessation of the government programs.
The Profit Motive
In the early part of the 20th century, the companies began to promote hybrids-- crosses of two (or more) different strains or species that exhibited some sort of "hybrid vigor"--offering greater production, tastier fruit, or some other desirable characteristic. Hybrids were a godsend to the companies, since they are often sterile or don't breed true, meaning that farmers needed to purchase (rather than save) seed each season.
The seed lobby eventually shifted public funding away from the free distribution of selected seedstocks to instead encouraging the USDA and universities to develop inbred parental lines and breeding stock that the seed trade could then use to create proprietary hybrid varieties. By 1960, farmers planted less than 5% of corn from saved seed; and less than 10% of soybeans by 2001. As on-farm familiarity with the saving of seed was forgotten, farmers became willing consumers of produced seed.
Enter GM Crops
Then in 1980, the Supreme Court decided that seed companies could patent new varieties if they contained distinct and novel genetic markers. This meant that farmers (in some countries) could now be required to sign licensing agreements to allow them to use the patented seed each season [37] (there is a hodge-podge of international patent laws in this regard [38]).
The Second "Green Revolution"
The first "green revolution" was based upon fertilizer, pesticides, and hybrid seed (and also resulted in forcing farmers onto "agricultural treadmills"-making them less self sufficient and sustainable, and more reliant upon purchased seed, pesticide and fertilizer use, and upon borrowed money).
In 1950 the Secretary of Agriculture Ezra Benson said to farmers, "Get big or get out." His 1970s successor, Earl Butts, repeated that message, and exhorted farmers to "plant fence row to fence row" and to "adapt or die." Politicians who understood that a well-fed electorate is a happy electorate promoted policies that resulted in the destruction of the small family farm. Our policy of price supports and favorable treatment of agribusiness has changed the face of the American farm and the composition of the American diet [39].
Today's "second green revolution" is based upon technological advances in plant genetics (including GM) and the (at least partial) replacement of nasty pesticides with "biologicals." As an environmentalist, I find the new revolution to be more promising for ecological sustainability, but it is not without its downside--the current consolidation of agribusiness. As I mentioned before, farms, seed companies, and chemical companies are all being bought up by a few main players. Philip Howard details this consolidation in a free download [40], from which I quote:
This consolidation is associated with a number of impacts that constrain the opportunities for renewable agriculture. Some of these include declining rates of saving and replanting seeds, as firms successfully convince a growing percentage of farmers to purchase their products year after year; a shift in both public and private research toward the most profitable proprietary crops and varieties, but away from the improvement of varieties that farmers can easily replant; and a reduction in seed diversity, as remaining firms eliminate less profitable lines from newly acquired subsidiaries.
He then speaks of the concept of the "treadmill":
For the majority of farmers, however, the result is that they must constantly increase yields in order to simply maintain the same revenue. [Monsanto's sales pitch is that economic success in farming is driven by yield per acre [41]. Those that are unable to keep up with this treadmill will "fall off," or exit farming altogether. Their land ends up being "cannibalized" by remaining farmers who seek to increase scale of production as another means of keeping up with the treadmill, leading to the increasing centralization of agriculture. Farmers who have managed to stay in business have adapted to this process, and are typically on the leading edge of the adoption of new technologies. As a result, they have a high degree of confidence in science and technological innovations.
However, this problem has nothing to do with GMO's, but is rather due to the public's unknowing acceptance of the practice. Capitalism inevitably leads to consolidation unless consumers stop supporting corporate agribusiness with their pocketbooks and their votes, and start demanding that their government enforce antitrust efforts and better support small farmers.
But we are allowing economics and politics to distract us from the topic at hand--the technology of genetic engineering in plant breeding.
Cautions About GM
The most vocal critic of genetic modification is Jeffrey Smith, fear-mongering author of Seeds of Deception, producer of the film Genetic Roulette, and executive director of the inappropriately-named Institute for Responsible Technology. Smith is a gifted and effective communicator, as well as being a practitioner of "yogic flying" [42]. I will be the first to say that Smith's anti-GMO claims [43] would scare the pants off of anyone, and make for compelling story! The problem is that he plays loose with the facts--most of his claims simply do not stand up to any sort of scientific scrutiny. I suggest that for an objective analysis of the facts, that you visit AcademicsReviewed.org, a website that tests popular claims against peer-reviewed science. They address each of Smith's alarming "facts" one by one [44]. It is a thrilling ride to open the two web pages side by side, first being shocked by Smith's wild and scary claims, and then reading the factual rebuttal to each! The thing that most bothers me about Smith's writing is that he treats GM cultivars generically, rather than specifically addressing the merits or concerns for them individually. This makes little sense, since any conventional crop has cultivars that cause human allergy or contain excessive levels of natural toxins, yet no one calls for the testing of each of them!
Perspectives On GM Crops
As you may have guessed by now, to me, the GM debate should not be about being pro or con, rather it should be about the intelligent discussion of reconciling its promise with its problems. The GE genie is out of the bottle, and I can't see that anyone is going to put it back in-so we might as well work with it! So let's cut through the hype and hysteria, the fears and judgments, and try to objectively look at the facts of the matter:
From a plant breeder standpoint, genetic engineering holds incredible promise for the development of crops that could be tremendously beneficial to humans or the environment. For example, "Transgenic cotton has reduced the need for conventional insecticides used against lepidopteran [pests] an average in the USA about 59.4% [and] Texas 74.7%...an average number of pesticide applications in conventional cotton has fallen from 4.3 in 1995 to 2.1 in the USA... with benefits to human health and the environment" [45].
GM is only a part of plant breeding--most advances continue to be in conventional breeding, now assisted by "marker assisted selection," which is embraced by environmentalists [46].
However, someone needs to pay for the research, and the taxpayer is not doing it! For a thoughtful discussion of the benefits of gene patents, see [47].
Novel genetic markers can be patented, and a licensing fee can be charged, despite the fact that they are not GM!
From a consumer standpoint, advanced breeding techniques can result in cheaper and more nutritious food, and less environmental impact from farming.
Consumers have erroneously been led to believe that GM crops are dangerous to their health, and call for application of the precautionary principle. My gosh, please read "Misconceptions about the causes of cancer" [48]. Few foods are entirely "safe"! And "safety" can never be proven--it can only be disproven. And no studies have ever disproven the safety of GM crops, nor have doctors noticed anyone ever getting sick from them, despite our eating them for 15 years!
In truth, some scientists argue that plants produced by classical breeding methods should undergo the same safety testing regime as genetically modified plants. There have been plenty of instances where plants bred using classical techniques have been unsuitable for human consumption, causing toxicity or allergic reactions.
Those that speak of applying the "precautionary principle" should read Jon Entine's trenchant analysis of the fallacy of overapplication of that principle [49]. In truth, our regulators (EPA and FDA) vigorously apply the precautionary principle in the form "reasonable certainty of no harm."
The benefits of seed biotechnology cannot be realized without good seed germplasm to start with. So a few large seed companies started buying up their competitors to acquire the most productive and desirable varieties.
The downside of the above practice is that by 2008, 85% of GM maize patents and 70% of non-maize GM plant patents in the U.S. were owned by the top three seed companies: Monsanto, DuPont, and Syngenta [50]. Note that economists figure that when four firms control 40% of a market, it is no longer competitive; in the case of GE crops, the top four seed firms control 56% of the global proprietary seed market!
On the flip side, these profits are an incentive for the large corporations to invest in innovative plant breeding research--Monsanto spends about $2 million a day on this. This is important to keep in mind in an increasingly hungry world.
On the dark side, Monsanto's nearly $12 billion in annual sales allows the company to lobby regulators, influence universities, and spin the news. These are standard business practices for any large corporation, but hardly make Monsanto uniquely evil.
Be aware that patented genes are of use only if inserted into high-producing cultivars-which are developed by conventional breeding (which constitutes nearly half of Monsanto's plant breeding budget). These desirable cultivars have no patent protection. Monsanto uses a non GE technology called SMART = Selection with Markers and Advanced Reproductive Technologies. SMART technology is warmly embraced by environmental groups [51].
Adding a genetic marker allows a company to identify its proprietary strains, like putting a nametag on a dog. But clever breeders can back engineer the desirable germplasm out from patent protection.
And remember that patents expire after 20 years. The patents for Roundup Ready soybeans expire in 2014--at which time farmers, universities, and seed companies will then be free to propagate and sell the variety [52]. Patents are granted in order to spur innovation; by filing for patent protection, a company must make its discoveries public knowledge. This is a good thing.
Monsanto invests 44% of its R&D on conventional (as opposed to GM breeding).
Monsanto has also given rights to some of their patented crops to poorer countries, and recently donated a database of some 4000 genetic markers from cotton to Texas A&M [53]. The university plant breeders are excited in that the information will assist them in their conventional (non-GM) breeding of cotton, to the benefit of the environment [54 ].
From the farmer's standpoint, he has the choice of purchasing GE varieties that may be more productive, reduce insecticide use, or reduce tillage costs [55]. Keep in mind that there is nothing keeping him from purchasing "conventional" non-GM seed--it is available (I checked, and it sells at about half the cost of GM seed). In our free enterprise system there is nothing to keep non-GM seed companies from selling an alternative product if there is a demand. Farmers who are unimpressed by GM varieties freely switch back to conventional seed.
From an agricultural standpoint, the widespread adoption of a few favored crop varieties (GM or not) can result in the irreplaceable loss of crop genetic diversity--this is of great concern to plant breeders. If you haven't yet seen the graphic of our loss of crop genetic diversity from National Geographic magazine, you should! [56]. Luckily, this does not appear to be occurring yet with maize in Oaxaca [57], but there is a legitimate concern that economics will force traditional farmers out of business, leading to the loss of heirloom varieties. However, this is not a GM issue, but rather an effect of consolidation.
From a sustainability standpoint, there is nothing to prevent constant breeding innovation to keep pace with pest evolution. Genetically engineered crops can play a role in sustainable farming as our agricultural practices begin to shift to more ecologically sustainable methods.
One should keep in mind how the simple splicing of a virus gene into the papaya saved the Hawaiian papaya growers from the ravages of ringspot virus--the GE papaya is the mainstay of the industry, and by virtue of keeping the virus in check actually allows nearby organic papayas to thrive. Yet ecoterrorists recently hacked down thousands of GM trees [58]. It's interesting to read the history of "Golden Rice" [59] to see how the anti-GMO lobby is specifically scared that the success of such a lifesaving crop might open the door for acceptance of other GM plants!
Update Jan 2013
News item: Leading Environmental Activist's Blunt Confession: I Was Completely Wrong To Oppose GMOs. Blog in Slate Magazine
"If you fear genetically modified food, you may have Mark Lynas to thank. By his own reckoning, British environmentalist helped spur the anti-GMO movement in the mid-'90s, arguing as recently at 2008 that big corporations' selfish greed would threaten the health of both people and the Earth. Thanks to the efforts of Lynas and people like him, governments around the world--especially in Western Europe, Asia, and Africa--have hobbled GM research, and NGOs like Greenpeace have spurned donations of genetically modified foods.
But Lynas has changed his mind--and he's not being quiet about it. On Thursday at the Oxford Farming Conference, Lynas delivered a blunt address: He got GMOs wrong."
Anyone opposed to GMO's should read Mr. Lynas' well thought out address: http://www.marklynas.org/2013/01/lecture-to-oxford-farming-conference-3-january-2013/
Update May 2014
I've compiled a list of recent worthwhile reading on the "other side" of the GMO debate at https://scientificbeekeeping.com/gmo-updates/
So What's The Problem?
The problem is that anti-GMO advocacy groups are determined to put a stop to all GE technology. They targeted California with Prop 37, which applied only to packaged foods and produce. A more cynical take on Prop 37 was that it was all about marketing: "If your produce is no different in terms of taste, safety and nutrition from a competitor, and costs more, apparently the only marketing option is to create a negative image of your competitor's product" [60].
If Prop 37 had been successful, the promoters would then have targeted restaurants, the meat and dairy industry, and the beverage industry. I personally feel that this is an extreme position, what with the human population growing hungrier every day, and climate change threatening agriculture worldwide with heat, drought, pestilence, and salinity problems. Not only that, but GM crops hold promise for cheap omega-3 fatty acids (so that we don't have to harvest fish for them), cost-effective biofuels, and less expensive pharmaceuticals.
A good blog on the problem with the anti-GMO fear campaign can be found at [61], from which I quote:
It would be bad enough if something like the Seralini study simply contributed to the unnecessary angst amongst consumers around the world. It also has very real political, economic and practical effects. For instance brand conscious food companies have used their leverage to prevent the development of GMO versions of potatoes, bananas, coffee and other crops because they fear controversy. Apple growers worried about the market response are opposing the introduction of a non-browning apple even though it was developed by one of their own fruit companies. French activists destroyed a government-run field trial of a virus-resistant root stock which could have made it possible to produce good wine on sites that have become useless because of contamination with sting nematodes and the virus they vector. California voters have the potential to pass a seriously flawed "GMO labeling" initiative next month that could only serve the purposes of the lawyers and "natural products" marketers who created it. More importantly, European and Japanese importers of wheat essentially blackmailed the North American wheat producers into blocking biotech wheat development because those companies were nervous about consumer response in countries where GMO angst is so high. This has delayed by decades not only specific desirable trait development, but also what might have been an enormous private investment in a crop that is critically important for feeding a lot more people than just those in those rich countries. There is a huge cost of "precaution" based on poor science.
I believe that people should be well informed before taking a stance on important issues. I'd like to suggest one last excellent blog by an independent U.C. Berkeley evolutionary biologist and medical researcher:"How Bt Corn and Roundup Ready Soy Work - And Why They Should Not Scare You [62].
Acknowledgements
As always, thanks to my friend and collaborator in research Peter Loring Borst, and to anyone who still reads my articles after finding out that I've collaborated with Monsanto!
References
[1] Key S, et al (2008) Genetically modified plants and human health. J R Soc Med.101(6):290-298. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2408621/
[2] For example: Antoniou, M, et al (2012) GMO myths and truths.
(Broken Link!) http://earthopensource.org/files/pdfs/GMO_Myths_and_Truths/GMO_Myths_and_Truths_1.3.pdf
[3] Chiba S, et al. (2011) Widespread endogenization of genome sequences of non-retroviral RNA viruses into plant genomes. PLoS Pathog 7(7): e1002146.
[4] Domingo, JL and JG Bordonaba (2011) A literature review on the safety assessment of genetically modified plants. Environment International 37: 734-742.
[5] Key (2008) op. cit.
[6] Smith, JM (2003) Seeds of Deception. Yes! Books
[7] Seralini, GE, et al (2012) Long term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize. Food and Chemical Toxicology (2012) http://foodpoisoningbulletin.com/wp-content/uploads/Toxicity-of-Roundup-Ready-Maize.pdf;
Reviews
http://www.forbes.com/sites/henrymiller/2012/09/25/scientists-smell-a-rat-in-fraudulent-genetic-engineering-study/2/
http://www.efsa.europa.eu/en/faqs/faqseralini.htm#9, http://www.emilywillinghamphd.com/2012/09/was-it-gmos-or-bpa-that-did-in-those.html,
(Broken Link!) http://www.ask-force.org/web/Seralini/Anonymous-Rat-List-Spaying-2003.pdfs, http://storify.com/vJayByrne/was-seralini-gmo-study-designed-to-generate-negati;
Benbrook, CM (2012) Impacts of genetically engineered crops on pesticide use in the U.S. -- the first sixteen years. Environmental Sciences Europe 24:24 http://www.enveurope.com/content/pdf/2190-4715-24-24.pdf,
Review http://weedcontrolfreaks.com/2012/10/do-genetically-engineered-crops-really-increase-herbicide-use/#more-432
[8] http://journals.tubitak.gov.tr/agriculture/issues/tar-04-28-6/tar-28-6-1-0309-5.pdf
[9] http://www.monsanto.com/whoweare/Pages/monsanto-history.aspx
[10] http://www.businessweek.com/stories/2010-01-10/monsanto-v-dot-food-inc-dot-over-how-to-feed-the-world
[11] Methods for genetic control of plant pest infestation and compositions thereof
http://www.freepatentsonline.com/8088976.html
http://www.freepatentsonline.com/7943819.html
[12] http://www.greenpeace.org/australia/PageFiles/348427/smart-breeding.pdf
[13] 2007 figures http://www.census.gov/compendia/statab/2012/tables/12s0835.pdf
[14] ETC Group (2008) Who owns nature? Corporate power and the final frontier in the commodification of life. http://www.etcgroup.org/sites/www.etcgroup.org/files/publication/707/01/etc_won_report_final_color.pdf
[15] Blakeney, M (2011) Trends in intellectual property rights relating to genetic resources for food and agriculture. http://www.fao.org/docrep/meeting/022/mb684e.pdf This document covers the hodge-podge of international patent laws regarding plants and animals.
[16] http://www.monsanto.com/products/Pages/biodirect-ag-biologicals.aspx
[17] History of Bt http://www.bt.ucsd.edu/bt_history.html
Mode of action http://www.bt.ucsd.edu/how_bt_work.html
[18] Gold 2002 Misconceptions about the causes of cancer http://potency.berkeley.edu/pdfs/Gold_Misconceptions.pdf A "MUST READ"!
[19] Buchmann CA, et al (2007) Dihydroxy-7-methoxy-1,4-benzoxazin-3-one (DIMBOA) and 2,4-dihydroxy-1,4-benzoxazin-3-one (DIBOA), two naturally occurring benzoxazinones contained in sprouts of Gramineae are potent aneugens in human-derived liver cells (HepG2). Cancer Lett. 246 (1-2):290-9.
[20] http://en.wikipedia.org/wiki/Endophyte
[21] Duan JJ, et al (2008) A meta-analysis of effects of Bt crops on honey bees (Hymenoptera: Apidae). PLoS ONE 3(1): e1415.
[22] Center for Environmental Risk Assessment (2011) A review of the environmental safety of the Cry1Ab protein. http://cera-gmc.org/docs/cera_publications/cry1ab_en.pdf
[23] Han, P, et al (2012) Does transgenic Cry1Ac + CpTI cotton pollen affect hypopharyngeal gland development and midgut proteolytic enzyme activity in the honey bee Apis mellifera L. (Hymenoptera, Apidae)? Ecotoxicology. 2012 Aug 7. [Epub ahead of print]
[24] Hendriksma HP, et al (2011) Testing pollen of single and stacked insect-resistant bt-maize on in vitro reared honey bee larvae. PLoS ONE 6(12): e28174.
[25] Benbrook, CM (2012) op. cit.
[26] Reviewed in http://www.sourcewatch.org/index.php/Glyphosate
[27] Mullin, C.A., J.L. Frazier, M.T. Frazier & T.J. Ciarlo - A primer on pesticide formulation 'inerts' and honey bees. http://www.extension.org/pages/58650/proceedings-of-the-american-bee-research-conference-2011
[28] Ciarlo TJ, CA Mullin, JL Frazier, DR Schmehl (2012) Learning impairment in honey bees caused by agricultural spray adjuvants. PLoS ONE 7(7): e40848.
[29] Johal, GS and DM Huber (2009) Glyphosate effects on diseases of plants. Europ. J. Agronomy 31: 144-152. http://www.organicconsumers.org/documents/huber-glyphosates-2009.pdf
Huber, DM (2010) Ag chemical and crop nutrient interactions - current update. http://www.calciumproducts.com/dealer_resources/Huber.pdf
Reviewed in (Broken Link!) http://www.weeds.iastate.edu/mgmt/2010/glyMndisease.pdf
[30] Kopsell et al. (2009) increase in nutritionally important sweet corn kernel carotenoids following mesotrione and atrazine applications. Journal of Agricultural and Food Chemistry 090619124509017 DOI: 10.1021/jf9013313
[31] Laws, F (2010) http://cornandsoybeandigest.com/issues/will-glyphosate-fall-wayside-resistance-grows
[32] http://www.nationalaglawcenter.org/assets/crs/RS20759.pdf
[33] http://www.ars.usda.gov/is/AR/archive/jul12/July2012.pdf
[34] http://www.misereor.org/fileadmin/redaktion/MISEREOR_no%20till.pdf
[35] http://www.acresusa.com/toolbox/reprints/Organic%20weed%20control_aug02.pdf
[36] http://www.seedalliance.org/Seed_News/SeminisMonsanto/
[37] (Broken Link!) http://earthopensource.org/files/pdfs/GMO_Myths_and_Truths/GMO_Myths_and_Truths_1.3a.pdf
[38] Blakeney, M (2011) Trends in intellectual property rights relating to genetic resources for food and agriculture. http://www.fao.org/docrep/meeting/022/mb684e.pdf This document covers the debate involved in international patent law regarding plants and animals.
[39] Philpott, T (2008) A reflection on the lasting legacy of 1970s USDA Secretary Earl Butz. http://grist.org/article/the-butz-stops-here/; but for a contrary view by an actual corn farmer, read Hurst, B (2010) No Butz About It. (Broken Link!) http://www.american.com/archive/2010/july/no-butz-about-it
[40] Howard, Philip H. 2009. Visualizing consolidation in the global seed industry: 1996-2008. Sustainability, 1(4), 1266-1287. http://www.mdpi.com/2071-1050/1/4/1266/pdf
[41] http://www.monsanto.com/investors/Documents/Whistle%20Stop%20Tour%20VI%20-%20Aug%202012/WST-Fraley_RD_Update.pdf
[42] http://academicsreview.org/reviewed-individuals/jeffrey-smith/
[43] http://responsibletechnology.org/docs/145.pdf
[44] http://academicsreview.org/reviewed-content/genetic-roulette/
[45] Greenberg, S, et al (2012) Economic and Environmental Impact Transgenically Modified Cotton Comparative with Synthetic Chemicals for Insect Control. Journal of Agricultural Science and Technology B 2 750-757.
[46] Greenpeace (2009) Smart Breeding. Marker-Assisted Selection: A non-invasive biotechnology alternative to genetic engineering of plant varieties. http://www.greenpeace.org/australia/PageFiles/348427/smart-breeding.pdf
[47] http://www.genengnews.com/gen-articles/in-defense-of-gene-patenting/2052/
[48] Gold 2002 Misconceptions about the causes of cancer http://potency.berkeley.edu/pdfs/Gold_Misconceptions.pdf
[49] Entine, J (2010) Crop Chemophobia: Will Precaution Kill the Green Revolution? http://www.jonentine.com/pdf/CROPCHEMOPHOBIApre-orderform.pdf
[50] Howard, Philip H. 2009. Visualizing consolidation in the global seed industry: 1996-2008. Sustainability, 1(4), 1266-1287. http://www.mdpi.com/2071-1050/1/4/1266/pdf
[51] http://www.greenpeace.org/australia/PageFiles/348427/smart-breeding.pdf
[52] http://www.monsanto.com/newsviews/Pages/roundup-ready-patent-expiration.aspx;
[53] http://www.cotton247.com/article/3401/monsanto-donates-marker-technology
[54] http://www.youtube.com/watch?v=dcZyFH_eITQ
[55] http://www.biofortified.org/2012/05/the-frustrating-lot-of-the-american-sweet-corn-grower/#more-8670
[56] http://ngm.nationalgeographic.com/2011/07/food-ark/food-variety-graphic If you didn't see this graphic in National Geographic, you should!
[57] (Broken Link!) http://researchnews.osu.edu/archive/mexmaize.htm
[58] http://www.huffingtonpost.com/2011/08/20/genetically-modified-papayas-attacked_n_932152.html
[59] http://en.wikipedia.org/wiki/Golden_rice
[60] http://westernfarmpress.com/blog/proposition-37-gone-probably-not-forgotten?
[61] http://appliedmythology.blogspot.com/2012/10/can-damage-from-agenda-driven-junk.html?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+AppliedMythology+%28Applied+Mythology%29
[62] http://www.science20.com/michael_eisen/how_bt_corn_and_roundup_ready_soy_work_and_why_they_should_not_scare_you
Category: Colony Health - Diseases, Viruses, CCD
Tags: collapse, colony, genetically, gm crops, gmo, modified, plants, sick bees | modified Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/modified/ |
Sick Bees - Part 18E: Colony Collapse Revisited - Genetically Modified Plants
First published in: ABJ December 2012
Genetically Modified Plants
What Is Genetic Modification?
There's Nothing New About Transgenics
GMOs
An Odd Series of Connections
The Vilifying of Monsanto
What Are They Up To?
Practicality Overrides Principle
Hold the Hate Mail
The Changing Face of Agriculture
Bt Crops
Roundup Ready
Direct Effects of Roundup Use
Indirect Effects of Roundup Use
The Future of Roundup
Reality Check
Looking Ahead: The Chemical Treadmill & Pest Resistance
Additional Discussion
The Back Story on Plant Breeding and GM Crops
The Profit Motive
Enter GM Crops
The Second "Green Revolution"
Cautions About GM
Perspectives on GM
So What's The Problem?
Acknowledgements
References
Sick Bees - Part 18E:
Colony Collapse Revisited - Genetically Modified Plants
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in Dec 2012
Genetically modified (or GM) plants have attracted a large amount of media attention in recent years and continue to do so. Despite this, the general public remains largely unaware of what a GM plant actually is or what advantages and disadvantages the technology has to offer, particularly with regard to the range of applications for which they can be used [1].
The above quote is certainly an understatement! Genetically Modified Organisms (GMO's) are a highly contentious topic these days, and blamed by some for the demise of bees. In researching the subject, I found the public discussion to be highly polarized--plant breeders and farmers are largely enthusiastic (with appropriate reservations) about the benefits of genetic engineering, whereas health and environmental advocacy groups tend to be fearful of the new technology [2]. I will largely save my review of the history and pros and cons of GM crops for my website, and focus this article upon how GMO's relate to honey bee health.
What Is Genetic Modification?
The knowledge of genetics was not applied to plant breeding until the 1920's; up 'til then breeders would blindly cross promising cultivars and hope for the best. With today's genetic engineering, breeders can now take a gene from one plant (or animal, fungus, or bacterium) and splice it into the DNA of another plant. If they get it just right, the new gene can confer resistance to frost, drought, pests, salinity, or disease. Or it could make the crop more nutritious, more flavorful, etc. Such genetically modified crops are also called "transgenic," "recombinant," "genetically engineered," or "bioengineered."
There's Nothing New About Transgenics
There is nothing new about transgenic organisms, in fact you (yes you) are one. Viruses regularly swap genes among unrelated organisms via a process called "horizontal gene transfer" [3]. For example, the gene which is responsible for the formation of the mammalian placenta was not originally a mammal gene--it was inserted into our distant ancestors by a virus. If a gene introduced by a virus confers a fitness advantage to the recipient, then that gene may eventually be propagated throughout that species' population. Until recently, we didn't even know that this process has occurred throughout the evolution of life, and didn't know or care whether a crop was "naturally" transgenic!
GMO's
Both the scientific community and industry have done a terrible job at explaining genetic engineering to a distrustful public. There are clearly potential issues with genetic engineering, but they are being carefully addressed by independent scientists [4] and regulatory agencies, especially in Europe:
From the first generation of GM crops, two main areas of concern have emerged, namely risk to the environment and risk to human health.... Although it is now commonplace for the press to adopt 'health campaigns', the information they publish is often unreliable and unrepresentative of the available scientific evidence [5].
Jeffrey Smith, in his book "Seeds of Deception" [6] details a number of legitimate issues and early missteps in bioengineering, as well as pointing out the substantial political influence firms such as Monsanto have upon researchers, regulators, and legislators. We should be cautious to take their assurances with a grain of salt. On the other hand, I've checked the claims of other anti-GMO crusaders for factual accuracy, and found that many simply don't hold water. For example, two headlined studies of late, one on rats fed GE corn and Roundup herbicide, and another on the purported increased use of herbicides due to GE crops simply do not stand up to objective scrutiny [7]. It bothers me that the public is being misled by myths and exaggeration from both sides.
From my point of view, GE holds incredible promise and should be pursued in earnest, yet must also be very carefully monitored and regulated. In any case, GE crops have been widely adopted in U.S. agriculture (Table 1), and thus are now a part of beekeeping.
Table 1. The genetically engineered traits available to farmers have evolved rapidly as technology improves and as such crops become more widely adopted. Table from http://www.census.gov/compendia/statab/2012/tables/12s0834.pdf.
An Odd Series Of Connections
In 1972, the dean of biological sciences at my university hired me to set up a "world class insectary" (which I did). I raised mass quantities of insects for hormone extraction, in the hope that we might develop a new generation of eco-friendly insecticides [8]. Several years later I was shocked when Monsanto-a widely-despised chemical company with a sordid history- then hired him to create "a world-class molecular biology company" (which he apparently did). In 2002, Monsanto was spun off as an independent agricultural company.
Jump forward to 2010, when I had the good fortune to work with an Israeli startup--Beeologics--and witnessed the efficacy of their eco-friendly dsRNA antiviral product for honey bees. But to bring the product to market, they needed more backing. To my utter astonishment, they recently sold themselves to Monsanto!
The Vilifying Of Monsanto
These days one can simply mention the name "Monsanto" in many circles, and immediately hear a kneejerk chorus of hisses and boos. Sure, it had been easy for me to enjoy the camaraderie of riding the anti-Monsanto bandwagon; but I realized that that I shouldn't allow that sort of fun to substitute for the responsibility of doing my homework and getting to the actual facts of the matter! When I did so, I found that some of Monsanto's actions did indeed deserve opprobrium; but that much of the criticism directed at the current company is undeserved (Monsanto suffers from an ingenerate inability to practice effective PR). Concurrent with the purchase of Beeologics, Monsanto hired well-respected apiarist (and columnist) Jerry Hayes to head up a new honey bee health division, and appointed some prominent beekeepers (not me) to its advisory board. It dismays me that some beekeepers then immediately jump to the erroneous conclusion that Jerry has sold his soul to the Devil--nothing could be further from the truth!
What Are They Up To?
Some beekeepers imaginatively feared that Monsanto was about to create a GM bee or was up to some other nefarious plot. But in reality, Monsanto's vision of its future direction is anything but evil--I suggest that you peruse their website for your own edification [9], [10]. Of course I was curious as to why they had purchased Beeologics, since the market for bee medicine is far too tiny to draw the interest of a giant corporation. But one needn't be some sort of psychic in order to figure out a corporation's plans--all you need do is to read its recent patents, which are a virtual crystal ball for seeing ten years into the future. So I searched out any patents containing the words "Monsanto" and "RNAi."
To my great relief, I found that Monsanto was not up to some evil plot--far from it! I suggest you read two of the patents yourself [11]:
Chemical pesticidal agents are not selective and exert their effects on non-target fauna as well...Some chemical pesticidal agents have been shown to accumulate in food, and to exhibit adverse effects on workers that manufacture and apply such chemical agents. Thus there has been a long felt need for methods for controlling or eradicating... pest infestation on or in plants, i.e., methods which are selective, environmentally inert, non-persistent, biodegradable, and that fit well into pest resistance management schemes. Plant biotechnology provides a means to control pest infestations by providing plants that express one or more pest control agents. Recombinant pest control agents have generally been reported to be proteins selectively toxic to a target pest that are expressed by the cells of a recombinant plant.
What the patents tell us is that Monsanto clearly sees that the public is sick of pesticides. Genetic RNAi technology would allow plant breeders to develop crop cultivars that control insect pests in the same manner that the plants naturally control viruses. All that the breeder need do would be to identify a unique target protein in a particular pest, and then splice a gene into the plant to produce a "blocking" dsRNA molecule that would prevent the pest from building that specific protein. The beauty is that dsRNA molecules are already naturally found in plant tissues, the blocking molecule would be entirely specific for that pest alone, completely nontoxic to humans or other non target species, and be rapidly biodegradable. It would be a win all around (except for the pest)--crop protection, no toxic pesticides, and a sustainable farming technology (as well as a market for Monsanto's products, since they would need to continually develop slightly different cultivars in order to avoid pest resistance). Who'd have guessed that Monsanto would be leading the way toward developing eco-friendly pest control? Life is full of surprises!
Practicality Overrides Principle
Some folk make GM crops out to be some sort of abomination of nature, and shun them with religious fervor. I'm not sure that this is the best course for environmentalists to take, and that perhaps, in the face of an expanding human population and a warming climate, we should leave all the possible plant breeding solutions on the table. The organic farming community wholeheartedly endorses the biotechnology of "marker assisted selection" [12], yet arbitrarily draws the line at the directed insertion of desirable genes. This may sound like heresy, but as an environmentalist, I suggest that GE holds great promise for developing more nutritious plants that don't require pesticides, fertilizer, or irrigation--all of which would be wins for organic farming.
From a biological standpoint, I simply don't see GM crops as being any more inherently dangerous than conventionally bred crops. Our domestic plants today are often far from "natural"--you wouldn't recognize the ancestors of many. Be aware that even conventionally bred cultivars of several crops (beans, potatoes, celery, etc.) often turn out to be too toxic for humans.
This is not by any means a fluff piece for Monsanto or agribusiness. Farming is not what it used to be. In the U.S., 85% of farm sales are produced by less than 10% of farms, which hold 44% of farm acreage [13]. A mere six companies collectively control around half of the proprietary seed market, and three quarters of the global agrochemical market [14]. I abhor such corporate domination; neither do I see today's high-input agricultural practices as being either sustainable or ecologically wise.
That said, human demands upon the Earth's finite ecosystem are growing. There are only about 4.5 acres of biologically productive land on the surface of the Earth available for each current human inhabitant. Depending upon the culture's lifestyle, we use anywhere from 25 acres (U.S.) to as little as 1 acre (Bangladesh) to feed and clothe each person. Unfortunately for the bee (and many other species), due to human population growth there are over 200,000 additional human mouths to feed every single day--each requiring the conversion of another couple of acres of natural habitat into farmland!
It doesn't take a mathematician to figure out that if we wish to conserve natural ecosystems that we need to get more yield out of existing cropland! And one of the best ways to do that is to breed crops that are more productive and pest-resistant. The plant scientists in the corporate labs are making huge strides in developing such cultivars, both by GM and conventional breeding. If they manage to file a patent [15], so what?--other breeders can easily "steal" the germplasm away from the patented genes, and in any case, the patents expire after 20 years!
Monsanto has seen the writing on the wall--farmers and consumers are demanding not only more food production, but also more eco-friendly agricultural practices. Monsanto research is heading in that direction with their conventional breeding programs, the development of "biological" insecticides [16], and the goal of producing pesticide-free dsRNA crops. Add to that that the company could actually bring to market dsRNA medications against bee viruses, nosema, and perhaps varroa. All would be huge wins for the honey bee and beekeepers!
Hold The Hate Mail
Full disclosure: so despite my innate aversion to corporate dominance and corporate agriculture, I feel that we beekeepers should work with Monsanto to develop products for the beekeeping industry, as well as bee-friendly cultivars of crop plants, and have thus personally decided to be a cooperator in their initial bee research trial. Is this some sort of Faustian bargain? I don't know, but as a condition of my cooperation, I asked, and Monsanto agreed, to allow me to share the data collected with the beekeeping community--which could be a big win for us, since Monsanto has some of the best analytic labs in the world! I feel that it is far better to have Monsanto working on the side of beekeepers, rather than perhaps against us. At this point, I'd like to leave the GM debate behind, and address the facts of the matter as to any relationship between GM crops and CCD.
The Changing Face Of Agriculture
Genetic engineering has clearly changed the face of agriculture in the U.S. (Fig. 1).
Figure 1. These three crops account for over half of all U.S. acreage planted to principal crops, and all are worked to some extent by bees. Data from http://www.ers.usda.gov/data-products/adoption-of-genetically-engineered-crops-in-the-us.aspx
As can be seen from the figure above, any bees near corn, soy, or cotton are going to be exposed to pollen and nectar from GM plants, as well as to indirect effects due to the technology. So could GM crops be the cause of CCD?
Bt Crops
Biological plausibility: the insecticidal Bt toxins in GM corn and cotton pollen could harm adult or larval bees.
Organic farmers have long used the spores of the bacterium Bacillus thuringiensis (Bt) to kill caterpillars. Bt spores germinate in the caterpillar gut, and the bacterium produces insecticidal crystalline proteins (Cry proteins) that bind to specific receptors on the insect intestinal wall. Since different insect species have different receptors on their gut cells, different strains of Bt have evolved to specifically kill various caterpillars, beetles, mosquitoes, etc. [17]. The proteins are so species specific that wax moths can be controlled on combs by Bt aizawai, which produces Cry proteins that are toxic to moth larvae, but not to bees.
Molecular biologists tweak these Cry proteins to make them even more species specific, and then insert them into plant DNA, so that the plant then produces the proteins itself, thus making its tissues toxic to the target species. In order to delay the inevitable evolution of Cry-resistant pests, growers plant a percentage of "refuge" crop not containing the Cry genes. Even so, any particular Cry gene will only be effective for some number of years until resistant pests show up.
People have expressed concern about a poisonous substance being introduced into plant tissues, and to them I highly recommend the paper "Misconceptions about the Causes of Cancer" [18]. The reality is that plant tissues are naturally awash in poisonous substances. Plants have needed to repel herbivores throughout their evolution, and since plants can't run, hide, or bite back, they do it chemically. Many of our most popular fruits, nuts, grains, and vegetables (and especially herbs and spices) contain powerful phytotoxins. Their wild ancestors required cooking or leaching before the plant was edible to humans. Plant breeders systematically select for cultivars with lower levels of (the often strongly flavored) toxins.
Plants that are naturally resistant to pests contain more phytotoxins, often produced in response to damage from insects. For example, the sprouts of wheat, corn, and rye produce potent mutagens (enjoy that cup of wheatgrass juice!) [19]. And some plants naturally contain symbiotic bacteria and fungi in their tissues, which produce non-plant chemicals [20]. There is absolutely nothing biologically novel about insecticidal toxins in plant tissues.
The toxicity (or lack thereof) of Cry proteins to non-target organisms, especially upon two "charismatic" species--the honey bee and the monarch butterfly--has been well studied [21], [22], [23]. A recent and very well-designed experiment on the effect of GM Bt corn pollen upon the growth and survival of honey bee larvae was recently performed by a team of independently-funded German researchers [24]. They added pollen from four different sources to a standard semi-artificial larval diet.
Results: surprisingly, the larvae fed the pollen from the "stacked" GM corn containing a combination of three different Cry proteins exhibited a higher survival rate (100%), than those fed non-GM corn pollen! To me, a big plus for this study was that they also included a positive control of pollen from a wild plant said to be harmful to bees--only about 30% of those larvae survived! This finding confirmed that even some natural pollens are quite toxic, and that we should compare any toxicity trials of pesticides with those of the natural phytotoxins in nature.
Analysis: CCD and colony mortality occur even in the absence of GM Bt crops; feeding GM Bt pollen to adult bees or larvae does not cause observable adverse effects.
Verdict on Bt crops: The specific Bt cry proteins used in GM crops were intentionally chosen to not cause harm to bees. There is no evidence to date that they do. On the other hand, Bt crops require less use of insecticides that are clearly toxic to bees [25].
Roundup Ready
Monsanto's pitch is that Roundup Ready®️ (RR) crops allow farmers to practice weed-free "no till" farming, which saves both topsoil and money. The catch is that farmers must then douse their fields with Monsanto's flagship product, Roundup (ensuring sales of that herbicide--a great marketing strategy). Bayer CropScience has followed suit by introducing crops resistant to its Liberty herbicide, which has a different mode of action.
Herbicide-resistant crops do indeed address several major environmental problems:
No till farming does in fact require less labor and reduces soil compaction.
Farmers get greater production due to less competition from weeds.
No till also reduces the amount of petrochemical fuel involved in tillage.
No till greatly reduces soil erosion, which has long been a major environmental concern.
No till may help to sequester carbon in the soil, and to rebuild soil.
So what's not to love about Roundup Ready? There are a few main complaints--(1) the massive spraying of the active ingredient, glyphosate, for which there is questionable evidence that it may be an endocrine disruptor [26], (2) claims of intimidation by Monsanto of farmers who choose not to plant RR seed, and (3) the environmental impact and sustainability of the sort of weed-free monoculture possible with RR crops.
So how do Roundup and RR crops relate to honey bees?
Direct Effects Of Roundup Use
Biological plausibility: either the active ingredient (glyphosate), or the adjuvants could cause bee toxicity.
The EPA has thoroughly reviewed the research and found glyphosate to be practically nontoxic to bees (and humans). They have found the same for Roundup's adjuvant polyoxyethylene-alkylamine. However, some beekeepers tell me that they see increased bee mortality following the spraying of glyphosate (Fig. 3), but are not sure whether it was a generic product, or perhaps contained additional ingredients (surfactants, fungicides, or insecticides) added to the tank mix.
Figure 3. A farmer spraying glyphosate herbicide over Roundup Ready corn seedlings. Photo courtesy of beekeeper Larry Garrett.
Analysis: there is no strong evidence that the spraying of Roundup or generic glyphosate herbicide is directly causing significant bee mortality. However, Drs. Jim and Maryann Frazier have legitimate concerns about the effect of some adjuvants--especially the organosilicones [27], [28].
Indirect Effects Of Roundup Use
Biological plausibility: the elimination of weeds reduces bee forage.
The success of Roundup Ready technology has allowed farmers to largely eliminate weeds from their fields (at least until the inevitable resistant weeds take over). But they don't stop there--nowadays they practice "clean farming" and use herbicides to burn off every weed along the fencerows and in the ditches--the very places that bees formerly had their best foraging. This elimination of flowering weeds severely reduces the amount of available of bee forage, plus kills off the host plants of native pollinators (such as monarch butterflies) and beneficial insects.
European honey bees evolved in Europe (hence the name), and are adapted to the nutrition provided by Old World flowering plants. Many of the weeds in North America are old friends of the honey bee. On the other hand, honey bees were never exposed to corn, soybeans, sunflowers, or squashes until recently; neither corn nor sunflowers supply complete amino acid profiles in their respective pollens. Until the advent of Roundup Ready, the weeds in an around crops provided alternative nectar and pollen sources for bees; today there is often nary a bee-nutritious weed to be seen in or around a field of corn or soybeans (Fig. 4).
Figure 4. I took this photo of a no-till herbicide-resistant corn field, prior to the shading canopy of the crop closing over. Note the total lack of any sort of bee forage (or any species of anything other than corn). The soil surface is a far cry from the original densely vegetated prairie sod. Prior to RR, there was more weedy forage for bees, and especially from the traditional weed-controlling crop rotation into legumes or pasture.
Update: there's a great deal of debate about the safely of Roundup (the formulated product with it's surfactants) and its active ingredient, glyphosate. From http://npic.orst.edu/factsheets/archive/glyphotech.html
"In plants, glyphosate disrupts the shikimic acid pathway through inhibition of the enzyme 5-enolpyruvylshikimate-3-phosphate (EPSP) synthase. The resulting deficiency in EPSP production leads to reductions in aromatic amino acids that are vital for protein synthesis and plant growth.
As far as the claims that glyphosate causes cancer (notably Non-Hodgkin's Lymphoma), I agree with the regulatory agencies that the case against glyphosate is very weak. As far as glyphosate being an endocrine disruptor, I'll leave it to the researchers and regulatory agencies to figure it out. As I type these words, I've actually got caged bees to which I'm feeding glyphosate (at a field-realistic dose) for a trial, and not seeing increased mortality. But some research indicates that it may be harmful to the gut microbiota. This sort of research takes time, and eventually we'll figure out just how safe or harmful glyphosate is to bees, humans, or the environment.
But nothing in nature is simple. Eliminating the competition of weeds and insects may allow plants to hold back from the production of natural toxins. And a surprising piece of research found corn kernels from plants sprayed with either of two different herbicides actually contain more of the healthful carotenoids [30]!
The Future Of Roundup
It took Monsanto several years to genetically engineer Roundup-resistant crops, yet took farmers only slightly longer to inadvertently produce Roundup-resistant weeds by the conventional breeding technique of applying a strong selective pressure-the continuous application of Roundup!
Weed management scientists consider glyphosate to be a once-in-a-100-year discovery--it works on 140 species of weeds, and is relatively environmentally friendly. However, its overuse has led to the creation of several "driver weeds" that could soon lead to its redundancy in corn, soy, and cotton acreage [31]. This will drive farmers to turn to other herbicides (which will also in time fail). We can only hope that someday they will be forced back into practicing crop rotation into legumes and pasture.
Reality Check
In order to clarify cause and effect, I often seek out extreme cases. Such would be the situation in the Corn Belt, where I could compare the USDA's hive and honey data from the old days to those under today's intense planting of GM crops (Fig. 5)!
Figure 5. The most intense planting of GM crops is in Iowa and Illinois (the dark green areas of the map above). U.S. farmers planted nearly 100 million acres of corn this year, and 76 million of soy. That is enough acreage to cover the entire state of Texas with GM crops!. Source: http://www.nass.usda.gov/Charts_and_Maps/Crops_County/pdf/CR-PL10-RGBChor.pdf
So I went through the tedious process of downloading and transcribing the NASS agricultural census figures for Iowa. I entered the amount of corn acreage, the total number of colonies in the state, and what I consider to be the best measure of colony health--honey yield per hive (which of course is largely weather dependent, but should show any trends). I plotted the data below (Fig. 6):
Figure 6. Bee and corn data from Iowa, and the dates of introduction of corn pest control technologies. The dotted line is median honey yield per colony. No factor appears to have affected honey production, but colony numbers have decreased since the arrival of varroa. Gaps are missing data. Source NASS.
Note: for non beekeepers, varroa is a parasitic mite that arrived in the U.S. around 1990 and quickly became, and still remains, the Number One problem in bee health-far more than any other factor.
Over the years, corn acreage increased by 18%. Other than the prodigious crop of 1988, honey production has averaged around 67 lbs per hive. The thing that stands out is the plot of number of colonies. Hive numbers jumped up in the late 1980's, likely due to federal honey price support payments, which peaked in 1988, and were cut off in 1994 [[i]]. Colony numbers peaked in 1990, the same year that varroa arrived in Ohio, and went down from there, leveling off to about half the number of hives present in the 1970's.
I fully expected honey yields to decrease concurrent with the adoption of Roundup Ready varieties, but they didn't! Colonies still produce as much honey today as they did in the past, but this might be partially due to having fewer bees working the same amount of land, or to increased soybean nectar (which saved a number of Midwestern beekeepers from disaster during this year's droughts).
Perhaps even more surprising is the fact that in a state covered in corn and soy, colony productivity did not appear to be affected by the introductions of either Bt or Roundup Ready corn, nor by the universal use of neonicotinoid seed treatments (between corn and soy, on over roughly two thirds of the entire state land area). Note that honey yields actually increased for a few years following the introduction of clothianidin seed treatment!
Tellingly, hive numbers started to decrease after the arrival of varroa, and plummeted in the late 1990's as fluvalinate failed as a miticide, and many beekeepers simply threw up their hands and quit the business.
Verdict on herbicide tolerant crops: from a nutritional standpoint, the increased use of herbicides, and the associated weed free "clean farming" has certainly not helped the bees in corn/soy areas, but it is hard to make a case for them causing colony collapse.
Verdict on GM crops in general: Allow me to quote from the USDA:
...there is no correlation between where GM crops are planted and the pattern of CCD incidents. Also, GM crops have been widely planted since the late 1990s, but CCD did not appear until 2006. In addition, CCD has been reported in countries that do not allow GM crops to be planted, such as
Switzerland [33].
Looking Ahead: The Chemical Treadmill & Pest Resistance
It is interesting to observe the evolution of agriculture from the perspective of a biologist. Simple systems in nature are inherently less stable than complex systems. The current agricultural model in the U.S. exemplifies simplicity to the extreme--plant a single species into bare soil year after year, killing any competitive weeds or insects with pesticides (either sprayed, systemic, or engineered into the plants), and attempt to maintain fertility by adding energy-costly fertilizer. From a biological perspective, such a strategy is little more than an intense selective breeding program for the most resistant pests, and doomed to escalating chemical and energy inputs until the system collapses under its own weight.
I'm anything but a salesman for either Bt nor RR crops. Both are mere short-term solutions--resistant bugs and weeds are already starting to spread. I also have questions about the benefits of herbicide-intense no till planting [34], and hope that farmers return to alternative methods of weed control [35]. Luckily, the system will likely be self correcting, eventually forcing humanity to practice more sustainable methods of farming the land. However, I suggest that those methods may well include the wise use of biotechnology.
Additional Discussion
The Back Story On Plant Breeding And GM Crops
Traditionally, farmers simply replanted with the seeds from the most desirable individual plants year after year; this is the simplest form of "selective breeding." For example, all the various cole crops (cabbage, kale, broccoli, cauliflower, kohlrabi, Brussels sprouts) were developed by intentionally selecting for unusual forms of the species (resulting from random recombination of the natural allelic diversity, spontaneous mutants, or natural hybrids). This sort of selective breeding tends to result in a diverse assembly of locally-adapted cultivars. In Oaxaca, Mexico- the birthplace of corn-some 150 traditional varieties of maize are grown without pesticides or herbicides, thereby maintaining an invaluable reservoir of genetically-diversity "germplasm," which breeders can then cross and backcross in order to develop new cultivars (e.g., for pest or drought resistance).
In the early years of the U.S., seeds from desirable cultivars were distributed to farmers by the government, and plant breeding was performed at universities and at the USDA [36]. But since every strain breeds true, a farmer could save the seed and replant, leaving little opportunity for seed companies to make a buck. So in 1883, they formed the American Seed Trade Association and began to lobby for the cessation of the government programs.
The Profit Motive
In the early part of the 20th century, the companies began to promote hybrids-- crosses of two (or more) different strains or species that exhibited some sort of "hybrid vigor"--offering greater production, tastier fruit, or some other desirable characteristic. Hybrids were a godsend to the companies, since they are often sterile or don't breed true, meaning that farmers needed to purchase (rather than save) seed each season.
The seed lobby eventually shifted public funding away from the free distribution of selected seedstocks to instead encouraging the USDA and universities to develop inbred parental lines and breeding stock that the seed trade could then use to create proprietary hybrid varieties. By 1960, farmers planted less than 5% of corn from saved seed; and less than 10% of soybeans by 2001. As on-farm familiarity with the saving of seed was forgotten, farmers became willing consumers of produced seed.
Enter GM Crops
Then in 1980, the Supreme Court decided that seed companies could patent new varieties if they contained distinct and novel genetic markers. This meant that farmers (in some countries) could now be required to sign licensing agreements to allow them to use the patented seed each season [37] (there is a hodge-podge of international patent laws in this regard [38]).
The Second "Green Revolution"
The first "green revolution" was based upon fertilizer, pesticides, and hybrid seed (and also resulted in forcing farmers onto "agricultural treadmills"-making them less self sufficient and sustainable, and more reliant upon purchased seed, pesticide and fertilizer use, and upon borrowed money).
In 1950 the Secretary of Agriculture Ezra Benson said to farmers, "Get big or get out." His 1970s successor, Earl Butts, repeated that message, and exhorted farmers to "plant fence row to fence row" and to "adapt or die." Politicians who understood that a well-fed electorate is a happy electorate promoted policies that resulted in the destruction of the small family farm. Our policy of price supports and favorable treatment of agribusiness has changed the face of the American farm and the composition of the American diet [39].
Today's "second green revolution" is based upon technological advances in plant genetics (including GM) and the (at least partial) replacement of nasty pesticides with "biologicals." As an environmentalist, I find the new revolution to be more promising for ecological sustainability, but it is not without its downside--the current consolidation of agribusiness. As I mentioned before, farms, seed companies, and chemical companies are all being bought up by a few main players. Philip Howard details this consolidation in a free download [40], from which I quote:
This consolidation is associated with a number of impacts that constrain the opportunities for renewable agriculture. Some of these include declining rates of saving and replanting seeds, as firms successfully convince a growing percentage of farmers to purchase their products year after year; a shift in both public and private research toward the most profitable proprietary crops and varieties, but away from the improvement of varieties that farmers can easily replant; and a reduction in seed diversity, as remaining firms eliminate less profitable lines from newly acquired subsidiaries.
He then speaks of the concept of the "treadmill":
For the majority of farmers, however, the result is that they must constantly increase yields in order to simply maintain the same revenue. [Monsanto's sales pitch is that economic success in farming is driven by yield per acre [41]. Those that are unable to keep up with this treadmill will "fall off," or exit farming altogether. Their land ends up being "cannibalized" by remaining farmers who seek to increase scale of production as another means of keeping up with the treadmill, leading to the increasing centralization of agriculture. Farmers who have managed to stay in business have adapted to this process, and are typically on the leading edge of the adoption of new technologies. As a result, they have a high degree of confidence in science and technological innovations.
However, this problem has nothing to do with GMO's, but is rather due to the public's unknowing acceptance of the practice. Capitalism inevitably leads to consolidation unless consumers stop supporting corporate agribusiness with their pocketbooks and their votes, and start demanding that their government enforce antitrust efforts and better support small farmers.
But we are allowing economics and politics to distract us from the topic at hand--the technology of genetic engineering in plant breeding.
Cautions About GM
The most vocal critic of genetic modification is Jeffrey Smith, fear-mongering author of Seeds of Deception, producer of the film Genetic Roulette, and executive director of the inappropriately-named Institute for Responsible Technology. Smith is a gifted and effective communicator, as well as being a practitioner of "yogic flying" [42]. I will be the first to say that Smith's anti-GMO claims [43] would scare the pants off of anyone, and make for compelling story! The problem is that he plays loose with the facts--most of his claims simply do not stand up to any sort of scientific scrutiny. I suggest that for an objective analysis of the facts, that you visit AcademicsReviewed.org, a website that tests popular claims against peer-reviewed science. They address each of Smith's alarming "facts" one by one [44]. It is a thrilling ride to open the two web pages side by side, first being shocked by Smith's wild and scary claims, and then reading the factual rebuttal to each! The thing that most bothers me about Smith's writing is that he treats GM cultivars generically, rather than specifically addressing the merits or concerns for them individually. This makes little sense, since any conventional crop has cultivars that cause human allergy or contain excessive levels of natural toxins, yet no one calls for the testing of each of them!
Perspectives On GM Crops
As you may have guessed by now, to me, the GM debate should not be about being pro or con, rather it should be about the intelligent discussion of reconciling its promise with its problems. The GE genie is out of the bottle, and I can't see that anyone is going to put it back in-so we might as well work with it! So let's cut through the hype and hysteria, the fears and judgments, and try to objectively look at the facts of the matter:
From a plant breeder standpoint, genetic engineering holds incredible promise for the development of crops that could be tremendously beneficial to humans or the environment. For example, "Transgenic cotton has reduced the need for conventional insecticides used against lepidopteran [pests] an average in the USA about 59.4% [and] Texas 74.7%...an average number of pesticide applications in conventional cotton has fallen from 4.3 in 1995 to 2.1 in the USA... with benefits to human health and the environment" [45].
GM is only a part of plant breeding--most advances continue to be in conventional breeding, now assisted by "marker assisted selection," which is embraced by environmentalists [46].
However, someone needs to pay for the research, and the taxpayer is not doing it! For a thoughtful discussion of the benefits of gene patents, see [47].
Novel genetic markers can be patented, and a licensing fee can be charged, despite the fact that they are not GM!
From a consumer standpoint, advanced breeding techniques can result in cheaper and more nutritious food, and less environmental impact from farming.
Consumers have erroneously been led to believe that GM crops are dangerous to their health, and call for application of the precautionary principle. My gosh, please read "Misconceptions about the causes of cancer" [48]. Few foods are entirely "safe"! And "safety" can never be proven--it can only be disproven. And no studies have ever disproven the safety of GM crops, nor have doctors noticed anyone ever getting sick from them, despite our eating them for 15 years!
In truth, some scientists argue that plants produced by classical breeding methods should undergo the same safety testing regime as genetically modified plants. There have been plenty of instances where plants bred using classical techniques have been unsuitable for human consumption, causing toxicity or allergic reactions.
Those that speak of applying the "precautionary principle" should read Jon Entine's trenchant analysis of the fallacy of overapplication of that principle [49]. In truth, our regulators (EPA and FDA) vigorously apply the precautionary principle in the form "reasonable certainty of no harm."
The benefits of seed biotechnology cannot be realized without good seed germplasm to start with. So a few large seed companies started buying up their competitors to acquire the most productive and desirable varieties.
The downside of the above practice is that by 2008, 85% of GM maize patents and 70% of non-maize GM plant patents in the U.S. were owned by the top three seed companies: Monsanto, DuPont, and Syngenta [50]. Note that economists figure that when four firms control 40% of a market, it is no longer competitive; in the case of GE crops, the top four seed firms control 56% of the global proprietary seed market!
On the flip side, these profits are an incentive for the large corporations to invest in innovative plant breeding research--Monsanto spends about $2 million a day on this. This is important to keep in mind in an increasingly hungry world.
On the dark side, Monsanto's nearly $12 billion in annual sales allows the company to lobby regulators, influence universities, and spin the news. These are standard business practices for any large corporation, but hardly make Monsanto uniquely evil.
Be aware that patented genes are of use only if inserted into high-producing cultivars-which are developed by conventional breeding (which constitutes nearly half of Monsanto's plant breeding budget). These desirable cultivars have no patent protection. Monsanto uses a non GE technology called SMART = Selection with Markers and Advanced Reproductive Technologies. SMART technology is warmly embraced by environmental groups [51].
Adding a genetic marker allows a company to identify its proprietary strains, like putting a nametag on a dog. But clever breeders can back engineer the desirable germplasm out from patent protection.
And remember that patents expire after 20 years. The patents for Roundup Ready soybeans expire in 2014--at which time farmers, universities, and seed companies will then be free to propagate and sell the variety [52]. Patents are granted in order to spur innovation; by filing for patent protection, a company must make its discoveries public knowledge. This is a good thing.
Monsanto invests 44% of its R&D on conventional (as opposed to GM breeding).
Monsanto has also given rights to some of their patented crops to poorer countries, and recently donated a database of some 4000 genetic markers from cotton to Texas A&M [53]. The university plant breeders are excited in that the information will assist them in their conventional (non-GM) breeding of cotton, to the benefit of the environment [54 ].
From the farmer's standpoint, he has the choice of purchasing GE varieties that may be more productive, reduce insecticide use, or reduce tillage costs [55]. Keep in mind that there is nothing keeping him from purchasing "conventional" non-GM seed--it is available (I checked, and it sells at about half the cost of GM seed). In our free enterprise system there is nothing to keep non-GM seed companies from selling an alternative product if there is a demand. Farmers who are unimpressed by GM varieties freely switch back to conventional seed.
From an agricultural standpoint, the widespread adoption of a few favored crop varieties (GM or not) can result in the irreplaceable loss of crop genetic diversity--this is of great concern to plant breeders. If you haven't yet seen the graphic of our loss of crop genetic diversity from National Geographic magazine, you should! [56]. Luckily, this does not appear to be occurring yet with maize in Oaxaca [57], but there is a legitimate concern that economics will force traditional farmers out of business, leading to the loss of heirloom varieties. However, this is not a GM issue, but rather an effect of consolidation.
From a sustainability standpoint, there is nothing to prevent constant breeding innovation to keep pace with pest evolution. Genetically engineered crops can play a role in sustainable farming as our agricultural practices begin to shift to more ecologically sustainable methods.
One should keep in mind how the simple splicing of a virus gene into the papaya saved the Hawaiian papaya growers from the ravages of ringspot virus--the GE papaya is the mainstay of the industry, and by virtue of keeping the virus in check actually allows nearby organic papayas to thrive. Yet ecoterrorists recently hacked down thousands of GM trees [58]. It's interesting to read the history of "Golden Rice" [59] to see how the anti-GMO lobby is specifically scared that the success of such a lifesaving crop might open the door for acceptance of other GM plants!
Update Jan 2013
News item: Leading Environmental Activist's Blunt Confession: I Was Completely Wrong To Oppose GMOs. Blog in Slate Magazine
"If you fear genetically modified food, you may have Mark Lynas to thank. By his own reckoning, British environmentalist helped spur the anti-GMO movement in the mid-'90s, arguing as recently at 2008 that big corporations' selfish greed would threaten the health of both people and the Earth. Thanks to the efforts of Lynas and people like him, governments around the world--especially in Western Europe, Asia, and Africa--have hobbled GM research, and NGOs like Greenpeace have spurned donations of genetically modified foods.
But Lynas has changed his mind--and he's not being quiet about it. On Thursday at the Oxford Farming Conference, Lynas delivered a blunt address: He got GMOs wrong."
Anyone opposed to GMO's should read Mr. Lynas' well thought out address: http://www.marklynas.org/2013/01/lecture-to-oxford-farming-conference-3-january-2013/
Update May 2014
I've compiled a list of recent worthwhile reading on the "other side" of the GMO debate at https://scientificbeekeeping.com/gmo-updates/
So What's The Problem?
The problem is that anti-GMO advocacy groups are determined to put a stop to all GE technology. They targeted California with Prop 37, which applied only to packaged foods and produce. A more cynical take on Prop 37 was that it was all about marketing: "If your produce is no different in terms of taste, safety and nutrition from a competitor, and costs more, apparently the only marketing option is to create a negative image of your competitor's product" [60].
If Prop 37 had been successful, the promoters would then have targeted restaurants, the meat and dairy industry, and the beverage industry. I personally feel that this is an extreme position, what with the human population growing hungrier every day, and climate change threatening agriculture worldwide with heat, drought, pestilence, and salinity problems. Not only that, but GM crops hold promise for cheap omega-3 fatty acids (so that we don't have to harvest fish for them), cost-effective biofuels, and less expensive pharmaceuticals.
A good blog on the problem with the anti-GMO fear campaign can be found at [61], from which I quote:
It would be bad enough if something like the Seralini study simply contributed to the unnecessary angst amongst consumers around the world. It also has very real political, economic and practical effects. For instance brand conscious food companies have used their leverage to prevent the development of GMO versions of potatoes, bananas, coffee and other crops because they fear controversy. Apple growers worried about the market response are opposing the introduction of a non-browning apple even though it was developed by one of their own fruit companies. French activists destroyed a government-run field trial of a virus-resistant root stock which could have made it possible to produce good wine on sites that have become useless because of contamination with sting nematodes and the virus they vector. California voters have the potential to pass a seriously flawed "GMO labeling" initiative next month that could only serve the purposes of the lawyers and "natural products" marketers who created it. More importantly, European and Japanese importers of wheat essentially blackmailed the North American wheat producers into blocking biotech wheat development because those companies were nervous about consumer response in countries where GMO angst is so high. This has delayed by decades not only specific desirable trait development, but also what might have been an enormous private investment in a crop that is critically important for feeding a lot more people than just those in those rich countries. There is a huge cost of "precaution" based on poor science.
I believe that people should be well informed before taking a stance on important issues. I'd like to suggest one last excellent blog by an independent U.C. Berkeley evolutionary biologist and medical researcher:"How Bt Corn and Roundup Ready Soy Work - And Why They Should Not Scare You [62].
Acknowledgements
As always, thanks to my friend and collaborator in research Peter Loring Borst, and to anyone who still reads my articles after finding out that I've collaborated with Monsanto!
References
[1] Key S, et al (2008) Genetically modified plants and human health. J R Soc Med.101(6):290-298. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2408621/
[2] For example: Antoniou, M, et al (2012) GMO myths and truths.
(Broken Link!) http://earthopensource.org/files/pdfs/GMO_Myths_and_Truths/GMO_Myths_and_Truths_1.3.pdf
[3] Chiba S, et al. (2011) Widespread endogenization of genome sequences of non-retroviral RNA viruses into plant genomes. PLoS Pathog 7(7): e1002146.
[4] Domingo, JL and JG Bordonaba (2011) A literature review on the safety assessment of genetically modified plants. Environment International 37: 734-742.
[5] Key (2008) op. cit.
[6] Smith, JM (2003) Seeds of Deception. Yes! Books
[7] Seralini, GE, et al (2012) Long term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize. Food and Chemical Toxicology (2012) http://foodpoisoningbulletin.com/wp-content/uploads/Toxicity-of-Roundup-Ready-Maize.pdf;
Reviews
http://www.forbes.com/sites/henrymiller/2012/09/25/scientists-smell-a-rat-in-fraudulent-genetic-engineering-study/2/
http://www.efsa.europa.eu/en/faqs/faqseralini.htm#9, http://www.emilywillinghamphd.com/2012/09/was-it-gmos-or-bpa-that-did-in-those.html,
(Broken Link!) http://www.ask-force.org/web/Seralini/Anonymous-Rat-List-Spaying-2003.pdfs, http://storify.com/vJayByrne/was-seralini-gmo-study-designed-to-generate-negati;
Benbrook, CM (2012) Impacts of genetically engineered crops on pesticide use in the U.S. -- the first sixteen years. Environmental Sciences Europe 24:24 http://www.enveurope.com/content/pdf/2190-4715-24-24.pdf,
Review http://weedcontrolfreaks.com/2012/10/do-genetically-engineered-crops-really-increase-herbicide-use/#more-432
[8] http://journals.tubitak.gov.tr/agriculture/issues/tar-04-28-6/tar-28-6-1-0309-5.pdf
[9] http://www.monsanto.com/whoweare/Pages/monsanto-history.aspx
[10] http://www.businessweek.com/stories/2010-01-10/monsanto-v-dot-food-inc-dot-over-how-to-feed-the-world
[11] Methods for genetic control of plant pest infestation and compositions thereof
http://www.freepatentsonline.com/8088976.html
http://www.freepatentsonline.com/7943819.html
[12] http://www.greenpeace.org/australia/PageFiles/348427/smart-breeding.pdf
[13] 2007 figures http://www.census.gov/compendia/statab/2012/tables/12s0835.pdf
[14] ETC Group (2008) Who owns nature? Corporate power and the final frontier in the commodification of life. http://www.etcgroup.org/sites/www.etcgroup.org/files/publication/707/01/etc_won_report_final_color.pdf
[15] Blakeney, M (2011) Trends in intellectual property rights relating to genetic resources for food and agriculture. http://www.fao.org/docrep/meeting/022/mb684e.pdf This document covers the hodge-podge of international patent laws regarding plants and animals.
[16] http://www.monsanto.com/products/Pages/biodirect-ag-biologicals.aspx
[17] History of Bt http://www.bt.ucsd.edu/bt_history.html
Mode of action http://www.bt.ucsd.edu/how_bt_work.html
[18] Gold 2002 Misconceptions about the causes of cancer http://potency.berkeley.edu/pdfs/Gold_Misconceptions.pdf A "MUST READ"!
[19] Buchmann CA, et al (2007) Dihydroxy-7-methoxy-1,4-benzoxazin-3-one (DIMBOA) and 2,4-dihydroxy-1,4-benzoxazin-3-one (DIBOA), two naturally occurring benzoxazinones contained in sprouts of Gramineae are potent aneugens in human-derived liver cells (HepG2). Cancer Lett. 246 (1-2):290-9.
[20] http://en.wikipedia.org/wiki/Endophyte
[21] Duan JJ, et al (2008) A meta-analysis of effects of Bt crops on honey bees (Hymenoptera: Apidae). PLoS ONE 3(1): e1415.
[22] Center for Environmental Risk Assessment (2011) A review of the environmental safety of the Cry1Ab protein. http://cera-gmc.org/docs/cera_publications/cry1ab_en.pdf
[23] Han, P, et al (2012) Does transgenic Cry1Ac + CpTI cotton pollen affect hypopharyngeal gland development and midgut proteolytic enzyme activity in the honey bee Apis mellifera L. (Hymenoptera, Apidae)? Ecotoxicology. 2012 Aug 7. [Epub ahead of print]
[24] Hendriksma HP, et al (2011) Testing pollen of single and stacked insect-resistant bt-maize on in vitro reared honey bee larvae. PLoS ONE 6(12): e28174.
[25] Benbrook, CM (2012) op. cit.
[26] Reviewed in http://www.sourcewatch.org/index.php/Glyphosate
[27] Mullin, C.A., J.L. Frazier, M.T. Frazier & T.J. Ciarlo - A primer on pesticide formulation 'inerts' and honey bees. http://www.extension.org/pages/58650/proceedings-of-the-american-bee-research-conference-2011
[28] Ciarlo TJ, CA Mullin, JL Frazier, DR Schmehl (2012) Learning impairment in honey bees caused by agricultural spray adjuvants. PLoS ONE 7(7): e40848.
[29] Johal, GS and DM Huber (2009) Glyphosate effects on diseases of plants. Europ. J. Agronomy 31: 144-152. http://www.organicconsumers.org/documents/huber-glyphosates-2009.pdf
Huber, DM (2010) Ag chemical and crop nutrient interactions - current update. http://www.calciumproducts.com/dealer_resources/Huber.pdf
Reviewed in (Broken Link!) http://www.weeds.iastate.edu/mgmt/2010/glyMndisease.pdf
[30] Kopsell et al. (2009) increase in nutritionally important sweet corn kernel carotenoids following mesotrione and atrazine applications. Journal of Agricultural and Food Chemistry 090619124509017 DOI: 10.1021/jf9013313
[31] Laws, F (2010) http://cornandsoybeandigest.com/issues/will-glyphosate-fall-wayside-resistance-grows
[32] http://www.nationalaglawcenter.org/assets/crs/RS20759.pdf
[33] http://www.ars.usda.gov/is/AR/archive/jul12/July2012.pdf
[34] http://www.misereor.org/fileadmin/redaktion/MISEREOR_no%20till.pdf
[35] http://www.acresusa.com/toolbox/reprints/Organic%20weed%20control_aug02.pdf
[36] http://www.seedalliance.org/Seed_News/SeminisMonsanto/
[37] (Broken Link!) http://earthopensource.org/files/pdfs/GMO_Myths_and_Truths/GMO_Myths_and_Truths_1.3a.pdf
[38] Blakeney, M (2011) Trends in intellectual property rights relating to genetic resources for food and agriculture. http://www.fao.org/docrep/meeting/022/mb684e.pdf This document covers the debate involved in international patent law regarding plants and animals.
[39] Philpott, T (2008) A reflection on the lasting legacy of 1970s USDA Secretary Earl Butz. http://grist.org/article/the-butz-stops-here/; but for a contrary view by an actual corn farmer, read Hurst, B (2010) No Butz About It. (Broken Link!) http://www.american.com/archive/2010/july/no-butz-about-it
[40] Howard, Philip H. 2009. Visualizing consolidation in the global seed industry: 1996-2008. Sustainability, 1(4), 1266-1287. http://www.mdpi.com/2071-1050/1/4/1266/pdf
[41] http://www.monsanto.com/investors/Documents/Whistle%20Stop%20Tour%20VI%20-%20Aug%202012/WST-Fraley_RD_Update.pdf
[42] http://academicsreview.org/reviewed-individuals/jeffrey-smith/
[43] http://responsibletechnology.org/docs/145.pdf
[44] http://academicsreview.org/reviewed-content/genetic-roulette/
[45] Greenberg, S, et al (2012) Economic and Environmental Impact Transgenically Modified Cotton Comparative with Synthetic Chemicals for Insect Control. Journal of Agricultural Science and Technology B 2 750-757.
[46] Greenpeace (2009) Smart Breeding. Marker-Assisted Selection: A non-invasive biotechnology alternative to genetic engineering of plant varieties. http://www.greenpeace.org/australia/PageFiles/348427/smart-breeding.pdf
[47] http://www.genengnews.com/gen-articles/in-defense-of-gene-patenting/2052/
[48] Gold 2002 Misconceptions about the causes of cancer http://potency.berkeley.edu/pdfs/Gold_Misconceptions.pdf
[49] Entine, J (2010) Crop Chemophobia: Will Precaution Kill the Green Revolution? http://www.jonentine.com/pdf/CROPCHEMOPHOBIApre-orderform.pdf
[50] Howard, Philip H. 2009. Visualizing consolidation in the global seed industry: 1996-2008. Sustainability, 1(4), 1266-1287. http://www.mdpi.com/2071-1050/1/4/1266/pdf
[51] http://www.greenpeace.org/australia/PageFiles/348427/smart-breeding.pdf
[52] http://www.monsanto.com/newsviews/Pages/roundup-ready-patent-expiration.aspx;
[53] http://www.cotton247.com/article/3401/monsanto-donates-marker-technology
[54] http://www.youtube.com/watch?v=dcZyFH_eITQ
[55] http://www.biofortified.org/2012/05/the-frustrating-lot-of-the-american-sweet-corn-grower/#more-8670
[56] http://ngm.nationalgeographic.com/2011/07/food-ark/food-variety-graphic If you didn't see this graphic in National Geographic, you should!
[57] (Broken Link!) http://researchnews.osu.edu/archive/mexmaize.htm
[58] http://www.huffingtonpost.com/2011/08/20/genetically-modified-papayas-attacked_n_932152.html
[59] http://en.wikipedia.org/wiki/Golden_rice
[60] http://westernfarmpress.com/blog/proposition-37-gone-probably-not-forgotten?
[61] http://appliedmythology.blogspot.com/2012/10/can-damage-from-agenda-driven-junk.html?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+AppliedMythology+%28Applied+Mythology%29
[62] http://www.science20.com/michael_eisen/how_bt_corn_and_roundup_ready_soy_work_and_why_they_should_not_scare_you
Category: Colony Health - Diseases, Viruses, CCD
Tags: collapse, colony, genetically, gm crops, gmo, modified, plants, sick bees | gm crops Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/gm-crops/ |
Sick Bees - Part 18E: Colony Collapse Revisited - Genetically Modified Plants
First published in: ABJ December 2012
Genetically Modified Plants
What Is Genetic Modification?
There's Nothing New About Transgenics
GMOs
An Odd Series of Connections
The Vilifying of Monsanto
What Are They Up To?
Practicality Overrides Principle
Hold the Hate Mail
The Changing Face of Agriculture
Bt Crops
Roundup Ready
Direct Effects of Roundup Use
Indirect Effects of Roundup Use
The Future of Roundup
Reality Check
Looking Ahead: The Chemical Treadmill & Pest Resistance
Additional Discussion
The Back Story on Plant Breeding and GM Crops
The Profit Motive
Enter GM Crops
The Second "Green Revolution"
Cautions About GM
Perspectives on GM
So What's The Problem?
Acknowledgements
References
Sick Bees - Part 18E:
Colony Collapse Revisited - Genetically Modified Plants
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in Dec 2012
Genetically modified (or GM) plants have attracted a large amount of media attention in recent years and continue to do so. Despite this, the general public remains largely unaware of what a GM plant actually is or what advantages and disadvantages the technology has to offer, particularly with regard to the range of applications for which they can be used [1].
The above quote is certainly an understatement! Genetically Modified Organisms (GMO's) are a highly contentious topic these days, and blamed by some for the demise of bees. In researching the subject, I found the public discussion to be highly polarized--plant breeders and farmers are largely enthusiastic (with appropriate reservations) about the benefits of genetic engineering, whereas health and environmental advocacy groups tend to be fearful of the new technology [2]. I will largely save my review of the history and pros and cons of GM crops for my website, and focus this article upon how GMO's relate to honey bee health.
What Is Genetic Modification?
The knowledge of genetics was not applied to plant breeding until the 1920's; up 'til then breeders would blindly cross promising cultivars and hope for the best. With today's genetic engineering, breeders can now take a gene from one plant (or animal, fungus, or bacterium) and splice it into the DNA of another plant. If they get it just right, the new gene can confer resistance to frost, drought, pests, salinity, or disease. Or it could make the crop more nutritious, more flavorful, etc. Such genetically modified crops are also called "transgenic," "recombinant," "genetically engineered," or "bioengineered."
There's Nothing New About Transgenics
There is nothing new about transgenic organisms, in fact you (yes you) are one. Viruses regularly swap genes among unrelated organisms via a process called "horizontal gene transfer" [3]. For example, the gene which is responsible for the formation of the mammalian placenta was not originally a mammal gene--it was inserted into our distant ancestors by a virus. If a gene introduced by a virus confers a fitness advantage to the recipient, then that gene may eventually be propagated throughout that species' population. Until recently, we didn't even know that this process has occurred throughout the evolution of life, and didn't know or care whether a crop was "naturally" transgenic!
GMO's
Both the scientific community and industry have done a terrible job at explaining genetic engineering to a distrustful public. There are clearly potential issues with genetic engineering, but they are being carefully addressed by independent scientists [4] and regulatory agencies, especially in Europe:
From the first generation of GM crops, two main areas of concern have emerged, namely risk to the environment and risk to human health.... Although it is now commonplace for the press to adopt 'health campaigns', the information they publish is often unreliable and unrepresentative of the available scientific evidence [5].
Jeffrey Smith, in his book "Seeds of Deception" [6] details a number of legitimate issues and early missteps in bioengineering, as well as pointing out the substantial political influence firms such as Monsanto have upon researchers, regulators, and legislators. We should be cautious to take their assurances with a grain of salt. On the other hand, I've checked the claims of other anti-GMO crusaders for factual accuracy, and found that many simply don't hold water. For example, two headlined studies of late, one on rats fed GE corn and Roundup herbicide, and another on the purported increased use of herbicides due to GE crops simply do not stand up to objective scrutiny [7]. It bothers me that the public is being misled by myths and exaggeration from both sides.
From my point of view, GE holds incredible promise and should be pursued in earnest, yet must also be very carefully monitored and regulated. In any case, GE crops have been widely adopted in U.S. agriculture (Table 1), and thus are now a part of beekeeping.
Table 1. The genetically engineered traits available to farmers have evolved rapidly as technology improves and as such crops become more widely adopted. Table from http://www.census.gov/compendia/statab/2012/tables/12s0834.pdf.
An Odd Series Of Connections
In 1972, the dean of biological sciences at my university hired me to set up a "world class insectary" (which I did). I raised mass quantities of insects for hormone extraction, in the hope that we might develop a new generation of eco-friendly insecticides [8]. Several years later I was shocked when Monsanto-a widely-despised chemical company with a sordid history- then hired him to create "a world-class molecular biology company" (which he apparently did). In 2002, Monsanto was spun off as an independent agricultural company.
Jump forward to 2010, when I had the good fortune to work with an Israeli startup--Beeologics--and witnessed the efficacy of their eco-friendly dsRNA antiviral product for honey bees. But to bring the product to market, they needed more backing. To my utter astonishment, they recently sold themselves to Monsanto!
The Vilifying Of Monsanto
These days one can simply mention the name "Monsanto" in many circles, and immediately hear a kneejerk chorus of hisses and boos. Sure, it had been easy for me to enjoy the camaraderie of riding the anti-Monsanto bandwagon; but I realized that that I shouldn't allow that sort of fun to substitute for the responsibility of doing my homework and getting to the actual facts of the matter! When I did so, I found that some of Monsanto's actions did indeed deserve opprobrium; but that much of the criticism directed at the current company is undeserved (Monsanto suffers from an ingenerate inability to practice effective PR). Concurrent with the purchase of Beeologics, Monsanto hired well-respected apiarist (and columnist) Jerry Hayes to head up a new honey bee health division, and appointed some prominent beekeepers (not me) to its advisory board. It dismays me that some beekeepers then immediately jump to the erroneous conclusion that Jerry has sold his soul to the Devil--nothing could be further from the truth!
What Are They Up To?
Some beekeepers imaginatively feared that Monsanto was about to create a GM bee or was up to some other nefarious plot. But in reality, Monsanto's vision of its future direction is anything but evil--I suggest that you peruse their website for your own edification [9], [10]. Of course I was curious as to why they had purchased Beeologics, since the market for bee medicine is far too tiny to draw the interest of a giant corporation. But one needn't be some sort of psychic in order to figure out a corporation's plans--all you need do is to read its recent patents, which are a virtual crystal ball for seeing ten years into the future. So I searched out any patents containing the words "Monsanto" and "RNAi."
To my great relief, I found that Monsanto was not up to some evil plot--far from it! I suggest you read two of the patents yourself [11]:
Chemical pesticidal agents are not selective and exert their effects on non-target fauna as well...Some chemical pesticidal agents have been shown to accumulate in food, and to exhibit adverse effects on workers that manufacture and apply such chemical agents. Thus there has been a long felt need for methods for controlling or eradicating... pest infestation on or in plants, i.e., methods which are selective, environmentally inert, non-persistent, biodegradable, and that fit well into pest resistance management schemes. Plant biotechnology provides a means to control pest infestations by providing plants that express one or more pest control agents. Recombinant pest control agents have generally been reported to be proteins selectively toxic to a target pest that are expressed by the cells of a recombinant plant.
What the patents tell us is that Monsanto clearly sees that the public is sick of pesticides. Genetic RNAi technology would allow plant breeders to develop crop cultivars that control insect pests in the same manner that the plants naturally control viruses. All that the breeder need do would be to identify a unique target protein in a particular pest, and then splice a gene into the plant to produce a "blocking" dsRNA molecule that would prevent the pest from building that specific protein. The beauty is that dsRNA molecules are already naturally found in plant tissues, the blocking molecule would be entirely specific for that pest alone, completely nontoxic to humans or other non target species, and be rapidly biodegradable. It would be a win all around (except for the pest)--crop protection, no toxic pesticides, and a sustainable farming technology (as well as a market for Monsanto's products, since they would need to continually develop slightly different cultivars in order to avoid pest resistance). Who'd have guessed that Monsanto would be leading the way toward developing eco-friendly pest control? Life is full of surprises!
Practicality Overrides Principle
Some folk make GM crops out to be some sort of abomination of nature, and shun them with religious fervor. I'm not sure that this is the best course for environmentalists to take, and that perhaps, in the face of an expanding human population and a warming climate, we should leave all the possible plant breeding solutions on the table. The organic farming community wholeheartedly endorses the biotechnology of "marker assisted selection" [12], yet arbitrarily draws the line at the directed insertion of desirable genes. This may sound like heresy, but as an environmentalist, I suggest that GE holds great promise for developing more nutritious plants that don't require pesticides, fertilizer, or irrigation--all of which would be wins for organic farming.
From a biological standpoint, I simply don't see GM crops as being any more inherently dangerous than conventionally bred crops. Our domestic plants today are often far from "natural"--you wouldn't recognize the ancestors of many. Be aware that even conventionally bred cultivars of several crops (beans, potatoes, celery, etc.) often turn out to be too toxic for humans.
This is not by any means a fluff piece for Monsanto or agribusiness. Farming is not what it used to be. In the U.S., 85% of farm sales are produced by less than 10% of farms, which hold 44% of farm acreage [13]. A mere six companies collectively control around half of the proprietary seed market, and three quarters of the global agrochemical market [14]. I abhor such corporate domination; neither do I see today's high-input agricultural practices as being either sustainable or ecologically wise.
That said, human demands upon the Earth's finite ecosystem are growing. There are only about 4.5 acres of biologically productive land on the surface of the Earth available for each current human inhabitant. Depending upon the culture's lifestyle, we use anywhere from 25 acres (U.S.) to as little as 1 acre (Bangladesh) to feed and clothe each person. Unfortunately for the bee (and many other species), due to human population growth there are over 200,000 additional human mouths to feed every single day--each requiring the conversion of another couple of acres of natural habitat into farmland!
It doesn't take a mathematician to figure out that if we wish to conserve natural ecosystems that we need to get more yield out of existing cropland! And one of the best ways to do that is to breed crops that are more productive and pest-resistant. The plant scientists in the corporate labs are making huge strides in developing such cultivars, both by GM and conventional breeding. If they manage to file a patent [15], so what?--other breeders can easily "steal" the germplasm away from the patented genes, and in any case, the patents expire after 20 years!
Monsanto has seen the writing on the wall--farmers and consumers are demanding not only more food production, but also more eco-friendly agricultural practices. Monsanto research is heading in that direction with their conventional breeding programs, the development of "biological" insecticides [16], and the goal of producing pesticide-free dsRNA crops. Add to that that the company could actually bring to market dsRNA medications against bee viruses, nosema, and perhaps varroa. All would be huge wins for the honey bee and beekeepers!
Hold The Hate Mail
Full disclosure: so despite my innate aversion to corporate dominance and corporate agriculture, I feel that we beekeepers should work with Monsanto to develop products for the beekeeping industry, as well as bee-friendly cultivars of crop plants, and have thus personally decided to be a cooperator in their initial bee research trial. Is this some sort of Faustian bargain? I don't know, but as a condition of my cooperation, I asked, and Monsanto agreed, to allow me to share the data collected with the beekeeping community--which could be a big win for us, since Monsanto has some of the best analytic labs in the world! I feel that it is far better to have Monsanto working on the side of beekeepers, rather than perhaps against us. At this point, I'd like to leave the GM debate behind, and address the facts of the matter as to any relationship between GM crops and CCD.
The Changing Face Of Agriculture
Genetic engineering has clearly changed the face of agriculture in the U.S. (Fig. 1).
Figure 1. These three crops account for over half of all U.S. acreage planted to principal crops, and all are worked to some extent by bees. Data from http://www.ers.usda.gov/data-products/adoption-of-genetically-engineered-crops-in-the-us.aspx
As can be seen from the figure above, any bees near corn, soy, or cotton are going to be exposed to pollen and nectar from GM plants, as well as to indirect effects due to the technology. So could GM crops be the cause of CCD?
Bt Crops
Biological plausibility: the insecticidal Bt toxins in GM corn and cotton pollen could harm adult or larval bees.
Organic farmers have long used the spores of the bacterium Bacillus thuringiensis (Bt) to kill caterpillars. Bt spores germinate in the caterpillar gut, and the bacterium produces insecticidal crystalline proteins (Cry proteins) that bind to specific receptors on the insect intestinal wall. Since different insect species have different receptors on their gut cells, different strains of Bt have evolved to specifically kill various caterpillars, beetles, mosquitoes, etc. [17]. The proteins are so species specific that wax moths can be controlled on combs by Bt aizawai, which produces Cry proteins that are toxic to moth larvae, but not to bees.
Molecular biologists tweak these Cry proteins to make them even more species specific, and then insert them into plant DNA, so that the plant then produces the proteins itself, thus making its tissues toxic to the target species. In order to delay the inevitable evolution of Cry-resistant pests, growers plant a percentage of "refuge" crop not containing the Cry genes. Even so, any particular Cry gene will only be effective for some number of years until resistant pests show up.
People have expressed concern about a poisonous substance being introduced into plant tissues, and to them I highly recommend the paper "Misconceptions about the Causes of Cancer" [18]. The reality is that plant tissues are naturally awash in poisonous substances. Plants have needed to repel herbivores throughout their evolution, and since plants can't run, hide, or bite back, they do it chemically. Many of our most popular fruits, nuts, grains, and vegetables (and especially herbs and spices) contain powerful phytotoxins. Their wild ancestors required cooking or leaching before the plant was edible to humans. Plant breeders systematically select for cultivars with lower levels of (the often strongly flavored) toxins.
Plants that are naturally resistant to pests contain more phytotoxins, often produced in response to damage from insects. For example, the sprouts of wheat, corn, and rye produce potent mutagens (enjoy that cup of wheatgrass juice!) [19]. And some plants naturally contain symbiotic bacteria and fungi in their tissues, which produce non-plant chemicals [20]. There is absolutely nothing biologically novel about insecticidal toxins in plant tissues.
The toxicity (or lack thereof) of Cry proteins to non-target organisms, especially upon two "charismatic" species--the honey bee and the monarch butterfly--has been well studied [21], [22], [23]. A recent and very well-designed experiment on the effect of GM Bt corn pollen upon the growth and survival of honey bee larvae was recently performed by a team of independently-funded German researchers [24]. They added pollen from four different sources to a standard semi-artificial larval diet.
Results: surprisingly, the larvae fed the pollen from the "stacked" GM corn containing a combination of three different Cry proteins exhibited a higher survival rate (100%), than those fed non-GM corn pollen! To me, a big plus for this study was that they also included a positive control of pollen from a wild plant said to be harmful to bees--only about 30% of those larvae survived! This finding confirmed that even some natural pollens are quite toxic, and that we should compare any toxicity trials of pesticides with those of the natural phytotoxins in nature.
Analysis: CCD and colony mortality occur even in the absence of GM Bt crops; feeding GM Bt pollen to adult bees or larvae does not cause observable adverse effects.
Verdict on Bt crops: The specific Bt cry proteins used in GM crops were intentionally chosen to not cause harm to bees. There is no evidence to date that they do. On the other hand, Bt crops require less use of insecticides that are clearly toxic to bees [25].
Roundup Ready
Monsanto's pitch is that Roundup Ready®️ (RR) crops allow farmers to practice weed-free "no till" farming, which saves both topsoil and money. The catch is that farmers must then douse their fields with Monsanto's flagship product, Roundup (ensuring sales of that herbicide--a great marketing strategy). Bayer CropScience has followed suit by introducing crops resistant to its Liberty herbicide, which has a different mode of action.
Herbicide-resistant crops do indeed address several major environmental problems:
No till farming does in fact require less labor and reduces soil compaction.
Farmers get greater production due to less competition from weeds.
No till also reduces the amount of petrochemical fuel involved in tillage.
No till greatly reduces soil erosion, which has long been a major environmental concern.
No till may help to sequester carbon in the soil, and to rebuild soil.
So what's not to love about Roundup Ready? There are a few main complaints--(1) the massive spraying of the active ingredient, glyphosate, for which there is questionable evidence that it may be an endocrine disruptor [26], (2) claims of intimidation by Monsanto of farmers who choose not to plant RR seed, and (3) the environmental impact and sustainability of the sort of weed-free monoculture possible with RR crops.
So how do Roundup and RR crops relate to honey bees?
Direct Effects Of Roundup Use
Biological plausibility: either the active ingredient (glyphosate), or the adjuvants could cause bee toxicity.
The EPA has thoroughly reviewed the research and found glyphosate to be practically nontoxic to bees (and humans). They have found the same for Roundup's adjuvant polyoxyethylene-alkylamine. However, some beekeepers tell me that they see increased bee mortality following the spraying of glyphosate (Fig. 3), but are not sure whether it was a generic product, or perhaps contained additional ingredients (surfactants, fungicides, or insecticides) added to the tank mix.
Figure 3. A farmer spraying glyphosate herbicide over Roundup Ready corn seedlings. Photo courtesy of beekeeper Larry Garrett.
Analysis: there is no strong evidence that the spraying of Roundup or generic glyphosate herbicide is directly causing significant bee mortality. However, Drs. Jim and Maryann Frazier have legitimate concerns about the effect of some adjuvants--especially the organosilicones [27], [28].
Indirect Effects Of Roundup Use
Biological plausibility: the elimination of weeds reduces bee forage.
The success of Roundup Ready technology has allowed farmers to largely eliminate weeds from their fields (at least until the inevitable resistant weeds take over). But they don't stop there--nowadays they practice "clean farming" and use herbicides to burn off every weed along the fencerows and in the ditches--the very places that bees formerly had their best foraging. This elimination of flowering weeds severely reduces the amount of available of bee forage, plus kills off the host plants of native pollinators (such as monarch butterflies) and beneficial insects.
European honey bees evolved in Europe (hence the name), and are adapted to the nutrition provided by Old World flowering plants. Many of the weeds in North America are old friends of the honey bee. On the other hand, honey bees were never exposed to corn, soybeans, sunflowers, or squashes until recently; neither corn nor sunflowers supply complete amino acid profiles in their respective pollens. Until the advent of Roundup Ready, the weeds in an around crops provided alternative nectar and pollen sources for bees; today there is often nary a bee-nutritious weed to be seen in or around a field of corn or soybeans (Fig. 4).
Figure 4. I took this photo of a no-till herbicide-resistant corn field, prior to the shading canopy of the crop closing over. Note the total lack of any sort of bee forage (or any species of anything other than corn). The soil surface is a far cry from the original densely vegetated prairie sod. Prior to RR, there was more weedy forage for bees, and especially from the traditional weed-controlling crop rotation into legumes or pasture.
Update: there's a great deal of debate about the safely of Roundup (the formulated product with it's surfactants) and its active ingredient, glyphosate. From http://npic.orst.edu/factsheets/archive/glyphotech.html
"In plants, glyphosate disrupts the shikimic acid pathway through inhibition of the enzyme 5-enolpyruvylshikimate-3-phosphate (EPSP) synthase. The resulting deficiency in EPSP production leads to reductions in aromatic amino acids that are vital for protein synthesis and plant growth.
As far as the claims that glyphosate causes cancer (notably Non-Hodgkin's Lymphoma), I agree with the regulatory agencies that the case against glyphosate is very weak. As far as glyphosate being an endocrine disruptor, I'll leave it to the researchers and regulatory agencies to figure it out. As I type these words, I've actually got caged bees to which I'm feeding glyphosate (at a field-realistic dose) for a trial, and not seeing increased mortality. But some research indicates that it may be harmful to the gut microbiota. This sort of research takes time, and eventually we'll figure out just how safe or harmful glyphosate is to bees, humans, or the environment.
But nothing in nature is simple. Eliminating the competition of weeds and insects may allow plants to hold back from the production of natural toxins. And a surprising piece of research found corn kernels from plants sprayed with either of two different herbicides actually contain more of the healthful carotenoids [30]!
The Future Of Roundup
It took Monsanto several years to genetically engineer Roundup-resistant crops, yet took farmers only slightly longer to inadvertently produce Roundup-resistant weeds by the conventional breeding technique of applying a strong selective pressure-the continuous application of Roundup!
Weed management scientists consider glyphosate to be a once-in-a-100-year discovery--it works on 140 species of weeds, and is relatively environmentally friendly. However, its overuse has led to the creation of several "driver weeds" that could soon lead to its redundancy in corn, soy, and cotton acreage [31]. This will drive farmers to turn to other herbicides (which will also in time fail). We can only hope that someday they will be forced back into practicing crop rotation into legumes and pasture.
Reality Check
In order to clarify cause and effect, I often seek out extreme cases. Such would be the situation in the Corn Belt, where I could compare the USDA's hive and honey data from the old days to those under today's intense planting of GM crops (Fig. 5)!
Figure 5. The most intense planting of GM crops is in Iowa and Illinois (the dark green areas of the map above). U.S. farmers planted nearly 100 million acres of corn this year, and 76 million of soy. That is enough acreage to cover the entire state of Texas with GM crops!. Source: http://www.nass.usda.gov/Charts_and_Maps/Crops_County/pdf/CR-PL10-RGBChor.pdf
So I went through the tedious process of downloading and transcribing the NASS agricultural census figures for Iowa. I entered the amount of corn acreage, the total number of colonies in the state, and what I consider to be the best measure of colony health--honey yield per hive (which of course is largely weather dependent, but should show any trends). I plotted the data below (Fig. 6):
Figure 6. Bee and corn data from Iowa, and the dates of introduction of corn pest control technologies. The dotted line is median honey yield per colony. No factor appears to have affected honey production, but colony numbers have decreased since the arrival of varroa. Gaps are missing data. Source NASS.
Note: for non beekeepers, varroa is a parasitic mite that arrived in the U.S. around 1990 and quickly became, and still remains, the Number One problem in bee health-far more than any other factor.
Over the years, corn acreage increased by 18%. Other than the prodigious crop of 1988, honey production has averaged around 67 lbs per hive. The thing that stands out is the plot of number of colonies. Hive numbers jumped up in the late 1980's, likely due to federal honey price support payments, which peaked in 1988, and were cut off in 1994 [[i]]. Colony numbers peaked in 1990, the same year that varroa arrived in Ohio, and went down from there, leveling off to about half the number of hives present in the 1970's.
I fully expected honey yields to decrease concurrent with the adoption of Roundup Ready varieties, but they didn't! Colonies still produce as much honey today as they did in the past, but this might be partially due to having fewer bees working the same amount of land, or to increased soybean nectar (which saved a number of Midwestern beekeepers from disaster during this year's droughts).
Perhaps even more surprising is the fact that in a state covered in corn and soy, colony productivity did not appear to be affected by the introductions of either Bt or Roundup Ready corn, nor by the universal use of neonicotinoid seed treatments (between corn and soy, on over roughly two thirds of the entire state land area). Note that honey yields actually increased for a few years following the introduction of clothianidin seed treatment!
Tellingly, hive numbers started to decrease after the arrival of varroa, and plummeted in the late 1990's as fluvalinate failed as a miticide, and many beekeepers simply threw up their hands and quit the business.
Verdict on herbicide tolerant crops: from a nutritional standpoint, the increased use of herbicides, and the associated weed free "clean farming" has certainly not helped the bees in corn/soy areas, but it is hard to make a case for them causing colony collapse.
Verdict on GM crops in general: Allow me to quote from the USDA:
...there is no correlation between where GM crops are planted and the pattern of CCD incidents. Also, GM crops have been widely planted since the late 1990s, but CCD did not appear until 2006. In addition, CCD has been reported in countries that do not allow GM crops to be planted, such as
Switzerland [33].
Looking Ahead: The Chemical Treadmill & Pest Resistance
It is interesting to observe the evolution of agriculture from the perspective of a biologist. Simple systems in nature are inherently less stable than complex systems. The current agricultural model in the U.S. exemplifies simplicity to the extreme--plant a single species into bare soil year after year, killing any competitive weeds or insects with pesticides (either sprayed, systemic, or engineered into the plants), and attempt to maintain fertility by adding energy-costly fertilizer. From a biological perspective, such a strategy is little more than an intense selective breeding program for the most resistant pests, and doomed to escalating chemical and energy inputs until the system collapses under its own weight.
I'm anything but a salesman for either Bt nor RR crops. Both are mere short-term solutions--resistant bugs and weeds are already starting to spread. I also have questions about the benefits of herbicide-intense no till planting [34], and hope that farmers return to alternative methods of weed control [35]. Luckily, the system will likely be self correcting, eventually forcing humanity to practice more sustainable methods of farming the land. However, I suggest that those methods may well include the wise use of biotechnology.
Additional Discussion
The Back Story On Plant Breeding And GM Crops
Traditionally, farmers simply replanted with the seeds from the most desirable individual plants year after year; this is the simplest form of "selective breeding." For example, all the various cole crops (cabbage, kale, broccoli, cauliflower, kohlrabi, Brussels sprouts) were developed by intentionally selecting for unusual forms of the species (resulting from random recombination of the natural allelic diversity, spontaneous mutants, or natural hybrids). This sort of selective breeding tends to result in a diverse assembly of locally-adapted cultivars. In Oaxaca, Mexico- the birthplace of corn-some 150 traditional varieties of maize are grown without pesticides or herbicides, thereby maintaining an invaluable reservoir of genetically-diversity "germplasm," which breeders can then cross and backcross in order to develop new cultivars (e.g., for pest or drought resistance).
In the early years of the U.S., seeds from desirable cultivars were distributed to farmers by the government, and plant breeding was performed at universities and at the USDA [36]. But since every strain breeds true, a farmer could save the seed and replant, leaving little opportunity for seed companies to make a buck. So in 1883, they formed the American Seed Trade Association and began to lobby for the cessation of the government programs.
The Profit Motive
In the early part of the 20th century, the companies began to promote hybrids-- crosses of two (or more) different strains or species that exhibited some sort of "hybrid vigor"--offering greater production, tastier fruit, or some other desirable characteristic. Hybrids were a godsend to the companies, since they are often sterile or don't breed true, meaning that farmers needed to purchase (rather than save) seed each season.
The seed lobby eventually shifted public funding away from the free distribution of selected seedstocks to instead encouraging the USDA and universities to develop inbred parental lines and breeding stock that the seed trade could then use to create proprietary hybrid varieties. By 1960, farmers planted less than 5% of corn from saved seed; and less than 10% of soybeans by 2001. As on-farm familiarity with the saving of seed was forgotten, farmers became willing consumers of produced seed.
Enter GM Crops
Then in 1980, the Supreme Court decided that seed companies could patent new varieties if they contained distinct and novel genetic markers. This meant that farmers (in some countries) could now be required to sign licensing agreements to allow them to use the patented seed each season [37] (there is a hodge-podge of international patent laws in this regard [38]).
The Second "Green Revolution"
The first "green revolution" was based upon fertilizer, pesticides, and hybrid seed (and also resulted in forcing farmers onto "agricultural treadmills"-making them less self sufficient and sustainable, and more reliant upon purchased seed, pesticide and fertilizer use, and upon borrowed money).
In 1950 the Secretary of Agriculture Ezra Benson said to farmers, "Get big or get out." His 1970s successor, Earl Butts, repeated that message, and exhorted farmers to "plant fence row to fence row" and to "adapt or die." Politicians who understood that a well-fed electorate is a happy electorate promoted policies that resulted in the destruction of the small family farm. Our policy of price supports and favorable treatment of agribusiness has changed the face of the American farm and the composition of the American diet [39].
Today's "second green revolution" is based upon technological advances in plant genetics (including GM) and the (at least partial) replacement of nasty pesticides with "biologicals." As an environmentalist, I find the new revolution to be more promising for ecological sustainability, but it is not without its downside--the current consolidation of agribusiness. As I mentioned before, farms, seed companies, and chemical companies are all being bought up by a few main players. Philip Howard details this consolidation in a free download [40], from which I quote:
This consolidation is associated with a number of impacts that constrain the opportunities for renewable agriculture. Some of these include declining rates of saving and replanting seeds, as firms successfully convince a growing percentage of farmers to purchase their products year after year; a shift in both public and private research toward the most profitable proprietary crops and varieties, but away from the improvement of varieties that farmers can easily replant; and a reduction in seed diversity, as remaining firms eliminate less profitable lines from newly acquired subsidiaries.
He then speaks of the concept of the "treadmill":
For the majority of farmers, however, the result is that they must constantly increase yields in order to simply maintain the same revenue. [Monsanto's sales pitch is that economic success in farming is driven by yield per acre [41]. Those that are unable to keep up with this treadmill will "fall off," or exit farming altogether. Their land ends up being "cannibalized" by remaining farmers who seek to increase scale of production as another means of keeping up with the treadmill, leading to the increasing centralization of agriculture. Farmers who have managed to stay in business have adapted to this process, and are typically on the leading edge of the adoption of new technologies. As a result, they have a high degree of confidence in science and technological innovations.
However, this problem has nothing to do with GMO's, but is rather due to the public's unknowing acceptance of the practice. Capitalism inevitably leads to consolidation unless consumers stop supporting corporate agribusiness with their pocketbooks and their votes, and start demanding that their government enforce antitrust efforts and better support small farmers.
But we are allowing economics and politics to distract us from the topic at hand--the technology of genetic engineering in plant breeding.
Cautions About GM
The most vocal critic of genetic modification is Jeffrey Smith, fear-mongering author of Seeds of Deception, producer of the film Genetic Roulette, and executive director of the inappropriately-named Institute for Responsible Technology. Smith is a gifted and effective communicator, as well as being a practitioner of "yogic flying" [42]. I will be the first to say that Smith's anti-GMO claims [43] would scare the pants off of anyone, and make for compelling story! The problem is that he plays loose with the facts--most of his claims simply do not stand up to any sort of scientific scrutiny. I suggest that for an objective analysis of the facts, that you visit AcademicsReviewed.org, a website that tests popular claims against peer-reviewed science. They address each of Smith's alarming "facts" one by one [44]. It is a thrilling ride to open the two web pages side by side, first being shocked by Smith's wild and scary claims, and then reading the factual rebuttal to each! The thing that most bothers me about Smith's writing is that he treats GM cultivars generically, rather than specifically addressing the merits or concerns for them individually. This makes little sense, since any conventional crop has cultivars that cause human allergy or contain excessive levels of natural toxins, yet no one calls for the testing of each of them!
Perspectives On GM Crops
As you may have guessed by now, to me, the GM debate should not be about being pro or con, rather it should be about the intelligent discussion of reconciling its promise with its problems. The GE genie is out of the bottle, and I can't see that anyone is going to put it back in-so we might as well work with it! So let's cut through the hype and hysteria, the fears and judgments, and try to objectively look at the facts of the matter:
From a plant breeder standpoint, genetic engineering holds incredible promise for the development of crops that could be tremendously beneficial to humans or the environment. For example, "Transgenic cotton has reduced the need for conventional insecticides used against lepidopteran [pests] an average in the USA about 59.4% [and] Texas 74.7%...an average number of pesticide applications in conventional cotton has fallen from 4.3 in 1995 to 2.1 in the USA... with benefits to human health and the environment" [45].
GM is only a part of plant breeding--most advances continue to be in conventional breeding, now assisted by "marker assisted selection," which is embraced by environmentalists [46].
However, someone needs to pay for the research, and the taxpayer is not doing it! For a thoughtful discussion of the benefits of gene patents, see [47].
Novel genetic markers can be patented, and a licensing fee can be charged, despite the fact that they are not GM!
From a consumer standpoint, advanced breeding techniques can result in cheaper and more nutritious food, and less environmental impact from farming.
Consumers have erroneously been led to believe that GM crops are dangerous to their health, and call for application of the precautionary principle. My gosh, please read "Misconceptions about the causes of cancer" [48]. Few foods are entirely "safe"! And "safety" can never be proven--it can only be disproven. And no studies have ever disproven the safety of GM crops, nor have doctors noticed anyone ever getting sick from them, despite our eating them for 15 years!
In truth, some scientists argue that plants produced by classical breeding methods should undergo the same safety testing regime as genetically modified plants. There have been plenty of instances where plants bred using classical techniques have been unsuitable for human consumption, causing toxicity or allergic reactions.
Those that speak of applying the "precautionary principle" should read Jon Entine's trenchant analysis of the fallacy of overapplication of that principle [49]. In truth, our regulators (EPA and FDA) vigorously apply the precautionary principle in the form "reasonable certainty of no harm."
The benefits of seed biotechnology cannot be realized without good seed germplasm to start with. So a few large seed companies started buying up their competitors to acquire the most productive and desirable varieties.
The downside of the above practice is that by 2008, 85% of GM maize patents and 70% of non-maize GM plant patents in the U.S. were owned by the top three seed companies: Monsanto, DuPont, and Syngenta [50]. Note that economists figure that when four firms control 40% of a market, it is no longer competitive; in the case of GE crops, the top four seed firms control 56% of the global proprietary seed market!
On the flip side, these profits are an incentive for the large corporations to invest in innovative plant breeding research--Monsanto spends about $2 million a day on this. This is important to keep in mind in an increasingly hungry world.
On the dark side, Monsanto's nearly $12 billion in annual sales allows the company to lobby regulators, influence universities, and spin the news. These are standard business practices for any large corporation, but hardly make Monsanto uniquely evil.
Be aware that patented genes are of use only if inserted into high-producing cultivars-which are developed by conventional breeding (which constitutes nearly half of Monsanto's plant breeding budget). These desirable cultivars have no patent protection. Monsanto uses a non GE technology called SMART = Selection with Markers and Advanced Reproductive Technologies. SMART technology is warmly embraced by environmental groups [51].
Adding a genetic marker allows a company to identify its proprietary strains, like putting a nametag on a dog. But clever breeders can back engineer the desirable germplasm out from patent protection.
And remember that patents expire after 20 years. The patents for Roundup Ready soybeans expire in 2014--at which time farmers, universities, and seed companies will then be free to propagate and sell the variety [52]. Patents are granted in order to spur innovation; by filing for patent protection, a company must make its discoveries public knowledge. This is a good thing.
Monsanto invests 44% of its R&D on conventional (as opposed to GM breeding).
Monsanto has also given rights to some of their patented crops to poorer countries, and recently donated a database of some 4000 genetic markers from cotton to Texas A&M [53]. The university plant breeders are excited in that the information will assist them in their conventional (non-GM) breeding of cotton, to the benefit of the environment [54 ].
From the farmer's standpoint, he has the choice of purchasing GE varieties that may be more productive, reduce insecticide use, or reduce tillage costs [55]. Keep in mind that there is nothing keeping him from purchasing "conventional" non-GM seed--it is available (I checked, and it sells at about half the cost of GM seed). In our free enterprise system there is nothing to keep non-GM seed companies from selling an alternative product if there is a demand. Farmers who are unimpressed by GM varieties freely switch back to conventional seed.
From an agricultural standpoint, the widespread adoption of a few favored crop varieties (GM or not) can result in the irreplaceable loss of crop genetic diversity--this is of great concern to plant breeders. If you haven't yet seen the graphic of our loss of crop genetic diversity from National Geographic magazine, you should! [56]. Luckily, this does not appear to be occurring yet with maize in Oaxaca [57], but there is a legitimate concern that economics will force traditional farmers out of business, leading to the loss of heirloom varieties. However, this is not a GM issue, but rather an effect of consolidation.
From a sustainability standpoint, there is nothing to prevent constant breeding innovation to keep pace with pest evolution. Genetically engineered crops can play a role in sustainable farming as our agricultural practices begin to shift to more ecologically sustainable methods.
One should keep in mind how the simple splicing of a virus gene into the papaya saved the Hawaiian papaya growers from the ravages of ringspot virus--the GE papaya is the mainstay of the industry, and by virtue of keeping the virus in check actually allows nearby organic papayas to thrive. Yet ecoterrorists recently hacked down thousands of GM trees [58]. It's interesting to read the history of "Golden Rice" [59] to see how the anti-GMO lobby is specifically scared that the success of such a lifesaving crop might open the door for acceptance of other GM plants!
Update Jan 2013
News item: Leading Environmental Activist's Blunt Confession: I Was Completely Wrong To Oppose GMOs. Blog in Slate Magazine
"If you fear genetically modified food, you may have Mark Lynas to thank. By his own reckoning, British environmentalist helped spur the anti-GMO movement in the mid-'90s, arguing as recently at 2008 that big corporations' selfish greed would threaten the health of both people and the Earth. Thanks to the efforts of Lynas and people like him, governments around the world--especially in Western Europe, Asia, and Africa--have hobbled GM research, and NGOs like Greenpeace have spurned donations of genetically modified foods.
But Lynas has changed his mind--and he's not being quiet about it. On Thursday at the Oxford Farming Conference, Lynas delivered a blunt address: He got GMOs wrong."
Anyone opposed to GMO's should read Mr. Lynas' well thought out address: http://www.marklynas.org/2013/01/lecture-to-oxford-farming-conference-3-january-2013/
Update May 2014
I've compiled a list of recent worthwhile reading on the "other side" of the GMO debate at https://scientificbeekeeping.com/gmo-updates/
So What's The Problem?
The problem is that anti-GMO advocacy groups are determined to put a stop to all GE technology. They targeted California with Prop 37, which applied only to packaged foods and produce. A more cynical take on Prop 37 was that it was all about marketing: "If your produce is no different in terms of taste, safety and nutrition from a competitor, and costs more, apparently the only marketing option is to create a negative image of your competitor's product" [60].
If Prop 37 had been successful, the promoters would then have targeted restaurants, the meat and dairy industry, and the beverage industry. I personally feel that this is an extreme position, what with the human population growing hungrier every day, and climate change threatening agriculture worldwide with heat, drought, pestilence, and salinity problems. Not only that, but GM crops hold promise for cheap omega-3 fatty acids (so that we don't have to harvest fish for them), cost-effective biofuels, and less expensive pharmaceuticals.
A good blog on the problem with the anti-GMO fear campaign can be found at [61], from which I quote:
It would be bad enough if something like the Seralini study simply contributed to the unnecessary angst amongst consumers around the world. It also has very real political, economic and practical effects. For instance brand conscious food companies have used their leverage to prevent the development of GMO versions of potatoes, bananas, coffee and other crops because they fear controversy. Apple growers worried about the market response are opposing the introduction of a non-browning apple even though it was developed by one of their own fruit companies. French activists destroyed a government-run field trial of a virus-resistant root stock which could have made it possible to produce good wine on sites that have become useless because of contamination with sting nematodes and the virus they vector. California voters have the potential to pass a seriously flawed "GMO labeling" initiative next month that could only serve the purposes of the lawyers and "natural products" marketers who created it. More importantly, European and Japanese importers of wheat essentially blackmailed the North American wheat producers into blocking biotech wheat development because those companies were nervous about consumer response in countries where GMO angst is so high. This has delayed by decades not only specific desirable trait development, but also what might have been an enormous private investment in a crop that is critically important for feeding a lot more people than just those in those rich countries. There is a huge cost of "precaution" based on poor science.
I believe that people should be well informed before taking a stance on important issues. I'd like to suggest one last excellent blog by an independent U.C. Berkeley evolutionary biologist and medical researcher:"How Bt Corn and Roundup Ready Soy Work - And Why They Should Not Scare You [62].
Acknowledgements
As always, thanks to my friend and collaborator in research Peter Loring Borst, and to anyone who still reads my articles after finding out that I've collaborated with Monsanto!
References
[1] Key S, et al (2008) Genetically modified plants and human health. J R Soc Med.101(6):290-298. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2408621/
[2] For example: Antoniou, M, et al (2012) GMO myths and truths.
(Broken Link!) http://earthopensource.org/files/pdfs/GMO_Myths_and_Truths/GMO_Myths_and_Truths_1.3.pdf
[3] Chiba S, et al. (2011) Widespread endogenization of genome sequences of non-retroviral RNA viruses into plant genomes. PLoS Pathog 7(7): e1002146.
[4] Domingo, JL and JG Bordonaba (2011) A literature review on the safety assessment of genetically modified plants. Environment International 37: 734-742.
[5] Key (2008) op. cit.
[6] Smith, JM (2003) Seeds of Deception. Yes! Books
[7] Seralini, GE, et al (2012) Long term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize. Food and Chemical Toxicology (2012) http://foodpoisoningbulletin.com/wp-content/uploads/Toxicity-of-Roundup-Ready-Maize.pdf;
Reviews
http://www.forbes.com/sites/henrymiller/2012/09/25/scientists-smell-a-rat-in-fraudulent-genetic-engineering-study/2/
http://www.efsa.europa.eu/en/faqs/faqseralini.htm#9, http://www.emilywillinghamphd.com/2012/09/was-it-gmos-or-bpa-that-did-in-those.html,
(Broken Link!) http://www.ask-force.org/web/Seralini/Anonymous-Rat-List-Spaying-2003.pdfs, http://storify.com/vJayByrne/was-seralini-gmo-study-designed-to-generate-negati;
Benbrook, CM (2012) Impacts of genetically engineered crops on pesticide use in the U.S. -- the first sixteen years. Environmental Sciences Europe 24:24 http://www.enveurope.com/content/pdf/2190-4715-24-24.pdf,
Review http://weedcontrolfreaks.com/2012/10/do-genetically-engineered-crops-really-increase-herbicide-use/#more-432
[8] http://journals.tubitak.gov.tr/agriculture/issues/tar-04-28-6/tar-28-6-1-0309-5.pdf
[9] http://www.monsanto.com/whoweare/Pages/monsanto-history.aspx
[10] http://www.businessweek.com/stories/2010-01-10/monsanto-v-dot-food-inc-dot-over-how-to-feed-the-world
[11] Methods for genetic control of plant pest infestation and compositions thereof
http://www.freepatentsonline.com/8088976.html
http://www.freepatentsonline.com/7943819.html
[12] http://www.greenpeace.org/australia/PageFiles/348427/smart-breeding.pdf
[13] 2007 figures http://www.census.gov/compendia/statab/2012/tables/12s0835.pdf
[14] ETC Group (2008) Who owns nature? Corporate power and the final frontier in the commodification of life. http://www.etcgroup.org/sites/www.etcgroup.org/files/publication/707/01/etc_won_report_final_color.pdf
[15] Blakeney, M (2011) Trends in intellectual property rights relating to genetic resources for food and agriculture. http://www.fao.org/docrep/meeting/022/mb684e.pdf This document covers the hodge-podge of international patent laws regarding plants and animals.
[16] http://www.monsanto.com/products/Pages/biodirect-ag-biologicals.aspx
[17] History of Bt http://www.bt.ucsd.edu/bt_history.html
Mode of action http://www.bt.ucsd.edu/how_bt_work.html
[18] Gold 2002 Misconceptions about the causes of cancer http://potency.berkeley.edu/pdfs/Gold_Misconceptions.pdf A "MUST READ"!
[19] Buchmann CA, et al (2007) Dihydroxy-7-methoxy-1,4-benzoxazin-3-one (DIMBOA) and 2,4-dihydroxy-1,4-benzoxazin-3-one (DIBOA), two naturally occurring benzoxazinones contained in sprouts of Gramineae are potent aneugens in human-derived liver cells (HepG2). Cancer Lett. 246 (1-2):290-9.
[20] http://en.wikipedia.org/wiki/Endophyte
[21] Duan JJ, et al (2008) A meta-analysis of effects of Bt crops on honey bees (Hymenoptera: Apidae). PLoS ONE 3(1): e1415.
[22] Center for Environmental Risk Assessment (2011) A review of the environmental safety of the Cry1Ab protein. http://cera-gmc.org/docs/cera_publications/cry1ab_en.pdf
[23] Han, P, et al (2012) Does transgenic Cry1Ac + CpTI cotton pollen affect hypopharyngeal gland development and midgut proteolytic enzyme activity in the honey bee Apis mellifera L. (Hymenoptera, Apidae)? Ecotoxicology. 2012 Aug 7. [Epub ahead of print]
[24] Hendriksma HP, et al (2011) Testing pollen of single and stacked insect-resistant bt-maize on in vitro reared honey bee larvae. PLoS ONE 6(12): e28174.
[25] Benbrook, CM (2012) op. cit.
[26] Reviewed in http://www.sourcewatch.org/index.php/Glyphosate
[27] Mullin, C.A., J.L. Frazier, M.T. Frazier & T.J. Ciarlo - A primer on pesticide formulation 'inerts' and honey bees. http://www.extension.org/pages/58650/proceedings-of-the-american-bee-research-conference-2011
[28] Ciarlo TJ, CA Mullin, JL Frazier, DR Schmehl (2012) Learning impairment in honey bees caused by agricultural spray adjuvants. PLoS ONE 7(7): e40848.
[29] Johal, GS and DM Huber (2009) Glyphosate effects on diseases of plants. Europ. J. Agronomy 31: 144-152. http://www.organicconsumers.org/documents/huber-glyphosates-2009.pdf
Huber, DM (2010) Ag chemical and crop nutrient interactions - current update. http://www.calciumproducts.com/dealer_resources/Huber.pdf
Reviewed in (Broken Link!) http://www.weeds.iastate.edu/mgmt/2010/glyMndisease.pdf
[30] Kopsell et al. (2009) increase in nutritionally important sweet corn kernel carotenoids following mesotrione and atrazine applications. Journal of Agricultural and Food Chemistry 090619124509017 DOI: 10.1021/jf9013313
[31] Laws, F (2010) http://cornandsoybeandigest.com/issues/will-glyphosate-fall-wayside-resistance-grows
[32] http://www.nationalaglawcenter.org/assets/crs/RS20759.pdf
[33] http://www.ars.usda.gov/is/AR/archive/jul12/July2012.pdf
[34] http://www.misereor.org/fileadmin/redaktion/MISEREOR_no%20till.pdf
[35] http://www.acresusa.com/toolbox/reprints/Organic%20weed%20control_aug02.pdf
[36] http://www.seedalliance.org/Seed_News/SeminisMonsanto/
[37] (Broken Link!) http://earthopensource.org/files/pdfs/GMO_Myths_and_Truths/GMO_Myths_and_Truths_1.3a.pdf
[38] Blakeney, M (2011) Trends in intellectual property rights relating to genetic resources for food and agriculture. http://www.fao.org/docrep/meeting/022/mb684e.pdf This document covers the debate involved in international patent law regarding plants and animals.
[39] Philpott, T (2008) A reflection on the lasting legacy of 1970s USDA Secretary Earl Butz. http://grist.org/article/the-butz-stops-here/; but for a contrary view by an actual corn farmer, read Hurst, B (2010) No Butz About It. (Broken Link!) http://www.american.com/archive/2010/july/no-butz-about-it
[40] Howard, Philip H. 2009. Visualizing consolidation in the global seed industry: 1996-2008. Sustainability, 1(4), 1266-1287. http://www.mdpi.com/2071-1050/1/4/1266/pdf
[41] http://www.monsanto.com/investors/Documents/Whistle%20Stop%20Tour%20VI%20-%20Aug%202012/WST-Fraley_RD_Update.pdf
[42] http://academicsreview.org/reviewed-individuals/jeffrey-smith/
[43] http://responsibletechnology.org/docs/145.pdf
[44] http://academicsreview.org/reviewed-content/genetic-roulette/
[45] Greenberg, S, et al (2012) Economic and Environmental Impact Transgenically Modified Cotton Comparative with Synthetic Chemicals for Insect Control. Journal of Agricultural Science and Technology B 2 750-757.
[46] Greenpeace (2009) Smart Breeding. Marker-Assisted Selection: A non-invasive biotechnology alternative to genetic engineering of plant varieties. http://www.greenpeace.org/australia/PageFiles/348427/smart-breeding.pdf
[47] http://www.genengnews.com/gen-articles/in-defense-of-gene-patenting/2052/
[48] Gold 2002 Misconceptions about the causes of cancer http://potency.berkeley.edu/pdfs/Gold_Misconceptions.pdf
[49] Entine, J (2010) Crop Chemophobia: Will Precaution Kill the Green Revolution? http://www.jonentine.com/pdf/CROPCHEMOPHOBIApre-orderform.pdf
[50] Howard, Philip H. 2009. Visualizing consolidation in the global seed industry: 1996-2008. Sustainability, 1(4), 1266-1287. http://www.mdpi.com/2071-1050/1/4/1266/pdf
[51] http://www.greenpeace.org/australia/PageFiles/348427/smart-breeding.pdf
[52] http://www.monsanto.com/newsviews/Pages/roundup-ready-patent-expiration.aspx;
[53] http://www.cotton247.com/article/3401/monsanto-donates-marker-technology
[54] http://www.youtube.com/watch?v=dcZyFH_eITQ
[55] http://www.biofortified.org/2012/05/the-frustrating-lot-of-the-american-sweet-corn-grower/#more-8670
[56] http://ngm.nationalgeographic.com/2011/07/food-ark/food-variety-graphic If you didn't see this graphic in National Geographic, you should!
[57] (Broken Link!) http://researchnews.osu.edu/archive/mexmaize.htm
[58] http://www.huffingtonpost.com/2011/08/20/genetically-modified-papayas-attacked_n_932152.html
[59] http://en.wikipedia.org/wiki/Golden_rice
[60] http://westernfarmpress.com/blog/proposition-37-gone-probably-not-forgotten?
[61] http://appliedmythology.blogspot.com/2012/10/can-damage-from-agenda-driven-junk.html?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+AppliedMythology+%28Applied+Mythology%29
[62] http://www.science20.com/michael_eisen/how_bt_corn_and_roundup_ready_soy_work_and_why_they_should_not_scare_you
Category: Colony Health - Diseases, Viruses, CCD
Tags: collapse, colony, genetically, gm crops, gmo, modified, plants, sick bees | genetically Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/genetically/ |
Neonicotinoids: Trying To Make Sense of the Science - Part 2
First published in: American Bee Journal, September, 2012
Neonicotinoids: Trying To Make Sense Of The Science
Part 2
Randy Oliver
ScientificBeekeeping.com
First published in ABJ September 2012
"Scientists have largely remained silent when the public discussion turns to the trade-off of benefits and risks from chemicals. They are often unwilling to engage controversial issues that could endanger their funding and research...The public interprets the unwillingness of scientists to engage those who campaign against chemicals as an implicit validation of their dangers. Those who do speak out are often...branded as industry apologists. Maybe the best we can hope for is that brave scientists, scientifically literate journalists and government officials who are responsible for translating science into regulatory policy will take the public's best interest into account...[and] resist the irrational and often regressive impulse stirred by the scare tactics that are so common today." 1
Thanks For The Feedback!
Following the publication of my article "The Extinction of the Honey Bee?" 2 in which I pointed out that honey bees were thriving at Ground Zero of neonicotinoid use, I fully expected to be excoriated by the anti-neonicotinoid True Believers. But to my great surprise, I was instead deluged by letters of support from beekeepers and researchers worldwide! A few examples:
"I'm an amateur beekeeper in France and I want to tell you that I strongly believe that CCD is not caused by pesticides. Like you, I'd like to find the culprit but so far it remains a mystery."
"I liked your article because here in Germany we are facing a hard discussion with bee keepers and other organizations regarding neonicotinoids and feel similar as you that often any scientific idea is missing and that it is a political mission," from a researcher at the major agricultural science institute.
"Likewise in USA, in Europe the discussion is more and more polarized, and in the hands of activists rather than scientists," a bee researcher from the Netherlands.
Thanks, Randy, for acting as a mythbuster," from a beekeeper from the Corn Belt.
Fortified by your vote of support, allow me to return to what I hope is an objective analysis of the neonicotinoid debate.
Innate Distrust Of Chemicals
I came of age in the '60's, and was profoundly influenced by Rachel Carson's book Silent Spring, which detailed how humans were poisoning the environment with pesticides. I have always had an innate distrust of manmade chemicals. I became an environmental activist, subscribed to Mother Earth News and Organic Gardening, moved to the woods, and began a lifelong quest to "walk the walk"--going solar, avoiding pesticides and manmade toxins in my personal environment, creating an organic garden and orchard. I'm a lifelong member of the Sierra Club and The Nature Conservancy, and am considered in my community to be about as green as you can get.
When I first heard reports from France that some new insecticides--the neonicotinoids--were causing massive bee mortality, I of course assumed, "Here we go again--the corporate recklessness of the chemical industry, coupled with government regulators asleep at the switch, has created yet another environmental catastrophe." 3 So, having a background in biology and chemistry, in my usual manner I began to investigate the subject deeply.
Boy, was I in for an education! I read the literature from both sides of the pesticide debate, and got to know the principal players--the beekeeper anti-neonic advocates (who I fully respect), bee researchers, ecotoxicologists, farmers, and scientists from the chemical companies and the EPA. I soon found out who I could trust for accurate information, and who was so biased that I had to take anything they said with a grain of salt. I had thought that I knew something about pesticides; but in reality, how little I knew!
Why Neonicotinoids?
"Until the mid-20th century, pest insect control in agriculture relied on largely inorganic and botanical insecticides, which were inadequate. Then, the remarkable insecticidal properties of several organochlorines, organophosphates, methylcarbamates, and pyrethroids were discovered, leading to an arsenal of synthetic organics. The effectiveness of these insecticides, however, diminished over time due to the emergence of resistant insect strains with less sensitive molecular targets in their nervous systems. This created a critical need for a new type of neuroactive insecticide with a different yet highly sensitive target. Nicotine in tobacco extract was for centuries the best available agent to prevent sucking insects from damaging crops, although this alkaloid was hazardous to people and not very effective. The search for unusual structures and optimization revealed a new class of potent insecticides, known as neonicotinoids, which are similar to nicotine in their structure and action." 4
The neonicotinoids had three other distinct advantages:
They are far more toxic to insects than to mammals, making them much safer for humans.
They are absorbed by plants and translocated via the vascular system, giving effective control of sap sucking and boring insects which other sprayed insecticides might not contact.
They can be applied as seed treatments (Fig. 1), thus being a solution to the longstanding problem that roughly 99% of sprayed treatments never actually hit a target pest, and thus are unnecessarily dumped into the environment. 5
Figure 1. Treated seed, dyed for identification. The purple ones on the left are canola. Seed treatment has a very long history[i], and has been popular in the U.S. for about 40 years. Treatment can consist of any number of fungicides or insecticides, often in "cocktails." The neonicotinoids, since they are transported by the plant vascular system, lend themselves well to this application. The treatments are diluted as the plants grow--in canola, they no longer kill aphids or flea beetles by the time the plants have grown for a month, and by bloom time, are nontoxic to bees.
[i] Munkvold, G (2006) Seed Treatment http://www.extension.iastate.edu/Publications/CS16.pdf
The neonicotinoid insecticides have become widely popular with farmers, and when used as seed treatments, drenches, or attentively applied foliar sprays, appear to indeed be more environmentally friendly than the alternatives. However, the problem lies in the delicate balance between applying them in a manner that targets the pests, without harming "off target" species, such as bees and native pollinators. So let's look at some of the questioned adverse effects.
Sublethal Effects
I can't think of any researcher who has more thoroughly investigated the effects of the neonicotinoids upon honey bee behavior than Dr. Axel Decourtye in France. In an extensive and excellent recent review, 7 he summarizes research on behavior:
Learning performance: Field-relevant doses do not appear to negatively affect learning, but higher doses may. "In general, results from these studies cannot be extrapolated to natural conditions. Moreover, imidacloprid can also have facilitatory effects on learning performances that complicate the interpretation at an ecological level." Yes, you understood him-a low dose of neonic may help bees to learn!
Orientation: "The lowest observed effect concentration on the frequentation of feeding site was 50 [ppb]" (normal field-realistic doses are usually less than 5 ppb).
Foraging: "Although these studies showed the absence of effect of neonicotinoids on foraging of treated plants, perturbations of the foraging behavior on artificial feeder were revealed in other experiments. Thus, for example, it was found a quick decrease in the foraging activity in honey bee colonies at about 20 ppb of imidacloprid. This is probably due to the anti-feedant character of the compound." This is a key point--bees appear to avoid nectar with high concentrations of neonicotinoids. Decourtye does mention that doses at the high end of field relevance may affect bee communication within the hive.
Immune function:
Stress due to exposure to any insecticide could plausibly affect bee immune response to pathogens. I find the research along this line less than compelling. What struck me was the lack of dose response, inconsistency of effect upon nosema replication, and lack of effect in field colonies. I'm sure that we will see further research on this subject.
Some beekeepers have been confused by the action of imidacloprid against termites, thinking that it suppressed the general termite immune function. This does not appear to be the case, as explained by Ramakrishnan (1999) 8: "Collectively, this evidence indicates that imidacloprid did not disrupt termite cellular defense mechanisms, and further suggests that social behaviors are the primary defense against pathogen infection." The social behavior he refers to is grooming, by which termites clean fungal spores off their bodies to prevent infection. Since grooming does not appear to be critical for bee defense against the most common pathogens, I find it difficult to extrapolate the action of imidacloprid against termites to bees.
Social interactions and task allocation:
It is plausible that intoxication by neonics could affect bee social behavior or alter the normal progression of age-related tasks (as proposed by Dr. James Frazier). However, if this were the case, it should affect overall colony performance, which hasn't been observed.
Putting sublethal effects into perspective:
People get hung up on the word "toxin." Perhaps it would help to consider the neonics as "stimulants." As I type these words, I'm enjoying the effects of a sublethal dose of the toxic alkaloid caffeine (plants produce caffeine to poison herbivores). Two cups of coffee supplies about 1/40th of the human LD50 (median lethal dose). 9 The way I brew my java, I'm at the high end of a sublethal dose! And I'll dose myself again late this afternoon.
So why don't I die from caffeine toxicity? Because my body quickly degrades the toxin. The same thing happens with nicotine, and with the neonicotinoids in bees. Suchail 10, 11 found that ingested imidacloprid is rapidly passed to the bee's rectum and excreted or degraded within hours. Very little makes it into the blood or rest of the body. Only about 5% is absorbed into the brain or flight muscles, where it is converted to the more toxic olefin metabolite, which then disappears within a day. Although the metabolite is more toxic on a dosage basis, understand that little of it actually formed.
This is the main problem with the hypothesis of Dr. Henk Tennekes 12, whose widely-cited publications attempt to make a case for the application the Druckrey-Kupfmuller equation for chronic toxicity to the neonics. I've corresponded at length with Dr. Tennekes, and asked him to explain why the neonics, which are also rapidly degraded by the bee, would have any more chronic toxicity than nicotine would to a human smoker. There is enough nicotine in a pack of cigarettes to easily kill a human, yet no one dies from nicotine toxicity (I watched in perverse horror as my high school biology teacher injected a rat with nicotine--its death was not a pretty sight). The point is, that nicotine and neonics appear to be so rapidly metabolized, that there is no buildup in the body (as there is in the case of DDT), the binding to the nerve receptors is reversible and insects recover fully, 13 and there is generally no increased mortality due to low-level chronic exposure.
Indeed, a number of studies have found that exposure to low doses of imidacloprid resulted in foragers being more active and carrying more pollen! 14 Some plants secrete nicotine or caffeine in their nectar; recent research 15 suggests that bees prefer a bit of stimulant "buzz" and are able to accurately self dose--avoiding syrup spiked to toxic levels.
Bottom line: Any number of scientists have diligently tried to find any sorts of sublethal effects of neonics on bees, but have failed to demonstrate adverse effects at the colony level at doses produced by seed treatments.
Effect Upon Brood
The surprising thing here is that bee larvae appear to be essentially immune to the effects of neonics! In fact no one's been able to come up with LD50's because you simply can't dissolve enough of the insecticide in syrup to cause 50% of the larvae to die! 16, 17
However, there could be indirect effects, should the nurse bees--the main consumers of pollen in the hive--be affected by neonics residues. It is plausible that the nurses may exhibit reduced brood feeding. Hatjina 18 found in a lab study that nurse bees fed field-realistic doses of imidacloprid had reduced hypopharyngeal glands (that produce jelly).
On the other hand, perhaps nurses amped up on stimulants work harder--Lu 19 found that field-realistic doses of imidacloprid actually increased broodrearing, and that even extremely high doses had no significant effect upon brood area.
Bottom line: if there were an effect on brood, we would expect to see it in field studies. Such studies do not show negative effects at realistic doses.
Vine Crops--Squashes And Melons
Colonies fare poorly on vine crops (cucurbits) unless they have alternate forage (pers obs). Exposure to pesticides likely exacerbates this problem. Two recent studies found that foliar, soil, or irrigation-applied imidacloprid may result in residues in squash or pumpkin nectar and pollen to levels at which some behavioral effects on bees may occur.
Dively 20 found that seed treatment of pumpkins was safe for bees, but that if neonics are applied close to bloom (as by chemigation or foliar application) that they may contaminate the pollen to the extent that one might expect some effects on the "pollen hogs" in the colony, that is, newly emerged workers and drones, or nurse bees.
Stoner 21 found that at allowed label rates for squash, neonic residues in nectar or pollen could push into the low range of observable behavioral effects. Such effects would likely only be serious to honey bees should lack of alternative forage be available. However, this would be different for the specialized native squash bees: "squash bees are specialists on Cucurbita, feeding their larvae exclusively on Cucurbita pollen, and also build their nests in soil, often directly beneath squash and pumpkin vines, so they could have much more exposure to the soil-applied insecticides used on these crops." 22
Sunflowers
Beekeepers in France emphatically blamed Gaucho seed treatment of sunflowers for colony losses. Bonmatin 23 (clearly on a mission against imidacloprid) found that sunflowers could recover imidacloprid from the soil following crops treated the previous year, and that the plants concentrated the residues in the flower head tissue (although he did not analyze nectar). Even so, he did not find residues that should have caused intoxication, even with seed treated at a much higher rate than on the U.S. label.
In Argentina, Stadler 24 placed hives in the center of large fields of flowering sunflowers from seed treated again at a higher rate than the U.S. label, and confirmed that at least 20% of the pollen in the combs was sunflower, and that the colonies had stored sunflower honey. They could not detect residues of imidacloprid in the pollen, and found that the colonies in the treated field actually performed better than in the untreated! They then moved the hives to natural pasture, and checked them again after 7 months, and found no differences between the groups.
So I don't understand the videos I've seen of trembling or lethargic bees on sunflower blossoms in France. If any U.S. beekeepers have had trouble with bees on seed-treated sunflowers, I'd like to hear!
Buildup In Soil
In some clay soils residues of the neonicotinoids bond tightly to soil particles and may degrade slowly. However, the question is whether the roots of subsequently planted crops are able to absorb them (a Bayer rep pointed out to me that if they did, the farmer wouldn't need to pay for seed treatment the next year). Data from canola fields in Canada (Fig. 2), in which treated seed has been planted year after year, do not support that residues escalate in the bloom, and a study is currently being run in California.
Figure 2. Some of Canadian beekeeper Cory Bacon's hives working canola this July. Lab studies aside, Canadian bees appear to do quite well on seed-treated canola year after year, and I don't hear the beekeepers complaining.
Native Pollinators
There are many other insects that feed on nectar and pollen. Native bees (Fig. 3) would be especially susceptible to systemic insecticides, since they do not fly far to forage, their larvae consume pollen directly, and due to their solitary nature, if the behavior of any female bee is disrupted, she may be unable to leave offspring. However, should native bee larvae have as high a tolerance of neonicotinoids as do honey bee larvae, the concern for larvae may be unfounded.
Figure 3. A sweat bee, Agapostemon virescens, on chicory flowering alongside an Indiana corn field. It is likely that solitary bees, such as this species, would be more negatively affected by neonicotinoids than would a honey bee colony. Photo by Larry Garrett, ID thanks to Dr. Robbin Thorpe.
Solitary native bees are an excellent bioindicator of whether systemic insecticides are causing problems, since they do not have a "reserve" as does a honey bee colony. As far as I can tell from the research, the decline in native bee populations appears to be mostly from habitat loss due to wall-to-wall tillage, not to mention spraying with old-school pesticides. There is scant evidence that field-relevant doses of neonics harm native pollinators, but this is an area that cries for additional research. Two good species to investigate would be our native squash and sunflower bees, since both forage predominately on the nectar and pollen of those plants, and since neonicotinoids are applied to both those crops.
Other Species Of Life
There is legitimate concern about the effects of seed treatments upon earthworms. Dittbrenner 25 found that some species moved less soil in response to imidacloprid. Other researchers 26 have found that some predatory species of insects or spiders may be negatively affected in treated fields, likely due to the suppression of aphid populations-seed treatment only suppresses aphids while plants are young. As plants grow, the insecticide becomes too diluted to affect either sap-sucking insects or (ideally) pollen- or nectar-feeding insects.
The seed treatments appear to be more environmentally friendly to birds (who learn to avoid the seeds) and mammals than the insecticides that they replace
Water Pollution
I've got a background in aquatic biology, and I agree with Dr. Henk Tennekes that levels of imidacloprid in surface waters in areas of heavy applications on non food crops (such as in the Netherlands) are of concern for aquatic ecosystems. Jody Johnson 27 found 7-30 ppb in some urban/suburban water, and up to 130 ppb in nursery puddles, and low levels in some streams. Neonics are relatively nontoxic to fish, but could affect the populations of the invertebrates upon which they feed.
Landscape/Ornamental Uses
Dr. Vera Krischik 28 has pointed out the potential dangers of landscape or ornamental uses of imidacloprid due to the possibility of extremely high doses making it into the nectar. Residues that would not be allowed in field crops are possible with landscape and nursery applications, and there are reports of bees dying from nectar from treated nursery plants. I concur with Dr. Krishik's concerns.
Tree Injections
In order to kill certain tree pests (lerp psyllids on eucalypts, borers in elm or ash) imidacloprid is registered for root or tree treatment. There is reason for concern about some of these registrations, as there is unpublished data of scary high concentrations in nectar.
Foliar Applications
Clearly the best uses for neonicotinoids are for seed application or soil drench. Foliar applications open a new can of worms, due to irregularity of application, translocation to bloom or extrafloral nectaries, or to adjacent flowering weeds. Foliar applications of neonicotinoids can clearly cause bee kills, and are much more subject to vagaries in application timing and other details than are seed treatments.
The registered uses as foliar applications should be safe for bees if label directions are followed exactly, but I simply haven't seen enough data to make an assessment. Beekeepers should file incident reports if there are problems.
Simple Overuse
Dr. Jim Frazier points out that the unrotated use of the same seed treatments is contrary to good pesticide resistance management. Already we are seeing calls to expand the refuge plantings of non Bt corn; 29 it would likely be wise to do the same with neonic treatments. My concern is that if the pests develop resistance, then farmers will have to use additional sprays.
The Absence Of Any "Smoking Gun"
If neonics were actually causing colony mortality, it should be child's play to demonstrate--just feed a colony syrup or pollen spiked with the insecticide and see how long it takes to kill it. The fact is, that try as they might, no research team has ever been able to induce colony mortality by exposing the bees to field-relevant doses of any neonicotinoid (although one can get a significant kill from corn planting dust). Nor has any investigation ever been able to link neonic residues in the hive to colony mortality. Every claim that neonics are causing serious bee mortality is unsupported supposition, not backed by any concrete evidence.
The Ignoring Of Negative Findings
What is interesting about the neonics and honey bees is that the adverse effects that one may see when testing individual bees in the lab don't necessarily translate into effects at the colony level in the field. I've spoken with several researchers who have tried to demonstrate harm to colonies by feeding them large amounts of imidacloprid, and found that it is hard to see any effect. 30
Such "negative findings" are rarely published--after all, who, other than the registrant or the EPA, would be interested in studies in which investigators expose bees to the chemical, and find that nothing happens? So the majority of such findings would only be published by the registrant, and of course no one trusts their research (damned if they do, damned if they don't)!
Reviews Of The Evidence
There has been a mountain of research done on the neonics, but most folk don't have time to review it all (even if they could get their hands on the papers), so they must depend upon a trusted other to do so. Please don't take my word for it-here are some (mostly) recent reviews; most are free downloads:
Reviews With A Pro Neonic Bias:
I find that documents coming from the chemical industry typically have a reassuring slant, but invariably get their facts straight (it would be foolish for them to get caught in a lie).
Maus, C, G Cure, R Schmuck (2003) Safety of imidacloprid seed dressings to honey bees: a comprehensive overview and compilation of the current state of knowledge. Written by Bayer scientists, but the facts are sound. http://www.bulletinofinsectology.org/pdfarticles/vol56-2003-051-057maus.pdf
Reviews With An Anti Neonic Bias:
Anti-neonic reviewers tend to cherry pick out several questionable studies, embellish the implications, and ignore on-the-ground beekeeper experience.
Small Blue Marble. Free downloads of a number of neonic papers. http://smallbluemarble.org.uk/research/
Pilatic, H (2012) Pesticides and Honey Bees: State of the Science. Decent summaries of many studies. http://www.panna.org/sites/default/files/Bees&Pesticides_SOS_FINAL_May2012.pdf
Relatively Objective Reviews:
Xerces Society (who advocate on behalf of native pollinators)-Are Neonicotinoids Killing Bees? http://www.xerces.org/neonicotinoids-and-bees/]--did not find any strong evidence that neonics are harming pollinators, but recommend caution with use and further study.
AFSSA (2010) Weakening, collapse and mortality of bee colonies The French Food Safety Agency conducted a thorough review of all suspected causes of colony mortality in Europe. They arrived at the politically unpopular finding that "The investigations and field work conducted to date do not lead to any conclusion that pesticides are a major cause of die-off of bee colonies in France." http://www.uoguelph.ca/canpolin/Publications/AFSSA%20Report%20SANT-Ra-MortaliteAbeillesEN.pdf
The European Food Safety Authority in their Statement on the findings in recent studies investigating sub-lethal effects in bees of some neonicotinoids in consideration of the uses currently authorised in Europe http://www.efsa.europa.eu/fr/efsajournal/pub/2752.htm, concluded that "Further data would be necessary before drawing a definite conclusion on the behavioural effects regarding sub-lethal exposure of foragers exposed to actual doses of neonicotinoids."
Blacquiere, et al (2012) Neonicotinoids in bees: a review on concentrations, side-effects and risk assessment http://www.gesundebiene.at/wp-content/uploads/2012/02/Neonicotinoide-in-bees.pdf This is a very thorough review of 15 year's worth of research (over 100 studies).
Cresswell (2011) A meta-analysis of experiments testing the effects of a neonicotinoid insecticide (imidacloprid) on honey bees. http://www.springerlink.com/content/j7v320r55510tr54/fulltext.pdf in reviewing 14 studies, estimated that "dietary imidacloprid at field-realistic levels in nectar will have no lethal effects, but will reduce expected performance in honey bees by between 6 and 20%."
Creswell, Desneux, and vanEngelsdorp (2012) Dietary traces of neonicotinoid pesticides as a cause of population declines in honey bees: an evaluation by Hill's epidemiological criteria. (Note the coauthor Dennis vanEngelsdprp, who has studied CCD as closely as anyone) "We conclude that dietary neonicotinoids cannot be implicated in honey bee declines, but this position is provisional because important gaps remain in current knowledge. We therefore identify avenues for further investigations to resolve this longstanding uncertainty."
Of course, all researchers cover their butts and qualify their statements by suggesting that additional research needs to be done. These insecticides have been on the market for about a decade, and we are still learning about them. We definitely want to learn more about their effects upon other non target species, interactions with parasites, synergies with other pesticides, and sublethal behavioral effects.
I would prefer that you read the studies yourself, and then form your own opinions, but in reality I don't expect you to read the hundreds of studies that I've read. It's likely that most of you won't even bother to read the reviews above!
Summary: The consensus opinion of the comprehensive reviews above, as well as of the vast majority of bee researchers that I've spoken with, mirrors Blacquiere's conclusion: "Many lethal and sublethal effects of neonicotinoid insecticides on bees have been described in laboratory studies, however, no effects were observed in field studies with field-realistic dosages."
The Elephant In The Living Room
Let's just put all scientific speculation aside, and look at the obvious--the survival and productivity of colonies actually exposed to neonics-treated crops. Not only is there no compelling evidence to date that exposure to seed-treated crops is causing harm to bees, but there are plenty of examples to the contrary, such as the thriving bee operations in the Corn Belt.
Neonicotinoid seed treatments actually appear to be living up to expectation as reduced-risk insecticides. When skeptical researchers have tested actual pollen and nectar from seed-treated crops, they invariably confirm that any neonicotinoid residues are indeed quite low. Bonmatin 32 sampled imidacloprid levels in corn pollen (Fig. 4) for three years running in France--they averaged 2.1 ppb. But contaminated pollen only made up about half of the pollen trapped at the entrances, so he revised his overall colony exposure via pollen to 0.6 ppb--a level at which no harmful effects have ever been observed.
Over the past two seasons Henderson and Bromenshenk (in press) sampled trapped nectar and/or pollen from hives in canola fields in Canada and corn across the Midwest; 95% contained less than 2.5 ppb of clothianidin residues.
Figure 3. A sweat bee, Agapostemon virescens, on chicory flowering alongside an Indiana corn field. It is likely that solitary bees, such as this species, would be more negatively affected by neonicotinoids than would a honey bee colony. Photo by Larry Garrett, ID thanks to Dr. Robbin Thorpe.
Colonies subsisting on corn pollen alone may indeed go downhill, but that would be due to its lack of certain amino acids. They do not appear to suffer from going into winter with a portion of their beebread consisting of pollen from seed-treated corn. No study (and there have been several) has been able to demonstrate that colonies suffer from foraging on seed-treated corn pollen, and some suggest that it was actually of benefit to them. 33
On the Canadian prairie, colonies build up and survive fine on a diet of canola nectar and pollen from treated fields. If neonicotinoid seed treatments were indeed causing the sort of colony mortality that some claim, the Midwestern and Canadian beekeepers should notice!
The Good, The Bad, And The Ugly
My personal assessment of our state of knowledge on the neonics:
The Good
Neonics are unquestionably reduced-risk insecticides as far as humans and wildlife are concerned, and their use as seed treatments appears to be an environmentally-friendlier way to put the pesticide exactly where it is needed.
Bees and other pollinators appear to be able to thrive on the pollen and nectar of seed-treated plants.
The Bad
There are clearly documented sublethal behavioral effects, but they do not appear to affect bees at field-relevant doses, and appear to be greatly mitigated at the colony level.
Misapplication by homeowners and nurseries can result in unacceptably high residues in nectar or pollen, as can chemigation (as in vine crops).
There is the possibility of residue buildup in soil, which should be monitored.
Landscape and ornamental use can result in runoff into aquatic ecosystems, as documented by Henk Tennkes.
I suggest that beekeepers work closely with regulators on these issues.
The Ugly
Foliar (spray) applications are less well studied than seed treatments, and have greater potential for inadvertent impact on pollinators. Applications to flowering (or soon to be flowering) plants could cause serious bee mortality, and should be carefully regulated.
Injections of, or root application to, nectar-producing trees. For the sake of pollinators these applications must be closely investigated and monitored.
Planting dust from sowing of corn. Although significant planting dust kills are rare, they are ugly. This issue is a bleeding wound to the beekeeping community, and needs to be addressed by the EPA and the registrants. Beekeepers should not be forced to suffer mortality to their livestock due to unregulated pneumatic planter dust. France and Germany have models that we can follow. Beekeepers rightfully feel strongly that the registrants should step forward and compensate beekeepers for their losses until the issue is resolved.
Conclusion
There is no conclusion. Neonics have only been on the market for about a decade, and we are learning how best to use and regulate them. There is plenty of current research and monitoring being done, and the world's main regulatory agencies are currently carefully reviewing their registrations.
Separating Fact From Fiction
Up 'til now this article has been my best shot at an objective review of the scientific data and on-the-ground assessments of the neonicotinoid insecticides. Now I am going to shift from statement of fact to my own personal opinions.
I don't want to hammer on the anti-neonic crowd, nor do I want to sound condescending. One can indeed make a circumstantial case against the neonics, and I feel for beekeepers who have watched their hives fall apart--especially from pesticide issues. What I found, however, is that if one really does their homework, that the case against the neonics largely falls apart.
What bothers me is when advocates embellish the facts to suit their case. I choke on the amount of mis- or disinformation in many of their publications. For example, a recent issue of Britain's The Beekeepers Quarterly 34 informs us that:
"in California [neonics] were applied to the entire almond crop for the last decade--which is why American bees collapsed so dramatically"
How easy it would have been to solve CCD if only that statement had any veracity! In truth, neonics were not used to any extent on almonds, a fact easy to check since California pesticide use reports are freely available. I find this sort of tossing about misinformation to be unethical.
The facts are that that when I checked the use reports for 2003, 2006, 2009, and 2010, there were zero neonic applications in the first two years, and only 96 and 1070 lbs of imidacloprid applied in 2009 and 2010 respectively (58 applications in 2010, and one app. of thiamethoxam of 0.17 lbs). To put those figures into perspective, about 20 million pounds of some 350 different pesticides are applied to almonds each season, predominately fungicides, which the growers spray liberally over the bees and bloom during wet springs. Yet colonies generally come out of almonds looking great!
It's true that Bayer withdrew the registration for imidacloprid for almonds, but rather than being an admission of a problem, 35 it simply wasn't worth it for Bayer to perform additional supportive studies for a product that not only wasn't being used, but had gone off patent and would have been sold by copycat manufacturers using Bayer's data (Dr. David Fischer, pers comm).
The problem with misinformation is that well-meaning folk then hop on the bandwagon to push their legislators to do something about an imagined problem. The more that I investigate pesticide issues, the more I find that policy has been driven by the politics of misinformation and fear, rather than by objective analysis of risks vs. benefits. I quoted the introduction to this article from a very readable book (a free download which I highly recommend) called "Scared to Death." 36 The author gives examples in which well-meaning advocacy groups have fomented enough public pressure to force the withdrawal of this or that chemical from the market, despite a lack of evidence that the chemical was in truth harmful!
Caution: If you are a lifelong environmentalist, reading a decidedly pro-chemical book such as this will take you out of your comfort zone, and may force you to reevaluate your established views. However, it is impossible to dismiss the author's analysis, since he does a pretty good job of backing up his claims with facts!
Overstepping The Bounds
I strongly support the pesticide watchdog groups, and frequently refer to their websites for information. However, I feel that they sometimes fall into Abraham Maslow's trap of: "If the only tool you have is a hammer, you tend to treat everything as if it were a nail." Some of these groups would have us believe that every health problem that humans or bees have can be blamed upon pesticides, a fear that I bought into in my younger days. But reality is not that simple.
For example, in researching the DPR database, I came across the figures for total pesticide use per county in California. 37 Aha, I thought, here's a chance to nail a correlation between pesticide exposure and cancer! So I ran down a map for incidence of cancer by county to compare. 38 To my utter surprise, Fresno and Kern, agricultural counties using 30 and 25 million pounds of pesticides, respectively, in 2010 had lower cancer rates than did the pristine Northern California coastal counties such as Humboldt and Mendocino (0.03 and 1 million pounds). That bastion of environmental activism and organic everything, Marin county (0.06 million lbs), was in the highest tier of cancer incidence! Astoundingly, all six of the Calif counties with the highest pesticide usage were in the lowest tiers of cancer rates. Go figure!
The neonicotinoids (generally lumped together with GMO's) have currently been pumped up to be a straw man that is responsible for the demise of the honey bee, and some advocacy groups are pulling out all stops in order to take them down. A problem happens when advocacy groups shift from merely informing our regulatory agencies, to the starting of public campaigns (that ignore actual evidence) to push lawmakers to overstep the regulators and ban a certain chemical anyway. This can result in unintended consequences to both humans and bees.
I have a vested interest in pesticides that are safer for humans, and the neonics fit that bill. In the case of bees, should seed treatment with clothianidin be banned, as PANNA is pushing, it's not like farmers are all going to suddenly go organic--they will simply substitute other insecticides, which will then pollute the environment (and likely cause bee mortality) to a much greater degree-even some "organic" pesticides are more harmful to bees or other beneficials than some synthetics. 39, 40
Not only that, but when emotion trumps science, what are farmers and the Plant Protection Product industry supposed to do? It takes millions of dollars to bring a new product to market--including the newer generation "biopesticides" and reduced-risk pesticides. Why should industry invest if their hard work all goes up in smoke as the result of an irrationally fearful public campaign?
Practical application: my concern is that the beekeeping community should be cautious about allowing itself to be used as a poster child for the "neonicotinoids are the cause of CCD and the extinction of the bee" NGO's. Some of these same advocates could well be campaigning next year against the natural toxins, or grains of GMO pollen, that are found in some honeys!
The EPA is actually doing a decent job. I've read their risk assessments for the neonics. They ask the right questions, and base their decisions on scientific evidence, not anecdote and emotion. I feel that when anti-chemical advocates or beekeepers bypass the system, that our society and the environment may suffer. The current focus on the neonicotinoids has drawn attention away from the incontrovertible damage caused to colonies every year by spray applications of other pesticides, as well as from important bee research which is finally elucidating the biological causes of colony mortality worldwide. To me, this misdirection of focus is a problem.
Folks, all regulatory agencies worldwide are fully aware of the questions regarding the neonicotinoid insecticides. The EPA is stuck between a hostile congress and farm lobby on one side, and the NGO advocacy groups and beekeepers on the other, and must stick to scientific evidence. There are plenty of watchdogs making sure that EPA does its job.
Let's Redirect Our Energy
Instead of putting unwarranted lobbying effort against the single insecticide clothianidin, the bee industry would better benefit by going after (as Darren Cox says) "the low-hanging fruit"--the all-too-common bee kills due to spray applications of other pesticides. This is a labeling, educational, and enforcement issue.
The EPA needs to better clarify its label requirements to prevent applicators from spraying onto flowering crops or allowing pesticide drift onto impact adjacent areas.
The EPA needs to reassess the impact of fungicides, surfactants, other adjuvants, or tank mixes upon bees.
Growers and applicators need to be better educated as to how to protect their crops without harming pollinators. Sometimes simply changing the timing of spraying can protect bees.
EPA needs to push state agencies to cooperate with (rather than discourage) beekeepers when they suffer damages.
State agencies need to take the lead in actually enforcing pesticide laws when violations occur.
The EPA has brought beekeepers to the regulatory table, and we are currently being well represented by the National Honey Bee Advisory Board, and by Darren Cox at the Pesticide Program Dialogue Committee. I'm greatly encouraged that the NHBAB currently includes beekeeper/growers--who see both sides of the issue of necessary plant protection vs. "acceptable damage" to bees. The commercial beekeepers are clearly letting the EPA know of the extent of their losses due to pesticides.
I want to also be clear that we should all be appreciative of the hard work done by the NGO's (overzealous or not) and especially by those beekeepers who, at considerable personal expense, donate their time toward the benefit of our industry by lobbying the regulators to pay attention to our very real issues.
Last Minute Update:
As I was getting ready to send this article off to press, the EPA denied the recent petition requesting emergency suspension of clothianidin based on imminent hazard, stating in its response:
"Based on the data, literature, and incidents cited in the petition and otherwise available to the Office of Pesticide Programs, the EPA does not find there currently is evidence adequate to demonstrate an imminent and substantial likelihood of serious harm occurring to bees and other pollinators from the use of clothianidin." 41
You can read the technical supporting documents yourself. 42 I do not for a moment doubt the earnestness of the petitioners, but I found that the EPA interpreted the research exactly as I have, and concur that there was simply not enough evidence (to date) that clothianidin poses a major threat to bees, beekeeping, or pollinators in general.
References
1 Entine, J (2011) Scared Death: How Chemophobia Threatens Public Health. http://www.acsh.org/include/docFormat_list.asp?docRecNo=1133&docType=0
2 July ABJ
3 Credit to Entine (2010) op. cit.
4 Tomizawa, M and JE Casida (2009) Molecular recognition of neonicotinoid insecticides: the determinants of life or death. Acc. Chem. Res. 42(2): 260-269.
5 Pimentel, D. 2001. Environmental effects of pesticides on public health, birds and other organisms. Rachel Carson and the Conservation Movement: Past Present and Future. Conference presented 10-12 August 2001, Shepherdstown, W.V. http://rachels-carson-of-today.blogspot.com/2011/02/environmental-effects-of-pesticides-on.html
6 Munkvold, G (2006) Seed Treatment http://www.extension.iastate.edu/Publications/CS16.pdf
7 Decourtye and Devillers (2010) Ecotoxicity of Neonicotinoid Insecticides to Bees. In, Insect Nicotinic Acetylcholine Receptors, Advances in Experimental Medicine and Biology 683: 85-95, DOI: 10.1007/978-1-4419-6445-8_8.
8 Ramakrishnan, R (1999) Imidacloprid-enhanced Reticulitermes flavipes (Kollar) (Isoptera: Rhinotermitidae) susceptibility to the entomopathogen Metarhizium anisopliae (Metsch.) Sorokin. J. Econ. Entomol 92:1125-1132.
9 Peters, J M (1967). Factors affecting caffeine toxicity: a review of the literature. The Journal of Clinical Pharmacology and the Journal of New Drugs (7): 131-141
10 Suchail, S, et al (2004a) Metabolism of imidacloprid in Apis mellifera. Pest Manag Sci 60:291-296
11 Suchail, S, et al (2004b) In vivo distribution and metabolisation of 14C-imidacloprid in different compartments of Apis mellifera L. Pest Manag Sci 60(11):1056-62 (2004b).
12 Tennekes HA. The significance of the Druckrey-Kupfmuller equation for risk assessment-the toxicity of neonicotinoid insecticides to arthropods is reinforced by exposure time. Toxicology 276(1):1-4.
13 Dr. John Casida, pers comm
14 Faucon, J-P, et al (2005) Experimental study on the toxicity of imidacloprid given in syrup to honey bee (Apis mellifera) colonies. Pest Manag Sci 61:111-125.
15 Are bees addicted to caffeine and nicotine?.ScienceDaily. Retrieved February 8, 2011, from http://www.sciencedaily.com/releases/2010/02/100210101504.htm
16 Lodesani, M, et al (2009) Effects of coated maize seed on honey bees: Effects on the brood. http://www.cra-api.it/online/immagini/Apenet_2009_eng.pdf
17 Lodesani, Marco, pers comm
18 Hatjina, F and T Dogaroglu (2010) Imidacloprid effect on honey bees under laboratory conditions using hoarding cages. http://www.coloss.org/publications/proceedings_workshop_bologna_2010
19 Lu,C, KM Warchol, RA Callahan (2012) In situ replication of honey bee colony collapse disorder. Bulletin of Insectology 65 (1): 99-106.
20 Dively, GP, Kamel A (2012) Insecticide residues in pollen and nectar of a cucurbit crop and their potential exposure to pollinators. J Agric Food Chem. 60: 4449-4456.
21 Stoner KA and BD Eitzer (2012) movement of soil-applied imidacloprid and thiamethoxam into nectar and pollen of squash (Cucurbita pepo). PLoS ONE 7(6): e39114. doi:10.1371/journal.pone.0039114
22 ibid
23 Bonmatin, JM, et al (2005) Quantification of imidacloprid uptake in maize crops. J. Agr. Food Chem. 53: 5336-5341.
24 Stadler T, et al (2003) Long-term toxicity assessment of imidacloprid to evaluate side effects on honey bees exposed to treated sunflower in Argentina, Bull Insect 2003; 56:77-81.
25 Dittbrenner, N, et al (2011) Assessment of short and long-term effects of imidacloprid on the burrowing behaviour of two earthworm species (Aporrectodea caliginosa and Lumbricus terrestris) by using 2D and 3D post-exposure techniques. Chemosphere 84(10): 1349-1355.
26 Albajes R, Lopez C, Pons X (2003) Predatory fauna in cornfields and response to imidacloprid seed treatment. J Econ Entomol. 96(6):1805-13.
27 Jody Johnson (2011 ABRC)
28 Krischik,VA, AI Landmark, and GE. Heimpel (2007) Soil-Applied Imidacloprid Is Translocated to Nectar and Kills Nectar-Feeding Anagyrus pseudococci (Girault) (Hymenoptera: Encyrtidae). Environ. Entomol. 36(5): 1238-1245.
29 http://www.sciencedaily.com/releases/2012/06/120605102846.htm)-it
30 Dively, GP, et al (2010) Sublethal and synergistic effects of pesticides http://agresearch.umd.edu/recs/WREC/files/2010Programs/EASSubletha%20Effects2010.pdf
31 Creswell, Desneux, and vanEngelsdorp (2012) Dietary traces of neonicotinoid pesticides as a cause of population declines in honey bees: an evaluation by Hill's epidemiological criteria. Pest Management Science 68(6): 819-827
32 Bonmatin (2005) Op. cit.
33 Nguyen BK, et al (2009) Does imidacloprid seed-treated maize have an impact on honey bee mortality? J Econ Entomol 102:616-623.
34 The Beekeepers Quarterly June 2012 (U.K.) Neonicotinoids--Our toxic countryside http://www.boerenlandvogels.nl/sites/default/files/BKQ%20108%20-%20Neonicotinoid%20Pesticides_0.pdf
35 http://www.panna.org/sites/default/files/BayerPullImidacloprid.pdf
36 Entine, op. cit.
37 http://www.cdpr.ca.gov/docs/pur/pur10rep/comrpt10.pdf
38 http://www.chcf.org/~/media/MEDIA%20LIBRARY%20Files/PDF/C/PDF%20CancerInCalifornia12.pdf
39 Bahlai, CA, et al (2010) Choosing organic pesticides over synthetic pesticides may not effectively mitigate environmental risk in soybeans. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0011250
40 http://www.organicfarming101.com/organic-pesticides/
41 Response to petition http://www.regulations.gov/#!documentDetail;D=EPA-HQ-OPP-2012-0334-0006
42 Technical supporting documents http://www.regulations.gov/#!documentDetail;D=EPA-HQ-OPP-2012-0334-0012
Category: Pesticide Issues
Tags: insecticides, neonicotinoids | insecticides Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/insecticides/ |
Testing of Bee Feed Syrups for Neonicotinoid Residues
First published in: American Bee Journal, August, 2012
Testing Of Bee Feed Syrups For Neonicotinoid Residues
Eric Mussen1 and Randy Oliver2
First Published in ABJ in August 2012
The widespread adoption of the systemic neonicotinoid insecticides has led a number of beekeepers to question whether the commercially available corn, beet, or cane sugar syrups might be contaminated with residues of those insecticides.
Introduction
Beekeepers often feed some form of sugar syrup to colonies for either buildup or winter stores. The raw materials for sugar production come mainly from three cultivated crops-traditionally sugar cane or sugar beets, from which sucrose is extracted; or from corn (maize), from which high fructose corn syrup (HFCS) is produced.
In recent years, growers have widely adopted the practice of treating corn and sugar beet seed with systemic neonicotinoid insecticides [1, 2, 3], and clothianidin may be used on sugar cane in some areas [4]. The understanding that these insecticides are "systemic" (transported throughout the plant tissues) has led some beekeepers to question whether residues may make it into the final sugar product.
We submitted samples of the bee feed syrups offered by two major U.S. suppliers for independent testing. Residues of neonicotinoid insecticides, as well as their degradation products, can be multiply-detected at as little as ppb levels by modern analytical instrumentation [5].
Materials And Methods
We solicited samples of syrups (Table 1) from Stuart Volby of Mann Lake Ltd. (Mann Lake, MN) and from Dadant (Chico, CA) branch manager John Gomez, which we reshipped for testing to Roger Simonds, Laboratory Manager of the USDA Agricultural Marketing Service lab. We requested analyses for neonicotinoid insecticides and their principal degradates.
Supplier Manufacturer Syrup Type
Mann Lake Ltd. Cargill Type 55 HFCS
Type 42 HFCS
Liquid sucrose (beet)
Liquid sucrose (cane)
Dadant & Sons, Inc. (Chico branch) Archer Daniels Midland (ADM) California blend:
50% Type 42 HFCS
50% Liquid sucrose (cane)
Table 1. Bee feed syrups submitted for analysis.
1 Extension Apiculturist, University of California, Davis, CA 95616
2 Proprietor, Golden West Apiaries, Grass Valley, CA 95945
Results
None of the tested samples contained detectable levels of either the neonicotinoid parent compounds or their degradates (Fig. 1).
Figure 1. Typical test results. The LOD is the "limit of detection," i.e., the lowest concentration in parts per billion (ppb) that the instrument can detect. The lab tested for both parent compounds (e.g., imidacloprid) as well as for the degradation products of the insecticides, which may also exhibit toxicity.
Discussion
Although no residues were detected in the syrup samples submitted for testing, the possibility exists that there were residues below the limit of detection (1 ppb for most of the parent compounds). However, levels below 1 ppb are generally accepted as being well below the no observable adverse effects concentration (NOAEC) [6].
These results are not surprising for HFCS, given that when the USDA tested 655 samples of corn grain in 2007 [7], no residues of neonicotinoid insecticides were detected. Although the tolerance level for clothianidin in sugar beets is 20 ppb [8], there are often no detectable residues from beets in the field [9]. Similarly, there were no detectable residues in the sample of beet sugar that we submitted.
Although this was a very limited sampling, it gave no evidence that beekeepers need to be concerned about neonicotinoid insecticide residues in feed syrups from the major suppliers.
Acknowledgements
Thanks to the cooperation of Stuart Volby and John Gomez for supplying samples, Roger Simonds for expediting the analyses, and to the U.C. Davis Extension Apiculture Program for providing funds for sample analyses.
References
[1] Anon (2012) 2012 Corn Insect Control Recommendations. http://eppserver.ag.utk.edu/redbook/pdf/corninsects.pdf
[2] Valent (2011) Valent USA Announces NipsIt™️ SUITE Sugar Beet Seed Treatment System. http://www.seedtoday.com/info/ST_articles.html?ID=113940
[3] Syngenta (2012) CRUISER FORCE sugar beet seed - the UK's number one choice. http://www.syngenta-crop.co.uk/pdfs/products/CruiserSB_uk_technical_update.pdf#view=fit
[4] APVMA (2010) Trade Advice Notice on clothianidin in the product Sumitomo Shield systemic insecticide http://www.apvma.gov.au/registration/assessment/docs/tan_clothianidin_60689.pdf
[5] http://quechers.cvua-stuttgart.de/
[6] Decourtye, A (2003) Learning performances of honeybees (Apis mellifera L) are differentially affected by imidacloprid according to the season. Pest Manag Sci 59: 269-278.
[7] USDA (2008) Pesticide Data Program Annual Summary, Calendar Year 2007, Appendix F Distribution of Residues by Pesticide in Corn Grain http://www.ams.usda.gov/AMSv1.0/getfile?dDocName=STELPRDC5074338
[8] Federal Register (2008) Clothianidin; Pesticide Tolerance. https://www.federalregister.gov/articles/2008/02/06/E8-1784/clothianidin-pesticide-tolerance
[9] FAO (2005) Clothianidin, Table 103. http://www.fao.org/fileadmin/templates/agphome/documents/Pests_Pesticides/JMPR/Evaluation10/Chlotiahinidin.pdf
Category: Pesticide Issues
Tags: bee feed syrups, insecticides, neonicotinoid, residues | residues Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/residues/ |
Sick Bees - Part 18E: Colony Collapse Revisited - Genetically Modified Plants
First published in: ABJ December 2012
Genetically Modified Plants
What Is Genetic Modification?
There's Nothing New About Transgenics
GMOs
An Odd Series of Connections
The Vilifying of Monsanto
What Are They Up To?
Practicality Overrides Principle
Hold the Hate Mail
The Changing Face of Agriculture
Bt Crops
Roundup Ready
Direct Effects of Roundup Use
Indirect Effects of Roundup Use
The Future of Roundup
Reality Check
Looking Ahead: The Chemical Treadmill & Pest Resistance
Additional Discussion
The Back Story on Plant Breeding and GM Crops
The Profit Motive
Enter GM Crops
The Second "Green Revolution"
Cautions About GM
Perspectives on GM
So What's The Problem?
Acknowledgements
References
Sick Bees - Part 18E:
Colony Collapse Revisited - Genetically Modified Plants
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in Dec 2012
Genetically modified (or GM) plants have attracted a large amount of media attention in recent years and continue to do so. Despite this, the general public remains largely unaware of what a GM plant actually is or what advantages and disadvantages the technology has to offer, particularly with regard to the range of applications for which they can be used [1].
The above quote is certainly an understatement! Genetically Modified Organisms (GMO's) are a highly contentious topic these days, and blamed by some for the demise of bees. In researching the subject, I found the public discussion to be highly polarized--plant breeders and farmers are largely enthusiastic (with appropriate reservations) about the benefits of genetic engineering, whereas health and environmental advocacy groups tend to be fearful of the new technology [2]. I will largely save my review of the history and pros and cons of GM crops for my website, and focus this article upon how GMO's relate to honey bee health.
What Is Genetic Modification?
The knowledge of genetics was not applied to plant breeding until the 1920's; up 'til then breeders would blindly cross promising cultivars and hope for the best. With today's genetic engineering, breeders can now take a gene from one plant (or animal, fungus, or bacterium) and splice it into the DNA of another plant. If they get it just right, the new gene can confer resistance to frost, drought, pests, salinity, or disease. Or it could make the crop more nutritious, more flavorful, etc. Such genetically modified crops are also called "transgenic," "recombinant," "genetically engineered," or "bioengineered."
There's Nothing New About Transgenics
There is nothing new about transgenic organisms, in fact you (yes you) are one. Viruses regularly swap genes among unrelated organisms via a process called "horizontal gene transfer" [3]. For example, the gene which is responsible for the formation of the mammalian placenta was not originally a mammal gene--it was inserted into our distant ancestors by a virus. If a gene introduced by a virus confers a fitness advantage to the recipient, then that gene may eventually be propagated throughout that species' population. Until recently, we didn't even know that this process has occurred throughout the evolution of life, and didn't know or care whether a crop was "naturally" transgenic!
GMO's
Both the scientific community and industry have done a terrible job at explaining genetic engineering to a distrustful public. There are clearly potential issues with genetic engineering, but they are being carefully addressed by independent scientists [4] and regulatory agencies, especially in Europe:
From the first generation of GM crops, two main areas of concern have emerged, namely risk to the environment and risk to human health.... Although it is now commonplace for the press to adopt 'health campaigns', the information they publish is often unreliable and unrepresentative of the available scientific evidence [5].
Jeffrey Smith, in his book "Seeds of Deception" [6] details a number of legitimate issues and early missteps in bioengineering, as well as pointing out the substantial political influence firms such as Monsanto have upon researchers, regulators, and legislators. We should be cautious to take their assurances with a grain of salt. On the other hand, I've checked the claims of other anti-GMO crusaders for factual accuracy, and found that many simply don't hold water. For example, two headlined studies of late, one on rats fed GE corn and Roundup herbicide, and another on the purported increased use of herbicides due to GE crops simply do not stand up to objective scrutiny [7]. It bothers me that the public is being misled by myths and exaggeration from both sides.
From my point of view, GE holds incredible promise and should be pursued in earnest, yet must also be very carefully monitored and regulated. In any case, GE crops have been widely adopted in U.S. agriculture (Table 1), and thus are now a part of beekeeping.
Table 1. The genetically engineered traits available to farmers have evolved rapidly as technology improves and as such crops become more widely adopted. Table from http://www.census.gov/compendia/statab/2012/tables/12s0834.pdf.
An Odd Series Of Connections
In 1972, the dean of biological sciences at my university hired me to set up a "world class insectary" (which I did). I raised mass quantities of insects for hormone extraction, in the hope that we might develop a new generation of eco-friendly insecticides [8]. Several years later I was shocked when Monsanto-a widely-despised chemical company with a sordid history- then hired him to create "a world-class molecular biology company" (which he apparently did). In 2002, Monsanto was spun off as an independent agricultural company.
Jump forward to 2010, when I had the good fortune to work with an Israeli startup--Beeologics--and witnessed the efficacy of their eco-friendly dsRNA antiviral product for honey bees. But to bring the product to market, they needed more backing. To my utter astonishment, they recently sold themselves to Monsanto!
The Vilifying Of Monsanto
These days one can simply mention the name "Monsanto" in many circles, and immediately hear a kneejerk chorus of hisses and boos. Sure, it had been easy for me to enjoy the camaraderie of riding the anti-Monsanto bandwagon; but I realized that that I shouldn't allow that sort of fun to substitute for the responsibility of doing my homework and getting to the actual facts of the matter! When I did so, I found that some of Monsanto's actions did indeed deserve opprobrium; but that much of the criticism directed at the current company is undeserved (Monsanto suffers from an ingenerate inability to practice effective PR). Concurrent with the purchase of Beeologics, Monsanto hired well-respected apiarist (and columnist) Jerry Hayes to head up a new honey bee health division, and appointed some prominent beekeepers (not me) to its advisory board. It dismays me that some beekeepers then immediately jump to the erroneous conclusion that Jerry has sold his soul to the Devil--nothing could be further from the truth!
What Are They Up To?
Some beekeepers imaginatively feared that Monsanto was about to create a GM bee or was up to some other nefarious plot. But in reality, Monsanto's vision of its future direction is anything but evil--I suggest that you peruse their website for your own edification [9], [10]. Of course I was curious as to why they had purchased Beeologics, since the market for bee medicine is far too tiny to draw the interest of a giant corporation. But one needn't be some sort of psychic in order to figure out a corporation's plans--all you need do is to read its recent patents, which are a virtual crystal ball for seeing ten years into the future. So I searched out any patents containing the words "Monsanto" and "RNAi."
To my great relief, I found that Monsanto was not up to some evil plot--far from it! I suggest you read two of the patents yourself [11]:
Chemical pesticidal agents are not selective and exert their effects on non-target fauna as well...Some chemical pesticidal agents have been shown to accumulate in food, and to exhibit adverse effects on workers that manufacture and apply such chemical agents. Thus there has been a long felt need for methods for controlling or eradicating... pest infestation on or in plants, i.e., methods which are selective, environmentally inert, non-persistent, biodegradable, and that fit well into pest resistance management schemes. Plant biotechnology provides a means to control pest infestations by providing plants that express one or more pest control agents. Recombinant pest control agents have generally been reported to be proteins selectively toxic to a target pest that are expressed by the cells of a recombinant plant.
What the patents tell us is that Monsanto clearly sees that the public is sick of pesticides. Genetic RNAi technology would allow plant breeders to develop crop cultivars that control insect pests in the same manner that the plants naturally control viruses. All that the breeder need do would be to identify a unique target protein in a particular pest, and then splice a gene into the plant to produce a "blocking" dsRNA molecule that would prevent the pest from building that specific protein. The beauty is that dsRNA molecules are already naturally found in plant tissues, the blocking molecule would be entirely specific for that pest alone, completely nontoxic to humans or other non target species, and be rapidly biodegradable. It would be a win all around (except for the pest)--crop protection, no toxic pesticides, and a sustainable farming technology (as well as a market for Monsanto's products, since they would need to continually develop slightly different cultivars in order to avoid pest resistance). Who'd have guessed that Monsanto would be leading the way toward developing eco-friendly pest control? Life is full of surprises!
Practicality Overrides Principle
Some folk make GM crops out to be some sort of abomination of nature, and shun them with religious fervor. I'm not sure that this is the best course for environmentalists to take, and that perhaps, in the face of an expanding human population and a warming climate, we should leave all the possible plant breeding solutions on the table. The organic farming community wholeheartedly endorses the biotechnology of "marker assisted selection" [12], yet arbitrarily draws the line at the directed insertion of desirable genes. This may sound like heresy, but as an environmentalist, I suggest that GE holds great promise for developing more nutritious plants that don't require pesticides, fertilizer, or irrigation--all of which would be wins for organic farming.
From a biological standpoint, I simply don't see GM crops as being any more inherently dangerous than conventionally bred crops. Our domestic plants today are often far from "natural"--you wouldn't recognize the ancestors of many. Be aware that even conventionally bred cultivars of several crops (beans, potatoes, celery, etc.) often turn out to be too toxic for humans.
This is not by any means a fluff piece for Monsanto or agribusiness. Farming is not what it used to be. In the U.S., 85% of farm sales are produced by less than 10% of farms, which hold 44% of farm acreage [13]. A mere six companies collectively control around half of the proprietary seed market, and three quarters of the global agrochemical market [14]. I abhor such corporate domination; neither do I see today's high-input agricultural practices as being either sustainable or ecologically wise.
That said, human demands upon the Earth's finite ecosystem are growing. There are only about 4.5 acres of biologically productive land on the surface of the Earth available for each current human inhabitant. Depending upon the culture's lifestyle, we use anywhere from 25 acres (U.S.) to as little as 1 acre (Bangladesh) to feed and clothe each person. Unfortunately for the bee (and many other species), due to human population growth there are over 200,000 additional human mouths to feed every single day--each requiring the conversion of another couple of acres of natural habitat into farmland!
It doesn't take a mathematician to figure out that if we wish to conserve natural ecosystems that we need to get more yield out of existing cropland! And one of the best ways to do that is to breed crops that are more productive and pest-resistant. The plant scientists in the corporate labs are making huge strides in developing such cultivars, both by GM and conventional breeding. If they manage to file a patent [15], so what?--other breeders can easily "steal" the germplasm away from the patented genes, and in any case, the patents expire after 20 years!
Monsanto has seen the writing on the wall--farmers and consumers are demanding not only more food production, but also more eco-friendly agricultural practices. Monsanto research is heading in that direction with their conventional breeding programs, the development of "biological" insecticides [16], and the goal of producing pesticide-free dsRNA crops. Add to that that the company could actually bring to market dsRNA medications against bee viruses, nosema, and perhaps varroa. All would be huge wins for the honey bee and beekeepers!
Hold The Hate Mail
Full disclosure: so despite my innate aversion to corporate dominance and corporate agriculture, I feel that we beekeepers should work with Monsanto to develop products for the beekeeping industry, as well as bee-friendly cultivars of crop plants, and have thus personally decided to be a cooperator in their initial bee research trial. Is this some sort of Faustian bargain? I don't know, but as a condition of my cooperation, I asked, and Monsanto agreed, to allow me to share the data collected with the beekeeping community--which could be a big win for us, since Monsanto has some of the best analytic labs in the world! I feel that it is far better to have Monsanto working on the side of beekeepers, rather than perhaps against us. At this point, I'd like to leave the GM debate behind, and address the facts of the matter as to any relationship between GM crops and CCD.
The Changing Face Of Agriculture
Genetic engineering has clearly changed the face of agriculture in the U.S. (Fig. 1).
Figure 1. These three crops account for over half of all U.S. acreage planted to principal crops, and all are worked to some extent by bees. Data from http://www.ers.usda.gov/data-products/adoption-of-genetically-engineered-crops-in-the-us.aspx
As can be seen from the figure above, any bees near corn, soy, or cotton are going to be exposed to pollen and nectar from GM plants, as well as to indirect effects due to the technology. So could GM crops be the cause of CCD?
Bt Crops
Biological plausibility: the insecticidal Bt toxins in GM corn and cotton pollen could harm adult or larval bees.
Organic farmers have long used the spores of the bacterium Bacillus thuringiensis (Bt) to kill caterpillars. Bt spores germinate in the caterpillar gut, and the bacterium produces insecticidal crystalline proteins (Cry proteins) that bind to specific receptors on the insect intestinal wall. Since different insect species have different receptors on their gut cells, different strains of Bt have evolved to specifically kill various caterpillars, beetles, mosquitoes, etc. [17]. The proteins are so species specific that wax moths can be controlled on combs by Bt aizawai, which produces Cry proteins that are toxic to moth larvae, but not to bees.
Molecular biologists tweak these Cry proteins to make them even more species specific, and then insert them into plant DNA, so that the plant then produces the proteins itself, thus making its tissues toxic to the target species. In order to delay the inevitable evolution of Cry-resistant pests, growers plant a percentage of "refuge" crop not containing the Cry genes. Even so, any particular Cry gene will only be effective for some number of years until resistant pests show up.
People have expressed concern about a poisonous substance being introduced into plant tissues, and to them I highly recommend the paper "Misconceptions about the Causes of Cancer" [18]. The reality is that plant tissues are naturally awash in poisonous substances. Plants have needed to repel herbivores throughout their evolution, and since plants can't run, hide, or bite back, they do it chemically. Many of our most popular fruits, nuts, grains, and vegetables (and especially herbs and spices) contain powerful phytotoxins. Their wild ancestors required cooking or leaching before the plant was edible to humans. Plant breeders systematically select for cultivars with lower levels of (the often strongly flavored) toxins.
Plants that are naturally resistant to pests contain more phytotoxins, often produced in response to damage from insects. For example, the sprouts of wheat, corn, and rye produce potent mutagens (enjoy that cup of wheatgrass juice!) [19]. And some plants naturally contain symbiotic bacteria and fungi in their tissues, which produce non-plant chemicals [20]. There is absolutely nothing biologically novel about insecticidal toxins in plant tissues.
The toxicity (or lack thereof) of Cry proteins to non-target organisms, especially upon two "charismatic" species--the honey bee and the monarch butterfly--has been well studied [21], [22], [23]. A recent and very well-designed experiment on the effect of GM Bt corn pollen upon the growth and survival of honey bee larvae was recently performed by a team of independently-funded German researchers [24]. They added pollen from four different sources to a standard semi-artificial larval diet.
Results: surprisingly, the larvae fed the pollen from the "stacked" GM corn containing a combination of three different Cry proteins exhibited a higher survival rate (100%), than those fed non-GM corn pollen! To me, a big plus for this study was that they also included a positive control of pollen from a wild plant said to be harmful to bees--only about 30% of those larvae survived! This finding confirmed that even some natural pollens are quite toxic, and that we should compare any toxicity trials of pesticides with those of the natural phytotoxins in nature.
Analysis: CCD and colony mortality occur even in the absence of GM Bt crops; feeding GM Bt pollen to adult bees or larvae does not cause observable adverse effects.
Verdict on Bt crops: The specific Bt cry proteins used in GM crops were intentionally chosen to not cause harm to bees. There is no evidence to date that they do. On the other hand, Bt crops require less use of insecticides that are clearly toxic to bees [25].
Roundup Ready
Monsanto's pitch is that Roundup Ready®️ (RR) crops allow farmers to practice weed-free "no till" farming, which saves both topsoil and money. The catch is that farmers must then douse their fields with Monsanto's flagship product, Roundup (ensuring sales of that herbicide--a great marketing strategy). Bayer CropScience has followed suit by introducing crops resistant to its Liberty herbicide, which has a different mode of action.
Herbicide-resistant crops do indeed address several major environmental problems:
No till farming does in fact require less labor and reduces soil compaction.
Farmers get greater production due to less competition from weeds.
No till also reduces the amount of petrochemical fuel involved in tillage.
No till greatly reduces soil erosion, which has long been a major environmental concern.
No till may help to sequester carbon in the soil, and to rebuild soil.
So what's not to love about Roundup Ready? There are a few main complaints--(1) the massive spraying of the active ingredient, glyphosate, for which there is questionable evidence that it may be an endocrine disruptor [26], (2) claims of intimidation by Monsanto of farmers who choose not to plant RR seed, and (3) the environmental impact and sustainability of the sort of weed-free monoculture possible with RR crops.
So how do Roundup and RR crops relate to honey bees?
Direct Effects Of Roundup Use
Biological plausibility: either the active ingredient (glyphosate), or the adjuvants could cause bee toxicity.
The EPA has thoroughly reviewed the research and found glyphosate to be practically nontoxic to bees (and humans). They have found the same for Roundup's adjuvant polyoxyethylene-alkylamine. However, some beekeepers tell me that they see increased bee mortality following the spraying of glyphosate (Fig. 3), but are not sure whether it was a generic product, or perhaps contained additional ingredients (surfactants, fungicides, or insecticides) added to the tank mix.
Figure 3. A farmer spraying glyphosate herbicide over Roundup Ready corn seedlings. Photo courtesy of beekeeper Larry Garrett.
Analysis: there is no strong evidence that the spraying of Roundup or generic glyphosate herbicide is directly causing significant bee mortality. However, Drs. Jim and Maryann Frazier have legitimate concerns about the effect of some adjuvants--especially the organosilicones [27], [28].
Indirect Effects Of Roundup Use
Biological plausibility: the elimination of weeds reduces bee forage.
The success of Roundup Ready technology has allowed farmers to largely eliminate weeds from their fields (at least until the inevitable resistant weeds take over). But they don't stop there--nowadays they practice "clean farming" and use herbicides to burn off every weed along the fencerows and in the ditches--the very places that bees formerly had their best foraging. This elimination of flowering weeds severely reduces the amount of available of bee forage, plus kills off the host plants of native pollinators (such as monarch butterflies) and beneficial insects.
European honey bees evolved in Europe (hence the name), and are adapted to the nutrition provided by Old World flowering plants. Many of the weeds in North America are old friends of the honey bee. On the other hand, honey bees were never exposed to corn, soybeans, sunflowers, or squashes until recently; neither corn nor sunflowers supply complete amino acid profiles in their respective pollens. Until the advent of Roundup Ready, the weeds in an around crops provided alternative nectar and pollen sources for bees; today there is often nary a bee-nutritious weed to be seen in or around a field of corn or soybeans (Fig. 4).
Figure 4. I took this photo of a no-till herbicide-resistant corn field, prior to the shading canopy of the crop closing over. Note the total lack of any sort of bee forage (or any species of anything other than corn). The soil surface is a far cry from the original densely vegetated prairie sod. Prior to RR, there was more weedy forage for bees, and especially from the traditional weed-controlling crop rotation into legumes or pasture.
Update: there's a great deal of debate about the safely of Roundup (the formulated product with it's surfactants) and its active ingredient, glyphosate. From http://npic.orst.edu/factsheets/archive/glyphotech.html
"In plants, glyphosate disrupts the shikimic acid pathway through inhibition of the enzyme 5-enolpyruvylshikimate-3-phosphate (EPSP) synthase. The resulting deficiency in EPSP production leads to reductions in aromatic amino acids that are vital for protein synthesis and plant growth.
As far as the claims that glyphosate causes cancer (notably Non-Hodgkin's Lymphoma), I agree with the regulatory agencies that the case against glyphosate is very weak. As far as glyphosate being an endocrine disruptor, I'll leave it to the researchers and regulatory agencies to figure it out. As I type these words, I've actually got caged bees to which I'm feeding glyphosate (at a field-realistic dose) for a trial, and not seeing increased mortality. But some research indicates that it may be harmful to the gut microbiota. This sort of research takes time, and eventually we'll figure out just how safe or harmful glyphosate is to bees, humans, or the environment.
But nothing in nature is simple. Eliminating the competition of weeds and insects may allow plants to hold back from the production of natural toxins. And a surprising piece of research found corn kernels from plants sprayed with either of two different herbicides actually contain more of the healthful carotenoids [30]!
The Future Of Roundup
It took Monsanto several years to genetically engineer Roundup-resistant crops, yet took farmers only slightly longer to inadvertently produce Roundup-resistant weeds by the conventional breeding technique of applying a strong selective pressure-the continuous application of Roundup!
Weed management scientists consider glyphosate to be a once-in-a-100-year discovery--it works on 140 species of weeds, and is relatively environmentally friendly. However, its overuse has led to the creation of several "driver weeds" that could soon lead to its redundancy in corn, soy, and cotton acreage [31]. This will drive farmers to turn to other herbicides (which will also in time fail). We can only hope that someday they will be forced back into practicing crop rotation into legumes and pasture.
Reality Check
In order to clarify cause and effect, I often seek out extreme cases. Such would be the situation in the Corn Belt, where I could compare the USDA's hive and honey data from the old days to those under today's intense planting of GM crops (Fig. 5)!
Figure 5. The most intense planting of GM crops is in Iowa and Illinois (the dark green areas of the map above). U.S. farmers planted nearly 100 million acres of corn this year, and 76 million of soy. That is enough acreage to cover the entire state of Texas with GM crops!. Source: http://www.nass.usda.gov/Charts_and_Maps/Crops_County/pdf/CR-PL10-RGBChor.pdf
So I went through the tedious process of downloading and transcribing the NASS agricultural census figures for Iowa. I entered the amount of corn acreage, the total number of colonies in the state, and what I consider to be the best measure of colony health--honey yield per hive (which of course is largely weather dependent, but should show any trends). I plotted the data below (Fig. 6):
Figure 6. Bee and corn data from Iowa, and the dates of introduction of corn pest control technologies. The dotted line is median honey yield per colony. No factor appears to have affected honey production, but colony numbers have decreased since the arrival of varroa. Gaps are missing data. Source NASS.
Note: for non beekeepers, varroa is a parasitic mite that arrived in the U.S. around 1990 and quickly became, and still remains, the Number One problem in bee health-far more than any other factor.
Over the years, corn acreage increased by 18%. Other than the prodigious crop of 1988, honey production has averaged around 67 lbs per hive. The thing that stands out is the plot of number of colonies. Hive numbers jumped up in the late 1980's, likely due to federal honey price support payments, which peaked in 1988, and were cut off in 1994 [[i]]. Colony numbers peaked in 1990, the same year that varroa arrived in Ohio, and went down from there, leveling off to about half the number of hives present in the 1970's.
I fully expected honey yields to decrease concurrent with the adoption of Roundup Ready varieties, but they didn't! Colonies still produce as much honey today as they did in the past, but this might be partially due to having fewer bees working the same amount of land, or to increased soybean nectar (which saved a number of Midwestern beekeepers from disaster during this year's droughts).
Perhaps even more surprising is the fact that in a state covered in corn and soy, colony productivity did not appear to be affected by the introductions of either Bt or Roundup Ready corn, nor by the universal use of neonicotinoid seed treatments (between corn and soy, on over roughly two thirds of the entire state land area). Note that honey yields actually increased for a few years following the introduction of clothianidin seed treatment!
Tellingly, hive numbers started to decrease after the arrival of varroa, and plummeted in the late 1990's as fluvalinate failed as a miticide, and many beekeepers simply threw up their hands and quit the business.
Verdict on herbicide tolerant crops: from a nutritional standpoint, the increased use of herbicides, and the associated weed free "clean farming" has certainly not helped the bees in corn/soy areas, but it is hard to make a case for them causing colony collapse.
Verdict on GM crops in general: Allow me to quote from the USDA:
...there is no correlation between where GM crops are planted and the pattern of CCD incidents. Also, GM crops have been widely planted since the late 1990s, but CCD did not appear until 2006. In addition, CCD has been reported in countries that do not allow GM crops to be planted, such as
Switzerland [33].
Looking Ahead: The Chemical Treadmill & Pest Resistance
It is interesting to observe the evolution of agriculture from the perspective of a biologist. Simple systems in nature are inherently less stable than complex systems. The current agricultural model in the U.S. exemplifies simplicity to the extreme--plant a single species into bare soil year after year, killing any competitive weeds or insects with pesticides (either sprayed, systemic, or engineered into the plants), and attempt to maintain fertility by adding energy-costly fertilizer. From a biological perspective, such a strategy is little more than an intense selective breeding program for the most resistant pests, and doomed to escalating chemical and energy inputs until the system collapses under its own weight.
I'm anything but a salesman for either Bt nor RR crops. Both are mere short-term solutions--resistant bugs and weeds are already starting to spread. I also have questions about the benefits of herbicide-intense no till planting [34], and hope that farmers return to alternative methods of weed control [35]. Luckily, the system will likely be self correcting, eventually forcing humanity to practice more sustainable methods of farming the land. However, I suggest that those methods may well include the wise use of biotechnology.
Additional Discussion
The Back Story On Plant Breeding And GM Crops
Traditionally, farmers simply replanted with the seeds from the most desirable individual plants year after year; this is the simplest form of "selective breeding." For example, all the various cole crops (cabbage, kale, broccoli, cauliflower, kohlrabi, Brussels sprouts) were developed by intentionally selecting for unusual forms of the species (resulting from random recombination of the natural allelic diversity, spontaneous mutants, or natural hybrids). This sort of selective breeding tends to result in a diverse assembly of locally-adapted cultivars. In Oaxaca, Mexico- the birthplace of corn-some 150 traditional varieties of maize are grown without pesticides or herbicides, thereby maintaining an invaluable reservoir of genetically-diversity "germplasm," which breeders can then cross and backcross in order to develop new cultivars (e.g., for pest or drought resistance).
In the early years of the U.S., seeds from desirable cultivars were distributed to farmers by the government, and plant breeding was performed at universities and at the USDA [36]. But since every strain breeds true, a farmer could save the seed and replant, leaving little opportunity for seed companies to make a buck. So in 1883, they formed the American Seed Trade Association and began to lobby for the cessation of the government programs.
The Profit Motive
In the early part of the 20th century, the companies began to promote hybrids-- crosses of two (or more) different strains or species that exhibited some sort of "hybrid vigor"--offering greater production, tastier fruit, or some other desirable characteristic. Hybrids were a godsend to the companies, since they are often sterile or don't breed true, meaning that farmers needed to purchase (rather than save) seed each season.
The seed lobby eventually shifted public funding away from the free distribution of selected seedstocks to instead encouraging the USDA and universities to develop inbred parental lines and breeding stock that the seed trade could then use to create proprietary hybrid varieties. By 1960, farmers planted less than 5% of corn from saved seed; and less than 10% of soybeans by 2001. As on-farm familiarity with the saving of seed was forgotten, farmers became willing consumers of produced seed.
Enter GM Crops
Then in 1980, the Supreme Court decided that seed companies could patent new varieties if they contained distinct and novel genetic markers. This meant that farmers (in some countries) could now be required to sign licensing agreements to allow them to use the patented seed each season [37] (there is a hodge-podge of international patent laws in this regard [38]).
The Second "Green Revolution"
The first "green revolution" was based upon fertilizer, pesticides, and hybrid seed (and also resulted in forcing farmers onto "agricultural treadmills"-making them less self sufficient and sustainable, and more reliant upon purchased seed, pesticide and fertilizer use, and upon borrowed money).
In 1950 the Secretary of Agriculture Ezra Benson said to farmers, "Get big or get out." His 1970s successor, Earl Butts, repeated that message, and exhorted farmers to "plant fence row to fence row" and to "adapt or die." Politicians who understood that a well-fed electorate is a happy electorate promoted policies that resulted in the destruction of the small family farm. Our policy of price supports and favorable treatment of agribusiness has changed the face of the American farm and the composition of the American diet [39].
Today's "second green revolution" is based upon technological advances in plant genetics (including GM) and the (at least partial) replacement of nasty pesticides with "biologicals." As an environmentalist, I find the new revolution to be more promising for ecological sustainability, but it is not without its downside--the current consolidation of agribusiness. As I mentioned before, farms, seed companies, and chemical companies are all being bought up by a few main players. Philip Howard details this consolidation in a free download [40], from which I quote:
This consolidation is associated with a number of impacts that constrain the opportunities for renewable agriculture. Some of these include declining rates of saving and replanting seeds, as firms successfully convince a growing percentage of farmers to purchase their products year after year; a shift in both public and private research toward the most profitable proprietary crops and varieties, but away from the improvement of varieties that farmers can easily replant; and a reduction in seed diversity, as remaining firms eliminate less profitable lines from newly acquired subsidiaries.
He then speaks of the concept of the "treadmill":
For the majority of farmers, however, the result is that they must constantly increase yields in order to simply maintain the same revenue. [Monsanto's sales pitch is that economic success in farming is driven by yield per acre [41]. Those that are unable to keep up with this treadmill will "fall off," or exit farming altogether. Their land ends up being "cannibalized" by remaining farmers who seek to increase scale of production as another means of keeping up with the treadmill, leading to the increasing centralization of agriculture. Farmers who have managed to stay in business have adapted to this process, and are typically on the leading edge of the adoption of new technologies. As a result, they have a high degree of confidence in science and technological innovations.
However, this problem has nothing to do with GMO's, but is rather due to the public's unknowing acceptance of the practice. Capitalism inevitably leads to consolidation unless consumers stop supporting corporate agribusiness with their pocketbooks and their votes, and start demanding that their government enforce antitrust efforts and better support small farmers.
But we are allowing economics and politics to distract us from the topic at hand--the technology of genetic engineering in plant breeding.
Cautions About GM
The most vocal critic of genetic modification is Jeffrey Smith, fear-mongering author of Seeds of Deception, producer of the film Genetic Roulette, and executive director of the inappropriately-named Institute for Responsible Technology. Smith is a gifted and effective communicator, as well as being a practitioner of "yogic flying" [42]. I will be the first to say that Smith's anti-GMO claims [43] would scare the pants off of anyone, and make for compelling story! The problem is that he plays loose with the facts--most of his claims simply do not stand up to any sort of scientific scrutiny. I suggest that for an objective analysis of the facts, that you visit AcademicsReviewed.org, a website that tests popular claims against peer-reviewed science. They address each of Smith's alarming "facts" one by one [44]. It is a thrilling ride to open the two web pages side by side, first being shocked by Smith's wild and scary claims, and then reading the factual rebuttal to each! The thing that most bothers me about Smith's writing is that he treats GM cultivars generically, rather than specifically addressing the merits or concerns for them individually. This makes little sense, since any conventional crop has cultivars that cause human allergy or contain excessive levels of natural toxins, yet no one calls for the testing of each of them!
Perspectives On GM Crops
As you may have guessed by now, to me, the GM debate should not be about being pro or con, rather it should be about the intelligent discussion of reconciling its promise with its problems. The GE genie is out of the bottle, and I can't see that anyone is going to put it back in-so we might as well work with it! So let's cut through the hype and hysteria, the fears and judgments, and try to objectively look at the facts of the matter:
From a plant breeder standpoint, genetic engineering holds incredible promise for the development of crops that could be tremendously beneficial to humans or the environment. For example, "Transgenic cotton has reduced the need for conventional insecticides used against lepidopteran [pests] an average in the USA about 59.4% [and] Texas 74.7%...an average number of pesticide applications in conventional cotton has fallen from 4.3 in 1995 to 2.1 in the USA... with benefits to human health and the environment" [45].
GM is only a part of plant breeding--most advances continue to be in conventional breeding, now assisted by "marker assisted selection," which is embraced by environmentalists [46].
However, someone needs to pay for the research, and the taxpayer is not doing it! For a thoughtful discussion of the benefits of gene patents, see [47].
Novel genetic markers can be patented, and a licensing fee can be charged, despite the fact that they are not GM!
From a consumer standpoint, advanced breeding techniques can result in cheaper and more nutritious food, and less environmental impact from farming.
Consumers have erroneously been led to believe that GM crops are dangerous to their health, and call for application of the precautionary principle. My gosh, please read "Misconceptions about the causes of cancer" [48]. Few foods are entirely "safe"! And "safety" can never be proven--it can only be disproven. And no studies have ever disproven the safety of GM crops, nor have doctors noticed anyone ever getting sick from them, despite our eating them for 15 years!
In truth, some scientists argue that plants produced by classical breeding methods should undergo the same safety testing regime as genetically modified plants. There have been plenty of instances where plants bred using classical techniques have been unsuitable for human consumption, causing toxicity or allergic reactions.
Those that speak of applying the "precautionary principle" should read Jon Entine's trenchant analysis of the fallacy of overapplication of that principle [49]. In truth, our regulators (EPA and FDA) vigorously apply the precautionary principle in the form "reasonable certainty of no harm."
The benefits of seed biotechnology cannot be realized without good seed germplasm to start with. So a few large seed companies started buying up their competitors to acquire the most productive and desirable varieties.
The downside of the above practice is that by 2008, 85% of GM maize patents and 70% of non-maize GM plant patents in the U.S. were owned by the top three seed companies: Monsanto, DuPont, and Syngenta [50]. Note that economists figure that when four firms control 40% of a market, it is no longer competitive; in the case of GE crops, the top four seed firms control 56% of the global proprietary seed market!
On the flip side, these profits are an incentive for the large corporations to invest in innovative plant breeding research--Monsanto spends about $2 million a day on this. This is important to keep in mind in an increasingly hungry world.
On the dark side, Monsanto's nearly $12 billion in annual sales allows the company to lobby regulators, influence universities, and spin the news. These are standard business practices for any large corporation, but hardly make Monsanto uniquely evil.
Be aware that patented genes are of use only if inserted into high-producing cultivars-which are developed by conventional breeding (which constitutes nearly half of Monsanto's plant breeding budget). These desirable cultivars have no patent protection. Monsanto uses a non GE technology called SMART = Selection with Markers and Advanced Reproductive Technologies. SMART technology is warmly embraced by environmental groups [51].
Adding a genetic marker allows a company to identify its proprietary strains, like putting a nametag on a dog. But clever breeders can back engineer the desirable germplasm out from patent protection.
And remember that patents expire after 20 years. The patents for Roundup Ready soybeans expire in 2014--at which time farmers, universities, and seed companies will then be free to propagate and sell the variety [52]. Patents are granted in order to spur innovation; by filing for patent protection, a company must make its discoveries public knowledge. This is a good thing.
Monsanto invests 44% of its R&D on conventional (as opposed to GM breeding).
Monsanto has also given rights to some of their patented crops to poorer countries, and recently donated a database of some 4000 genetic markers from cotton to Texas A&M [53]. The university plant breeders are excited in that the information will assist them in their conventional (non-GM) breeding of cotton, to the benefit of the environment [54 ].
From the farmer's standpoint, he has the choice of purchasing GE varieties that may be more productive, reduce insecticide use, or reduce tillage costs [55]. Keep in mind that there is nothing keeping him from purchasing "conventional" non-GM seed--it is available (I checked, and it sells at about half the cost of GM seed). In our free enterprise system there is nothing to keep non-GM seed companies from selling an alternative product if there is a demand. Farmers who are unimpressed by GM varieties freely switch back to conventional seed.
From an agricultural standpoint, the widespread adoption of a few favored crop varieties (GM or not) can result in the irreplaceable loss of crop genetic diversity--this is of great concern to plant breeders. If you haven't yet seen the graphic of our loss of crop genetic diversity from National Geographic magazine, you should! [56]. Luckily, this does not appear to be occurring yet with maize in Oaxaca [57], but there is a legitimate concern that economics will force traditional farmers out of business, leading to the loss of heirloom varieties. However, this is not a GM issue, but rather an effect of consolidation.
From a sustainability standpoint, there is nothing to prevent constant breeding innovation to keep pace with pest evolution. Genetically engineered crops can play a role in sustainable farming as our agricultural practices begin to shift to more ecologically sustainable methods.
One should keep in mind how the simple splicing of a virus gene into the papaya saved the Hawaiian papaya growers from the ravages of ringspot virus--the GE papaya is the mainstay of the industry, and by virtue of keeping the virus in check actually allows nearby organic papayas to thrive. Yet ecoterrorists recently hacked down thousands of GM trees [58]. It's interesting to read the history of "Golden Rice" [59] to see how the anti-GMO lobby is specifically scared that the success of such a lifesaving crop might open the door for acceptance of other GM plants!
Update Jan 2013
News item: Leading Environmental Activist's Blunt Confession: I Was Completely Wrong To Oppose GMOs. Blog in Slate Magazine
"If you fear genetically modified food, you may have Mark Lynas to thank. By his own reckoning, British environmentalist helped spur the anti-GMO movement in the mid-'90s, arguing as recently at 2008 that big corporations' selfish greed would threaten the health of both people and the Earth. Thanks to the efforts of Lynas and people like him, governments around the world--especially in Western Europe, Asia, and Africa--have hobbled GM research, and NGOs like Greenpeace have spurned donations of genetically modified foods.
But Lynas has changed his mind--and he's not being quiet about it. On Thursday at the Oxford Farming Conference, Lynas delivered a blunt address: He got GMOs wrong."
Anyone opposed to GMO's should read Mr. Lynas' well thought out address: http://www.marklynas.org/2013/01/lecture-to-oxford-farming-conference-3-january-2013/
Update May 2014
I've compiled a list of recent worthwhile reading on the "other side" of the GMO debate at https://scientificbeekeeping.com/gmo-updates/
So What's The Problem?
The problem is that anti-GMO advocacy groups are determined to put a stop to all GE technology. They targeted California with Prop 37, which applied only to packaged foods and produce. A more cynical take on Prop 37 was that it was all about marketing: "If your produce is no different in terms of taste, safety and nutrition from a competitor, and costs more, apparently the only marketing option is to create a negative image of your competitor's product" [60].
If Prop 37 had been successful, the promoters would then have targeted restaurants, the meat and dairy industry, and the beverage industry. I personally feel that this is an extreme position, what with the human population growing hungrier every day, and climate change threatening agriculture worldwide with heat, drought, pestilence, and salinity problems. Not only that, but GM crops hold promise for cheap omega-3 fatty acids (so that we don't have to harvest fish for them), cost-effective biofuels, and less expensive pharmaceuticals.
A good blog on the problem with the anti-GMO fear campaign can be found at [61], from which I quote:
It would be bad enough if something like the Seralini study simply contributed to the unnecessary angst amongst consumers around the world. It also has very real political, economic and practical effects. For instance brand conscious food companies have used their leverage to prevent the development of GMO versions of potatoes, bananas, coffee and other crops because they fear controversy. Apple growers worried about the market response are opposing the introduction of a non-browning apple even though it was developed by one of their own fruit companies. French activists destroyed a government-run field trial of a virus-resistant root stock which could have made it possible to produce good wine on sites that have become useless because of contamination with sting nematodes and the virus they vector. California voters have the potential to pass a seriously flawed "GMO labeling" initiative next month that could only serve the purposes of the lawyers and "natural products" marketers who created it. More importantly, European and Japanese importers of wheat essentially blackmailed the North American wheat producers into blocking biotech wheat development because those companies were nervous about consumer response in countries where GMO angst is so high. This has delayed by decades not only specific desirable trait development, but also what might have been an enormous private investment in a crop that is critically important for feeding a lot more people than just those in those rich countries. There is a huge cost of "precaution" based on poor science.
I believe that people should be well informed before taking a stance on important issues. I'd like to suggest one last excellent blog by an independent U.C. Berkeley evolutionary biologist and medical researcher:"How Bt Corn and Roundup Ready Soy Work - And Why They Should Not Scare You [62].
Acknowledgements
As always, thanks to my friend and collaborator in research Peter Loring Borst, and to anyone who still reads my articles after finding out that I've collaborated with Monsanto!
References
[1] Key S, et al (2008) Genetically modified plants and human health. J R Soc Med.101(6):290-298. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2408621/
[2] For example: Antoniou, M, et al (2012) GMO myths and truths.
(Broken Link!) http://earthopensource.org/files/pdfs/GMO_Myths_and_Truths/GMO_Myths_and_Truths_1.3.pdf
[3] Chiba S, et al. (2011) Widespread endogenization of genome sequences of non-retroviral RNA viruses into plant genomes. PLoS Pathog 7(7): e1002146.
[4] Domingo, JL and JG Bordonaba (2011) A literature review on the safety assessment of genetically modified plants. Environment International 37: 734-742.
[5] Key (2008) op. cit.
[6] Smith, JM (2003) Seeds of Deception. Yes! Books
[7] Seralini, GE, et al (2012) Long term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize. Food and Chemical Toxicology (2012) http://foodpoisoningbulletin.com/wp-content/uploads/Toxicity-of-Roundup-Ready-Maize.pdf;
Reviews
http://www.forbes.com/sites/henrymiller/2012/09/25/scientists-smell-a-rat-in-fraudulent-genetic-engineering-study/2/
http://www.efsa.europa.eu/en/faqs/faqseralini.htm#9, http://www.emilywillinghamphd.com/2012/09/was-it-gmos-or-bpa-that-did-in-those.html,
(Broken Link!) http://www.ask-force.org/web/Seralini/Anonymous-Rat-List-Spaying-2003.pdfs, http://storify.com/vJayByrne/was-seralini-gmo-study-designed-to-generate-negati;
Benbrook, CM (2012) Impacts of genetically engineered crops on pesticide use in the U.S. -- the first sixteen years. Environmental Sciences Europe 24:24 http://www.enveurope.com/content/pdf/2190-4715-24-24.pdf,
Review http://weedcontrolfreaks.com/2012/10/do-genetically-engineered-crops-really-increase-herbicide-use/#more-432
[8] http://journals.tubitak.gov.tr/agriculture/issues/tar-04-28-6/tar-28-6-1-0309-5.pdf
[9] http://www.monsanto.com/whoweare/Pages/monsanto-history.aspx
[10] http://www.businessweek.com/stories/2010-01-10/monsanto-v-dot-food-inc-dot-over-how-to-feed-the-world
[11] Methods for genetic control of plant pest infestation and compositions thereof
http://www.freepatentsonline.com/8088976.html
http://www.freepatentsonline.com/7943819.html
[12] http://www.greenpeace.org/australia/PageFiles/348427/smart-breeding.pdf
[13] 2007 figures http://www.census.gov/compendia/statab/2012/tables/12s0835.pdf
[14] ETC Group (2008) Who owns nature? Corporate power and the final frontier in the commodification of life. http://www.etcgroup.org/sites/www.etcgroup.org/files/publication/707/01/etc_won_report_final_color.pdf
[15] Blakeney, M (2011) Trends in intellectual property rights relating to genetic resources for food and agriculture. http://www.fao.org/docrep/meeting/022/mb684e.pdf This document covers the hodge-podge of international patent laws regarding plants and animals.
[16] http://www.monsanto.com/products/Pages/biodirect-ag-biologicals.aspx
[17] History of Bt http://www.bt.ucsd.edu/bt_history.html
Mode of action http://www.bt.ucsd.edu/how_bt_work.html
[18] Gold 2002 Misconceptions about the causes of cancer http://potency.berkeley.edu/pdfs/Gold_Misconceptions.pdf A "MUST READ"!
[19] Buchmann CA, et al (2007) Dihydroxy-7-methoxy-1,4-benzoxazin-3-one (DIMBOA) and 2,4-dihydroxy-1,4-benzoxazin-3-one (DIBOA), two naturally occurring benzoxazinones contained in sprouts of Gramineae are potent aneugens in human-derived liver cells (HepG2). Cancer Lett. 246 (1-2):290-9.
[20] http://en.wikipedia.org/wiki/Endophyte
[21] Duan JJ, et al (2008) A meta-analysis of effects of Bt crops on honey bees (Hymenoptera: Apidae). PLoS ONE 3(1): e1415.
[22] Center for Environmental Risk Assessment (2011) A review of the environmental safety of the Cry1Ab protein. http://cera-gmc.org/docs/cera_publications/cry1ab_en.pdf
[23] Han, P, et al (2012) Does transgenic Cry1Ac + CpTI cotton pollen affect hypopharyngeal gland development and midgut proteolytic enzyme activity in the honey bee Apis mellifera L. (Hymenoptera, Apidae)? Ecotoxicology. 2012 Aug 7. [Epub ahead of print]
[24] Hendriksma HP, et al (2011) Testing pollen of single and stacked insect-resistant bt-maize on in vitro reared honey bee larvae. PLoS ONE 6(12): e28174.
[25] Benbrook, CM (2012) op. cit.
[26] Reviewed in http://www.sourcewatch.org/index.php/Glyphosate
[27] Mullin, C.A., J.L. Frazier, M.T. Frazier & T.J. Ciarlo - A primer on pesticide formulation 'inerts' and honey bees. http://www.extension.org/pages/58650/proceedings-of-the-american-bee-research-conference-2011
[28] Ciarlo TJ, CA Mullin, JL Frazier, DR Schmehl (2012) Learning impairment in honey bees caused by agricultural spray adjuvants. PLoS ONE 7(7): e40848.
[29] Johal, GS and DM Huber (2009) Glyphosate effects on diseases of plants. Europ. J. Agronomy 31: 144-152. http://www.organicconsumers.org/documents/huber-glyphosates-2009.pdf
Huber, DM (2010) Ag chemical and crop nutrient interactions - current update. http://www.calciumproducts.com/dealer_resources/Huber.pdf
Reviewed in (Broken Link!) http://www.weeds.iastate.edu/mgmt/2010/glyMndisease.pdf
[30] Kopsell et al. (2009) increase in nutritionally important sweet corn kernel carotenoids following mesotrione and atrazine applications. Journal of Agricultural and Food Chemistry 090619124509017 DOI: 10.1021/jf9013313
[31] Laws, F (2010) http://cornandsoybeandigest.com/issues/will-glyphosate-fall-wayside-resistance-grows
[32] http://www.nationalaglawcenter.org/assets/crs/RS20759.pdf
[33] http://www.ars.usda.gov/is/AR/archive/jul12/July2012.pdf
[34] http://www.misereor.org/fileadmin/redaktion/MISEREOR_no%20till.pdf
[35] http://www.acresusa.com/toolbox/reprints/Organic%20weed%20control_aug02.pdf
[36] http://www.seedalliance.org/Seed_News/SeminisMonsanto/
[37] (Broken Link!) http://earthopensource.org/files/pdfs/GMO_Myths_and_Truths/GMO_Myths_and_Truths_1.3a.pdf
[38] Blakeney, M (2011) Trends in intellectual property rights relating to genetic resources for food and agriculture. http://www.fao.org/docrep/meeting/022/mb684e.pdf This document covers the debate involved in international patent law regarding plants and animals.
[39] Philpott, T (2008) A reflection on the lasting legacy of 1970s USDA Secretary Earl Butz. http://grist.org/article/the-butz-stops-here/; but for a contrary view by an actual corn farmer, read Hurst, B (2010) No Butz About It. (Broken Link!) http://www.american.com/archive/2010/july/no-butz-about-it
[40] Howard, Philip H. 2009. Visualizing consolidation in the global seed industry: 1996-2008. Sustainability, 1(4), 1266-1287. http://www.mdpi.com/2071-1050/1/4/1266/pdf
[41] http://www.monsanto.com/investors/Documents/Whistle%20Stop%20Tour%20VI%20-%20Aug%202012/WST-Fraley_RD_Update.pdf
[42] http://academicsreview.org/reviewed-individuals/jeffrey-smith/
[43] http://responsibletechnology.org/docs/145.pdf
[44] http://academicsreview.org/reviewed-content/genetic-roulette/
[45] Greenberg, S, et al (2012) Economic and Environmental Impact Transgenically Modified Cotton Comparative with Synthetic Chemicals for Insect Control. Journal of Agricultural Science and Technology B 2 750-757.
[46] Greenpeace (2009) Smart Breeding. Marker-Assisted Selection: A non-invasive biotechnology alternative to genetic engineering of plant varieties. http://www.greenpeace.org/australia/PageFiles/348427/smart-breeding.pdf
[47] http://www.genengnews.com/gen-articles/in-defense-of-gene-patenting/2052/
[48] Gold 2002 Misconceptions about the causes of cancer http://potency.berkeley.edu/pdfs/Gold_Misconceptions.pdf
[49] Entine, J (2010) Crop Chemophobia: Will Precaution Kill the Green Revolution? http://www.jonentine.com/pdf/CROPCHEMOPHOBIApre-orderform.pdf
[50] Howard, Philip H. 2009. Visualizing consolidation in the global seed industry: 1996-2008. Sustainability, 1(4), 1266-1287. http://www.mdpi.com/2071-1050/1/4/1266/pdf
[51] http://www.greenpeace.org/australia/PageFiles/348427/smart-breeding.pdf
[52] http://www.monsanto.com/newsviews/Pages/roundup-ready-patent-expiration.aspx;
[53] http://www.cotton247.com/article/3401/monsanto-donates-marker-technology
[54] http://www.youtube.com/watch?v=dcZyFH_eITQ
[55] http://www.biofortified.org/2012/05/the-frustrating-lot-of-the-american-sweet-corn-grower/#more-8670
[56] http://ngm.nationalgeographic.com/2011/07/food-ark/food-variety-graphic If you didn't see this graphic in National Geographic, you should!
[57] (Broken Link!) http://researchnews.osu.edu/archive/mexmaize.htm
[58] http://www.huffingtonpost.com/2011/08/20/genetically-modified-papayas-attacked_n_932152.html
[59] http://en.wikipedia.org/wiki/Golden_rice
[60] http://westernfarmpress.com/blog/proposition-37-gone-probably-not-forgotten?
[61] http://appliedmythology.blogspot.com/2012/10/can-damage-from-agenda-driven-junk.html?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+AppliedMythology+%28Applied+Mythology%29
[62] http://www.science20.com/michael_eisen/how_bt_corn_and_roundup_ready_soy_work_and_why_they_should_not_scare_you
Category: Colony Health - Diseases, Viruses, CCD
Tags: collapse, colony, genetically, gm crops, gmo, modified, plants, sick bees | gmo Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/gmo/ |
Sick Bees - Part 18F7: Colony Collapse Revisited - Pesticide Exposure
First published in: American Bee Journal, October and November 2013
Pesticide Exposure
Oh No, Not Pesticides Again!
Reality Checks
The Two Worlds of Beekeeping
Pesticides and Bee-pocalypse
A Comparison To Some "Control Groups"
The Four Horsemen And The Tip Point
Could Pesticides Cause Colony Mortality And CCD?
Short Memories
The Heart Of The Hive - The Nursery
Industry's Arguments
But Don't We Already Know That It's The Neonicotinoids?
An "Acid Test" Of Neonic Seed Treatment
So Which Pesticides Are Actually To Blame?
The Evidence
Oh Boy, Let's Do Some Math!
And How About The "Inerts"?
Choosing To Ignore The Obvious
Blinded By Bias
No More Safe Home To Return To
A Historical Artifact
The Beekeeper Contribution To Shifting The Tip Point
Stop Right There!
Undetectable Levels And Hormesis
Wrap Up
Acknowledgements
References
Sick Bees Part 18f7: Colony Collapse Revisited
Pesticide Exposure
Randy Oliver
ScientificBeekeeping.com
Originally published in ABJ Oct and Nov 2013
Oh No, Not Pesticides Again!
Some readers may wonder why I am spending so much time on the issue of pesticides, since to many (if not most) beekeepers, pesticides are a non issue. In answer, the main reason is that the public (and our lawmakers) are being hammered by the twin messages that the honey bee is on the verge of extinction, and that the reason is pesticides. In my writings, I'm attempting to address the validity of both of those claims. Let's start with the first.
Reality Checks
Honey bees have clearly (and deservedly) become one of today's most charismatic environmental poster children, and as such are a useful bioindicator that our human activities are having a negative impact upon pollinators, and wildlife in general.
But I also feel that we take care to not overstate or exaggerate our case. One of my greatest concerns is that beekeepers are allowing the media to scare the public with all the hue and cry of an impending bee-pocalypse (and that it is due to a certain type of pesticide). Our complicity in this message (as we enjoy the luxury of basking in the warmth of all the public support) may backfire on us one of these days--putting us into the position of the little boy who cried wolf. Some in the media are starting to notice that the facts don't support the claim that bees are disappearing (Fig. 1).
Figure 1. It's true that it's more difficult to keep bees healthy these days, but it doesn't look like bee-pocalypse is imminent (as evidenced by this recently-published chart). Whenever honey and pollination prices are high enough to make beekeeping profitable, resourceful beekeepers somehow manage to recover their colony losses [[i]]. Chart courtesy Shawn Regan [[ii]].
[i] Rucker, RR and WN Thurman (2012) Colony collapse disorder: the market response to bee disease. http://perc.org/sites/default/files/ps50.pdf
[ii] (Broken Link) http://perc.org/articles/everyone-calm-down-there-no-bee-pocalypse
In the rest of the world, the number of managed hives has actually been increasing [3]. And as far as claims that pesticides are driving bees to extinction, Hannah Nordhaus, the author of the excellent book The Beekeeper's Lament writes:
Reflexively blaming pesticides for all of the honey bee's problems may in fact slow the search for solutions. Honey bees have enough to do without having to serve as our exoskeletal canaries in a coalmine. Dying bees have become symbols of environmental sin, of faceless corporations out to ransack nature. Such is the story environmental journalism tells all too often. But it's not always the story that best helps us understand how we live in this world of nearly seven billion hungry people, or how we might square our ecological concerns and commitments with that reality. By engaging in simplistic and sometimes misleading environmental narratives -- by exaggerating the stakes and brushing over the inconvenient facts that stand in the way of foregone conclusions -- we do our field, and our subjects, a disservice [4].
Further reading: for a detailed and sober analysis of the factors that affect managed bee populations, I highly recommend the review by Drs. vanEngelsdorp and Meixner [5].
The reality is that it is not the honey bee that is being driven to extinction--it is instead the commercial beekeeper who is finding that his traditional business model is becoming less profitable due to today's greater degree of colony losses and the decreasing availability of good summer forage.
The question is, to what extent are pesticides involved in those problems?
The Two Worlds Of Beekeeping
There are two very different worlds of beekeeping--small scale (hobbyists, who constitute the vast majority of beekeepers by number) and large scale (commercialized professionals, who manage the vast majority of hives), with a small continuum of sideliners bridging the gap.
Hobby beekeeping is currently enjoying a bubble of resurgence, but in the Big Picture in the U.S., hobbyists manage an insignificant number of hives. And those small-scale beekeepers tend to keep their hives close to home, largely avoiding serious exposure to pesticides. But that's not to say that small-scale beekeepers are immune to pesticide kills; I've heard of several this season, and what with all the spraying for West Nile virus and the citrus psyllid, we can expect more of the same. And since there are far more small-scale beekeepers to put pressure on regulators and legislators, I feel that it is a good idea for them to be informed about pesticide issues.
Large-scale beekeepers, on the other hand, typically run migratory operations--moving their hives to almond pollination, and then to other agricultural areas (it's problematic to keep apiaries of hundreds of hives in the suburbs). The fate of those bees (and their keepers) is largely determined by agricultural land use practices and their degree of exposure to agricultural pesticides.
It is some of those large-scale beekeepers for whom extinction is a valid concern. The reason (as with any other enterprise) is financial--they can only survive so long unless their businesses continue to be profitable [6]. In recent years, they've had two things going for them--sky-high honey prices and elevated pollination fees. But all is not rosy--there are reasons for those prices going up; these days it's simply more costly to produce honey or to provide bees for pollination.
Today's breathtakingly-high high almond rental rates typically don't even cover operating costs--even if most of one's colonies make it through the winter! Today's 30% average winter loss rate is bleeding profitability from many operations. Not only does the beekeeper need to rebuild his numbers after almonds, but to stay in the black he must also make additional income from paid pollinations or a decent honey crop. And that may no longer be as easy as it used to be for various reasons:
Formerly bee-friendly farmland has been turned into agri-deserts devoid of any bee forage.
Honey producers on field crops (such as alfalfa, sunflowers, or cotton) get hammered time and again by pesticide spraying, sometimes watching whole yards of colonies dwindle or go queenless weeks afterwards.
Paid summer pollination contracts (such as for vine crops) may leave colonies in poor shape for the winter, due to the heavy stocking, the lack of nutritious pollen, and the exposure to multiple pesticides.
These days, the sad fact is that many good beekeepers are barely keeping their heads above water. So the beekeeper's lament continues--varroa, high winter mortality, and lack of good forage are driving a number of operations into the red.
Practical application: although the "extinction of the honey bee" makes for a good rallying cry, the real concern is the possible extinction of the migratory beekeeper who supplies necessary pollination services to agriculture. So far, the almond industry has been economically propping up the bee industry, but I'm not sure how long that arrangement will be sustainable.
Pestcides And Bee-Pocalypse
For some beekeepers, "bee-pocalypse" has already occurred. New York beekeeper Jim Doan, whose case I detailed in a previous article [7], sadly gave it up this year. Here is a beekeeper whose apiaries had been in the same locations for many years without noticeable pesticide problems, but who apparently suffered from devastating spray or dust kills this season and last, as evidenced by piles of fresh dead bees in front of his hives in spring.
Residue analysis of those dead bees clearly showed that they had been exposed to several pesticides, but none of the detects were at levels that would be expected to cause such carnage--so we don't even know which pesticides or practices to point the finger at! To my scientific mind, this is very frustrating--that our "system" was not able to identify the cause of Jim's bee kills, to change anything to keep them from recurring, nor compensate an innocent beekeeper for the loss of his livestock and livelihood.
As unlucky as Jim has been, his case is not necessarily the norm. Overall, the issue of environmental toxins is improving. In my own lifetime I've seen us clean up our pollution of the air and water, cease atmospheric testing of nuclear weapons, ban DDT, fluorocarbons, and PCB's, phase out the worst pesticides, and raise the general environmental consciousness. Humans still inflict far too damaging an environmental footprint on Earth, but we are moving in the right direction, and should give ourselves some credit for that!
There is no doubt that pesticides are often involved in bee health issues, but can we blame them for all our problems? That question is best answered by considering the health of those colonies that are not exposed to pesticides:
A Comparison To Some "Control Groups"
There are plenty of beekeepers in non agricultural areas whose apiaries are not exposed to pesticides to any extent. Those hives serve as a "control group," whose health we can compare to those colonies that do have to deal with pesticides.
For instance, in my own operation of about a thousand hives, their only exposure to pesticides is to the fungicides in the almond orchards (from which they don't appear to suffer to any serious extent). I haven't used synthetic miticides in over a decade, rotate my combs, and rarely feed syrup.
Yet, I've experienced CCD firsthand, see more queenlessness, unsuccessful supersedure, and experience somewhat higher winter losses than in the old days (meaning before varroa). I hear the same from many others in the pesticide-free control group. The simple fact is that these days it requires better husbandry to maintain productive colonies. Yet we in the "control group" can hardly blame pesticides to be the cause.
And then there are the stationary "treatment free" beekeepers in the middle of intense agriculture who suffer no higher colony loss rates than the norm, despite their apiaries being surrounded by corn and soy [8]. How the heck do we reconcile their success to the problems that the commercial guys experience in the same areas?
Do they owe their success to keeping fewer hives in a yard? To keeping locally-adapted survivor stock? To their placement within flight range of patches of undisturbed forage? To the fact that they don't move to multiple crops? Or is it because they aren't contaminating their combs with miticides? Believe me, if I knew the answer, I'd tell you!
As (the very successful) beekeeper Dave Mendes observes, colonies just seem to be more "fragile" these days. It's no surprise then that the addition of toxins of any sort can help to tip a colony over. The Ericksons [9] put it this way:
Pesticides and their residues in the hive stress bees as do other factors such as weather extremes, food shortages, pests, predators, and disease. Conversely, stress induced by other factors undoubtedly has a significant impact on the level of damage that a pesticide inflicts on a colony.
Note that the above words were written prior to our colonies having to deal with varroa, the varroa-vectored viruses, Nosema ceranae, our evolving brood diseases, GMO's, neonicotinoids, or Roundup Ready corn.
The Four Horsemen And The Tip Point
Colony growth is a function of the recruitment rate via successful broodrearing vs. the attrition rate of workers due to age, disease, the altruistic departure of sick bees, or the loss of foragers in the field. When recruitment exceeds attrition, colonies grow; when attrition exceeds recruitment, the colony population shrinks. Environmental factors, including toxins, can shift the tip point for colony growth (Fig. 2).
Figure 2. Any colony with a good laying queen has the potential to grow rapidly--the greater the rate of recruitment (successful broodrearing), the steeper the slope of the growth curve. In the real world, such potential growth is often held back by the lack of nutritious pollen, or by the stresses of toxins, chilling, or pathogens (especially the mite-associated viruses, nosema, or EFB). Any of those can strongly shift the tip point, slowing, or even reversing, the rate of colony growth.
In the last decade, something appears to have shifted that tip point--colonies today seem to more readily go into a downhill spiral and queens no longer hold up as well. Could it be due to pesticides?
Could Pesticides Cause Colony Mortality And CCD?
Of course they could! In 2010, after closely observing the progression of experimentally-induced CCD with my collaborator Dr. Eric Mussen, I published the flow chart below (Fig. 3) to detail the interactions and feedback loops involved in the step-by-step collapse of a colony [10]. At the time, I fully intended to further elaborate upon the contribution of toxins, but didn't get around to it until now.
Figure 3. The positive feedback loops that can lead to colony dwindling and/or sudden depopulation. I've since observed this process take place in sick colonies time and again.
In the above chart, I called out toxins (which would include pesticides) as one of the "Four Horsemen of Bee Apocolypse" (the four factors at top left). Below I've indicated in red those points at which toxins may exacerbate the downhill process (Fig. 4).
Figure 4. Note that toxins can exert lethal or sublethal effects (red bubbles) at every step in the process of colony dwindling or collapse. Pesticides may in some cases be the prime cause of colony mortality; more frequently they might be "contributory factors," especially due the prolonged sublethal effects of residues in the beebread or wax.
Please note that in these charts I'm referring to toxins generically, not specifically to manmade pesticides. Such toxins would include natural plant allelochemicals, industrial pollutants, metals such as arsenic or selenium in soil and dust, fungal and bacterial toxins (which may be altered in beebread by the presence of pesticide residues), beekeeper-applied varroacides, HMF in overheated corn syrup, all in addition to any agricultural pesticides. In the words of ecotoxicologist Dr. Helen Thompson, we must pay attention to the total toxin load of the hive, plus any interactions between those chemicals, as well as other contributory factors [11]--a sentiment also echoed by the Fraziers at Penn State [12]. So, back to our original question: Can toxins, including synthetic pesticides, cause colony morbidity or mortality?
Verdict #1: clearly, synthetic pesticides and varroacides may constitute the most serious toxin load for managed bees in agricultural areas, and have the potential kill a colony outright, or to exacerbate positive feedback loops that can result in dwindling, poor overwintering, or collapse.
But does any pesticide specifically cause CCD--"the disappearance of most, if not all, of the adult honey bees in a colony, leaving behind honey and brood but no dead bee bodies" [13] (and no sign of brood diseases or varroa-induced DWV collapse).
Analysis: The most direct way to answer that question is to see whether we can fulfill Koch's third postulate [14]: can we experimentally create the symptoms of CCD by treating a healthy hive with the pesticide in question?
Verdict #2: to the best of my knowledge, no one has yet duplicated the symptoms of CCD by treating a colony with any pesticide (the most obvious difference being that there are generally plenty of dead bees present in the case of pesticide toxicity). This is notably true for the neonicotinoids, for which any number of researchers have attempted to duplicate CCD symptoms by continually feeding colonies neonic-tainted syrup or pollen.
Hold on--drop those stones! I am not saying that pesticides cannot contributeto CCD or colony morbidity or mortality in general--my chart above clearly illustrates that they have the potential to do so. Yet even those beekeepers who manage to completely avoid pesticides may still experience sudden colony depopulations, dwindling, or excessive winter losses due to some combination the Four Horseman (as in the perfect storm detailed at [15]).
I feel that it is a serious error for us to try to link CCD to pesticides. Pesticides have always been an issue to beekeepers, but CCD-like events have historically come and gone (as in Disappearing Disease--read the description at [16]). Pesticides will remain an issue long after the term "CCD" is forgotten.
Bottom line: Despite the fact that the evidence at hand does not support the case that CCD is directly caused by any pesticide, that fact certainly does not mean that we should ignore pesticide issues. If anything, we beekeepers ourselves have helped to make pesticides even more of an issue these days.
Short Memories
There is a popular myth going around that pesticides only started to become an issue to honey bee colony survival in 2007. In fact, the sublethal effects of pesticides were well known to beekeepers and researchers long before then. If we review the older literature [17], we find that it was already well known that contaminated pollen was a more serious issue to colony health than the in-field kill of foragers. We knew that colonies might collect such tainted pollen from miles away, that dusts were worse than sprays, that young bees may be more susceptible than older bees, and that temperature and humidity had a great deal to do with pesticide toxicity. Pesticide issues were actually far worse in the 1960's and '70's than they are today, and have generally improved since then (not to say that some new issues haven't arisen).
On the other hand, the overall contamination of combs with pesticides has increased in recent years due to the direct contribution by we beekeepers ourselves. In virtually any residue analysis of beebread or beeswax these days in any country with varroa, the most prevalent toxins are the beekeeper-applied varroacides [18]-you may wish to refer back to my chart of the "toxicological eras of honey bee evolution [19].
So one question is, To what degree we have shifted the tip point of colony health by contaminating our brood combs with miticides? Let's explore the broodnest...
The Heart Of The Hive - The Nursery
The insidious, long-term effects of total toxin load (including pesticide and varroacide residues) would be from those that made it into the heart of the hive--the critical stored beebread and the wax of the brood combs (Fig. 5). Note: Dr. David Fischer of Bayer brings to my attention that in the case of imidacloprid, the results of his testing indicates that bees in the hive are more affected by residues in the nectar than by those in the pollen.
Figure 5. Long after a pesticide-sprayed field force has been replaced by newly-recruited foragers, the colony may still need to deal with the lingering effects of pesticide residues in the combs, and especially in the all-important stores of beebread. It is here that such persistent residues can affect colony health and buildup for many months after the initial exposure, and exactly where we should focus our attention.
Here's some food for thought: a toxin need not actually kill a single bee to mess up a colony. There are many ways in which sublethal levels of toxins can negatively affect the colony population curve. A few examples would be:
By decreasing the survival rate of larvae (as from residues of varroacides [20, 21], or fungicides [22]) , or by increasing their development time (as effected by various pollutants, plant alleleochemicals, pesticides, or miticides).
By affecting the proper fermentation of beebread (fungicides).
By affecting the sensitive nurse bees that must digest that beebread and produce the critical jelly used to feed the brood, queen, and other workers (natural plant toxins, pollutants, or pesticides).
By affecting the normal behavioral progression of the workers. E.g., if workers initiate foraging prematurely, this greatly reduces their overall longevity, and results in severe depression of colony growth [23] (much more research is crying to be done, but many chemicals would be suspect).
By requiring bees to allocate precious resources toward the detoxification of the poisons (as per my leaky boat analogy [24]).
By increasing the virulence of varroa, nosema, or viruses (any number of pesticides and miticides have been implicated [25, 26])
By affecting normal colony homeostasis, such as thermoregulation of the brood, which is dependent upon the proper assessment of temperature, and the ability to effectively generate heat by the vibration of the wing muscles (neurotoxins would be expected to affect this ability).
By affecting the longevity of the queen, the viability of spermatozoa, or the ability of a colony to successfully supersede (coumaphos notably had this effect)
By affecting the production of, or normal communication via pheromones (which include the recognition of brood and the queen) [27] (essential oils, formic acid, other pesticides?)
By affecting foragers' ability to communicate by dance, to navigate, to learn (a wide range of pesticides [28]), or to react properly to normal stimuli (neonics can clearly do this [29]; but similar effects could be due to any number of other pesticides).
Bottom line: the toxin load in the broodnest can greatly affect a colony in many ways, generally (but not necessarily always) negatively. The greater the total toxin load with which the colony is forced to deal, the more likely that it will suffer from the combined ill effects.
Industry's Arguments
In order to present an objective review of pesticide issues, we should also hear Industry's side of the argument. The industry-funded think tank OPERA [30] takes the position that:
Although, based on the facts outlined above, there does not appear to be any strong evidence that sublethal effects of pesticides play a key role as causative factors behind bee colony mortality (which is likewise supported by the fact that in several monitoring projects no correlation has been found between colony losses and pesticide exposure), sublethal effects are certainly a point where more fundamental research is needed to obtain a clearer picture of the nature of the issue.
The above statements are factually correct in that there is to date no compelling evidence that pesticides are at the root of the elevated rates of colony mortality seen in recent years, and that more fundamental research is clearly needed. But a long history of practical experience by beekeepers with the sublethal (as well as lethal) effects of pesticides leaves no doubt that pesticides certainly have the potential to cause colony health issues.
But Don't We Already Know That It's The Neonicotinoids?
The media have already tried and convicted the neonicotinoids as the cause of all bee problems, and it's currently fashionable to celebrate the restrictions recently imposed on them by the European Union. But it is rational? No one has ever shown convincing evidence that neonics are linked to colony collapse; conversely, there is abundant experimental and on-the-ground evidence that the residues from seed-treated plants do not appear to cause observable harm to colonies [31].
Planting dust, soil drenches, or foliar applications are a different story, but these are generally drift or misapplication issues, hitting individual apiaries, not the bee population as a whole. Our regulators are well aware of these issues, and working to fix the problems.
Regarding the completely unacceptable bee kills due to the dust from corn seeding, of interest is a recent paper by Drs. Chris Cutler and Cynthia Scott-Dupree [32]--environmental toxicologists from Canada's Dalhousie University--who analyzed the 110 pesticide incident reports received by Canada's PMRA since 2007. Ranking the reports by the degree of severity of the bee kill, they found that there were over five times as many "major incidents" due to non-neonicotinoid products (including carbofuran, chlorpyrifos, coumaphos, diazinon, dimethoate, fluvalinate, formic acid, permethrin, and phosmet) as there were due to neonics, yet that these incidents are largely ignored by the press and beekeepers, who for some reason single-mindedly focus upon the neonics.
Hey, I'm as concerned about pollinators and pesticides as anyone. A recent review by Goulson [33] points out the excessive use of neonics (actually all pesticides are greatly overused), and details the many environmental questions about this class of chemicals. But here's the thing--I can read studies all day long, but what I prefer to seek out are actual on-the-ground, real-life observations. Let me share one with you:
An "Acid Test" Of Neonic Seed Treatment
Activists are calling for a ban on clothianidin--the most common neonicotinoid seed treatment. Although honey bees appear to do just fine on seed-treated canola, their species has an advantage over solitary bees and other pollinators, due to their foraging on multiple plant species over a wide area, their social structure, and their processing of the pollen by nurse bees. So honey bees may not be the best indicator of neonic toxicity.
On the other hand, solitary bee species may be a better indicator as to whether neonic residues cause subtle adverse effects. Many solitary bees are "monovoltine," meaning that they only raise a single generation per year. Because of this, a negative effect on any single female bee could prevent the production of the next generation. It occurred to me that the Alfalfa Leafcutter Bee (Megachile rotundata), which is used to pollinate clothianidin-treated canola (Fig. 6), would provide an excellent "acid test" of clothianidin for several reasons:
Clothianidin has been shown to be highly toxic to leafcutter bees by topical application [34]. Since neonics are typically an order of magnitude more toxic by oral exposure [35], it is reasonable to expect that the leafcutter bee would be even more susceptible to residues consumed in food.
Leafcutter bees do all their foraging within a few hundred feet of the nest [36], so those placed in the middle of a canola field would forage solely upon treated canola.
Each individual female alone forages and provisions her nest, feeding upon the contaminated pollen and nectar as her sole protein and energy sources. If the insecticide negatively affected her behavior, navigational ability, health, or longevity she would be unable to reproduce effectively.
The male bees use canola nectar as their sole energy source, and if the insecticide residues interfered with their behavior or longevity, the female bees might not get properly mated.
The larvae consume a diet consisting solely of unprocessed contaminated pollen and nectar (rather than royal jelly), and thus every item in their diet would contain verified concentrations of clothianidin (approximately 1.7 ppb in the pollen; 0.8 ppb in the nectar [37]). Note: as with honey bees, neonicotinoids are virtually nontoxic to the larvae of the leafcutter bee [38].
The female constructs her nest by cutting (with her mouthparts) leaves from the treated canola plants, which contain even higher residues of clothianidin than the pollen, thus exposing her to even more of the chemical. The larva then develops surrounded by these contaminated leaves, and the pupa overwinters in them.
Figure 6. Tents covering Alfalfa Leafcutter bee nest boxes in a canola field.
In short, the leafcutter bees would constitute the most severe test case for clothianidin exposure from a seed-treated crop. So I phoned a commercial supplier of leafcutter bees in Ontario (who declined to be named) and asked him whether he had any problems with his bees reproducing or overwintering after being set in clothianidin seed-treated canola. He said that he had been rearing them on such fields for many years and did not observe any problem. I put a good deal of faith into such unbiased field experience by a commercial bee man. You can draw your own conclusions.
So Which Pesticides Are Actually To Blame?
It's pretty easy to diagnose an acute bee kill, what with piles of twitching bees in front of the hives (see "Signs and symptoms of bee poisoning" at [39]), and in many cases the responsible pesticide can be identified. To sidetrack briefly, remember when I mentioned a few articles back that the residues in Jim Doan's bee kills did not indicate that the bees contained lethal doses of the chemicals? This made me strongly suspect that we can't apply the LD50 data (in nanograms per bee) to the values obtained from actual field samples of dead bees. The recent report from Canada [40] confirms this. The highest residue level of clothianidin (from corn planting dust) found in any sample of dead bees from the entrances of a hive was 24 ppb, which works out to about a tenth of the theoretical amount necessary to kill a bee . This finding could be due to the metabolic degradation of the insecticide, but it certainly suggest that the LD50 value should be adjusted lower for samples of dead bees! I am greatly heartened that Canada is moving forward in addressing this issue of bee kills from corn planting dust [41].
Overt bee kills aside, more insidious are the residual effects due to contaminated dust, pollen, or nectar that foragers bring back into the broodnest. I'm told by beekeepers with far more experience with pesticides than I, that after exposure to certain pesticides, colony growth and production come to a standstill, sometimes for months, until the colony clears itself of residues and perhaps eventually recovers (or not). The problem is that few beekeepers (if any) can look inside a hive and diagnose which pesticide (or combination thereof) is causing the problem. He may notice spotty brood, poor buildup, winter dwindling, or queenlessness, but it is very hard to isolate the effect any particular pesticide residue, especially in today's stew of residues in combs. But that doesn't mean that we are completely blind...
The Evidence
Due to the rapid turnover of bees in a hive (other than the queen or "winter bees"), if a pesticide were indeed exerting a long-term effect upon colony health, then there would by necessity need to be residues of that pesticide or its degradation products persisting in the combs. With today's testing equipment, we can detect residues to the parts per billion level, and have quite a large database of residue analyses of beebread samples, which we can perhaps use to either finger or exonerate certain pesticides suspected of being involved in colony health issues.
In a court of law, all evidence would be laid out before the court to determine whether it was substantial enough to make a case against a particular suspect. We can do something similar by reviewing two large publicly-available datasets of actual pesticide analyses of beebread from across the country--one by the Penn State team , the other by the USDA (Tables 1 and 2). I've condensed their data to only those pesticide detects that were found in at least 10% (Penn State) or 5% (USDA) of the samples, following this reasoning:
If a pesticide isn't present in at least 10% of samples, then it isn't likely to be the cause of widespread problems.
I've also color-coded the results as to the type of pesticide, and included the median detection level (to help us to determine whether that dose would be expected to cause colony health problems, or whether it would be insignificant).
Pesticide
Present in percent of samples*
Median detection if positive for target (ppb)
Type of pesticide
Fluvalinate
88.3
40.2
Beekeeper-applied miticide
Coumaphos
75.1
13.1
Beekeeper-applied miticide
Chlorpyrifos
43.7
4.4
Insecticide
Chlorothalonil
52.9
35
Fungicide
Pendimethalin
45.7
13.4
Herbicide
Endosulfan I
28
4.2
Insecticide
Endosulfan sulfate
26.3
2.2
Insecticide
DMPF (amitraz)
31.2
75
Beekeeper-applied miticide
Atrazine
20.3
8.9
Herbicide
Endosulfan II
20
3.8
Insecticide
Fenpropathrin
18
7
Insecticide
Azoxystrobin
15.1
10.2
Fungicide
Metolachlor
14.9
8.1
Herbicide
THPI (Captan)
14.2
227
Fungicide
Captan
12.9
103
Fungicide
Esfenvalerate
11.7
3.3
Insecticide
Carbaryl
10.9
36.7
Insecticide
Cyhalothrin
10.9
1.7
Insecticide
Table 1. The 2010 survey by the Penn State team [42], based upon (depending upon the pesticide) either 350 or 247 samples. This study (plus numerous others worldwide) clearly point out that the predominant pesticide residues in brood combs are typically those from the beekeeper-applied miticides (yellow).
Table 2. This 2012 survey by the USDA [43] echoes the previous findings--the only pesticides found in at least 10% of the samples were from either beekeeper-applied miticides or chlorpyrifos. The 99 analyzed samples came from Alabama, California, Colorado, Florida, Idaho, Indiana, New York, South Dakota, Tennessee, Texas, and Wisconsin.
Keep in mind that the above surveys screen only for 174 chosen pesticides--compare this number to the roughly 1000 pesticide active ingredients and adjuvants registered for use in California. I've discussed the composition of this list with USDA's Roger Simonds, who runs the tests. It is prohibitively costly to test for every possible pesticide, so one must arbitrarily draw up a limited list of the chemicals of most concern. All are aware that this is a difficult task, since we don't even know which toxins with which we should be most concerned!
Note that in both surveys, the most common insecticide present was chlorpyrifos- an "old school" (introduced in 1965) organophosphate neurotoxin classified as being "highly toxic" to bees, and marketed as Dursban and Lorsban. Chlorpyrifos was previously widely used by homeowners and residential pest control companies. EPA has since restricted its use due to its toxicity to wildlife and aquatic organisms, and possible links to human health issues [44]--some of the reasons that EPA favors the neonicotinoids as "reduced risk" products.
Oh Boy, Let's Do Some Math!
But just because a pesticide is present, doesn't necessarily mean that it is causing measureable harm. A nurse bee may consume about 10 mg of beebread per day [45], so if she consumed that amount of pollen contaminated with chlorpyrifos at 6.5 ppb, then she would have been dosed with 0.065 ng (1 nanogram = 1 billionth of a gram) of the chemical. The question then is, how much chlorpyrifos does it take to actually harm a bee?
One commonly cited figure is that the LD50 for chlorpyrifos given orally is 360 ng/bee. Compare those figures (360 ng for toxicity vs. 0.065 in the daily diet)! Even though chlorpyrifos is a disturbingly common comb contaminant, it is unlikely that the median detected concentration (alone) would be causing colony health problems (not to say that higher doses don't hurt colonies).
But, you say, some of the neonics are even more toxic than chlorpyrifos. How about the mean 31 ppb found by the USDA in the few samples positive for imidacloprid? The typical nurse bee would consume 0.31 ng, compared to the oral LD50 of about 4-40 ng, so she'd be eating a tenth to a hundredth of the lethal dose. This would be cause for concern, tempered by the fact that a bee can easily metabolize that amount of imidacloprid a day [46]. Such consumption could legitimately be suspected of causing sublethal effects. However, keep in mind that that 31 ppb was an average, which was strongly skewed by a few samples with very high concentrations (which I'd fully expect to cause colony health problems). Plus this is not simply a matter of the average amount of contamination; one must also look at the percentage of positive detects. The Penn State team [47] puts it well:
Our residue results based on 1120 samples which include Mullin et al. (2010) and subsequently more than 230 additional samples do not support sufficient amounts and frequency of imidacloprid in pollen to broadly impact bees.
OK, so how about the varoacides fluvalinate at 40 ppb or the amitraz degradate DMPF at 100 ppb? Surprisingly, I can't find an oral LD50 for fluvalinate, so the contact toxicity figure (200 ng/bee) will need to suffice. Those residues work out to about 1/500th expected toxicity.
Amitraz scored a bit better, with the nurse bees consuming about 0.01 ng--far below the lethal dose. But a recent study found that an oral dose of 0.2 ng of amitraz causes more than a doubling of the heart rate of a bee [48]--that's at 1/20th of the average detect! The authors dryly state:
The above responses clearly show that the heart of the honeybee is extremely vulnerable to amitraz, which is nevertheless still used inside beehives, ostensibly to "protect" the honeybees against their main parasite, Varroa destructor.
How vulnerable? Frazier [49] observed that "Dead and dying bees collected around colonies in association with corn had only residues of 2,4-DMPF at 5,160 ppb." Looks like perhaps the beekeeper inadvertently killed his own bees with an off-label mite treatment that may have overworked their little hearts!
And if those miticide and insecticide residue weren't enough alone, some of the toxicity of these chemicals is additive or synergistic. The Penn State team again says it well:
[The] pyrethroids... were found in 79.4% of samples at 36-times higher amounts than the neonicotinoids, on average... The mean neonicotinoid residue was 37 ppb (scoring non-detects as 0 ppb), of which only 6.7 ppb was imidacloprid. Pyrethroids, by comparison, were present at a mean residue of 106 ppb and a frequency of 80.3% in pollen samples... Indeed, if a relative hazard to honey bees is calculated as the product of mean residue times frequency detected divided by the LD50, the hazard due to pyrethroid residues is three-times greater than that of neonicotinoids detected in pollen samples [emphasis mine].
The pyrethroids are popular because they are relatively nontoxic to humans. But they can sure kill honey bees. More so, they can cause sublethal effects, such as irreversible inhibition of olfactory learning ability [50].
Hey, we're only getting rolling! Mussen [51] pointed out a decade ago that fungicides could kill larvae; recent research from the Tucson lab [52] and elsewhere confirm that fungicide residues can mess up the colony (we sometimes observe this in almonds). Of note is that colonies treated with some fungicides were unsuccessful at requeening themselves! And recent research by Zhu [53] found that the relative toxicity of larvae to the commonly-detected fungicide chlorothalanil was almost 40 times higher than that of chlorpyrifos. Fungicides are frequently found at high concentrations in beebread.
I cannot help from returning to the refrain that instead of limiting our concern to any single pesticide, that we should be looking at the total toxin load that the colony is forced to deal with.
And How About The "Inerts"?
The pesticide detection analyses above do not look at the "inert" adjuvants in the pesticide "formulation." These chemicals not only help to disperse the pesticide over the waxy leaf surface, but also aid in its penetration through the insect cuticle, thus making the pesticide relatively more toxic to the bee!
Mullin and Ciarlo [54, 55] found that:
Formulations usually contain inerts at higher amounts than active ingredients, and these penetrating enhancers, surfactants and adjuvants can be more toxic on non-targets than the active ingredients. For example, we found that the miticide formulation Taktic®️ was four time more orally toxic to adult honey bees than the respective active ingredient amitraz. Impacts of 'inerts' in pollen and nectar alone or in combination with coincident pesticide residues on honey bee survival and behavior are unknown.
The researchers also found that:
Learning was [rapidly] impaired after ingestion of 20 ug of any of the four tested organosilicone adjuvants, indicating harmful effects on honey bees caused by agrochemicals previously believed to be innocuous.
One of the common adjuvants is a solvent NMP, described by BASF [56]:
NMP can be used as a solvent or co-solvent for the formulation of insecticides, fungicides, herbicides, seed treatment products and bioregulators where highly polar compounds are required. NMP is given preference over other highly polar solvents because it is exempt from the requirement of a tolerance when used as a solvent or co-solvent in pesticide formulations applied to growing crops, and it possesses a favorable toxicological and environmental profile.
The key words above are that these toxic solvents are "exempt from tolerance" [57], so they are sprayed all over crops along with the active ingredients of pesticides (including imidacloprid). Yet Zhu [58] recently reported that NMP can rapidly kill bee larvae. The authors conclude that:
Our study suggests that fungicide, the inert ingredient and pesticide interaction should be of high concern to honey bee larvae and overall colony health. None of these factors can be neglected in the pesticide risk assessment for honey bees.
Choosing To Ignore The Obvious
There is no doubt that neonics have the potential to harm bees, but the question is, do they really cause as much problem in the real world as we've been led to believe? This is not a matter of convincing the masses; this is an investigation of fact and evidence. For a pesticide to cause harm to a colony of bees, two necessary elements must occur:
The bees must be exposed to the pesticide. Evidence for this is best determined by chemical analysis of the pollen in the combs, since residues in the bodies of dead bees may be degraded, and because water-soluble insecticides such as the neonics are not absorbed into the wax (residues in the wax do document the history of exposure to lipophilic pesticides).
The pesticide must be present at a concentration above a trivial level.
When we take the time to determine which pesticides bees are actually found in the combs of hives, neonicotinoids are seldom present, or if detected are often at biologically irrelevant concentrations. Imidacloprid was detected in fewer than 3% of Mullin's 350 samples, and clothianidin not at all! Similarly, there were zero detects for clothianidin in the 99 USDA samples; imidacloprid was only present in 9%. Likewise, a number of European studies have shown similar results (reviewed in [59]).
In a recent study, the Fraziers [60] looked at hives placed in cotton, corn, alfalfa, apples, pumpkins, almonds, melons, blueberries, or wild flowers, and identified the residues in collected pollen, in returning foragers, and in dead or dying bees near the hives. Again, the only neonic noted was thiamethoxam in alfalfa (in which dying bees contained residues of ten different pesticides). However, there were alarmingly high detects of fungicides, the insecticide acephate, and the metabolite of the beekeeper-applied miticide amitraz.
The latest data comes from Dr. Jeff Pettis [61], whose group determined the pesticides in bee-collected pollen from six crops: apple, blueberry, cranberry, cucumber, pumpkin, and watermelon. Of the 35 pesticides detected, beekeeper-applied miticides and ag fungicides predominated (sometimes at alarming levels), followed by common organophosphate, pyrethroid, and cyclodiene insecticides (again sometimes at alarming levels). In the 17 samples tested, residues of neonics were only found in the samples from the apple orchards, and only one was found at a biologically-relevant concentration.
So my question is why the heck are so many activists pursuing the single-minded focus upon the neonics, when the clear evidence is that neonics are not commonly found in bee-collected pollen, and if present, are generally at levels that do not appear to negatively affect colony health [62]?
There is a lot more to pesticide issues than the neonics alone, and by focusing our attention solely upon them, we ignore the often far more serious effects of other pesticides.
Blinded By Bias
During the intense focus upon neonicotinoids the past few years, we've learned that exposure of bees to these insecticides can result in all sorts of sublethal effects. Unfortunately, many researchers appear to be wearing blinders as to the effects of other pesticides. The resulting narrowness of these studies skews our perspective--if we only look for effects from the neonics, we don't know how to rank the biological relevance of those effects relative to the effects of all the other toxins to which bees are exposed, generally to greater extent.
A practical complaint to researchers: if you are going to look for sublethal effects of neonics, please include positive controls of some other pesticides, so that we can learn whether the neonics are better or worse than the alternatives!
I commend one group that recently decided to take a look at the effects of a common herbicide upon the development of bee larvae [63]. The results of this straightforward and meticulous study are an eye opener!
The researchers found that exposing bee larvae to even infinitesimal amounts of the herbicide paraquat prevented them from fully developing their critical oenocyte cells (see box).
Oenocyte cells are not only involved in the production of lipids and lipoproteins, but they also appear to play a role in the constitution of external cuticle in both larvae and adults. In addition, they are involved in intermediary metabolism and synthesize hydrocarbons to waterproof cuticle or to make beeswax. Furthermore, oenocytes secrete hormones, especially those involved in larval and adult development. They are also described as the major cells expressing cytochrome P450 reductase, which is involved in detoxification of toxins [information paraphrased from the cited paper].
Exposure to even a part per trillion of paraquat suppressed the development of these extremely important cells. The authors conclude:
This study is the first which reports an effect of a pesticide at the very low concentration of 1 ng/kg, a concentration below the detection limits of the most efficient analytic methods. It shows that chemicals, including pesticides, are likely to have a potential impact at such exposure levels.
Who woulda thunk? Paraquat isn't included in the standard screening for pesticide residues, so we don't even know how prevalent it is in hives! The above findings should make it clear that we need to go back to the beginning if we are to understand the sublethal effects of pesticides (and adjuvants), even at perhaps undetectable levels.
We do know that here were 812,000 lbs of paraquat applied in California in 2010, as opposed to only 266,000 lbs of imidacloprid. Paraquat shows strong adverse effects upon bee larvae at a part per trillion, as compared to imidacloprid, which is so minimally toxic to bee larvae that no one has even been able to determine an LD50! So the amount of paraquat applied has far greater potential to cause problems to bees in agricultural areas (Fig. 7).
Figure 7. The herbicide paraquat appears to be harmful to bee larvae at levels as low as 1 part per trillion. Note the wide variety of crops, and the extensive areas to which it is applied.
So here we have clear scientific data from a well-designed laboratory experiment that a commonly-applied pesticide has the ability to cause immune suppression and other adverse effects in developing bees, yet these results have been virtually ignored by beekeepers and environmental groups. I just don't understand it!
No More Safe Home To Return To
Out of their protective hive, honey bees live in a hostile world, full of predators, deadly weather, and toxic agents (both natural and manmade). But the bees of old could generally return to a "safe" home, in which the transmission of natural toxins was largely minimized by the behavior of foragers, and by the processes of the conversion of nectar to honey, and of pollen into jelly (via the digestion of beebread by nurse bees). Both of these processes help to prevent the transmission of toxins from the foragers to the queen and the brood.
With the advent manmade pesticides, bees may no longer have that "safe" home to return to. Beebread and the wax combs nowadays are often contaminated with any number of pesticides (in addition to natural plant toxins and industrial pollutants). But this is not a "new" problem:
A Historical Artifact
Even before we had the ability to detect pesticide residues in combs to the parts per billion level, pesticide analyses often found easily-detectable levels of insecticides in bee hives. As a frame of reference, I sought out a historical artifact--the residues in the beeswax that had been rendered by beekeepers and reprocessed into a sheet of "clean" foundation. I was lucky enough to find that such a sample had recently been analyzed by the Tucson Bee Lab. Dr. Diana Sammataro forwarded me the results of the analysis of an undated "very old" piece of wax foundation from the Northeast (Table 3).
THIS IS THE TABLE !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!
Pesticides in an old piece of beeswax foundation.
Positive residue detect
ppb
Pendimethalin
13.1
Endrin
156
Dieldrin
160
Trifluralin
3.6
DDT p,p'
32.7
Heptachlor
35.1
Malathion
4.3
Chlorpyrifos
4.6
Dicofol
6.8
PCB's
8190
Chlorothalonil
84.6
Table 3. We can narrow down the foundation's date of manufacture by the residues present. Pendimethalin was first registered in 1972 (the same year that DDT was banned), and since there were no residues of fluvalinate, the foundation was clearly produced prior to the arrival of varroa around 1990. Thanks to Dr. Diana Sammataro and the Tucson Bee Lab.
Clearly, pesticide-contaminated combs are hardly a new phenomenon. In the above example, the beeswax batch used to produce the foundation came not from a single hive, but rather from the combined wax from many hives, likely from many beekeepers, and thus would represent an average sample of the degree of contamination somewhere in that 1972-1990 time frame. And that doesn't take into account whether the raw wax came mainly from cappings (which would have been minimally contaminated), or whether it went through the common practice of being filtered through activated carbon. But any colony started on such foundation purchased from a beekeeping supply house would clearly have had to deal with at least the residues of these lipophilic toxins from the get go!
An aside: perhaps of interest is something that I noticed years ago when I switched from dipping my own wax queen cell cups to using plastic cups. My "take" rate became better and more consistent. Was that because the beeswax at the time was contaminated with residues?
The Beekeeper Contribution To Shifting The Tip Point
One thing that is "new" is that since the arrival of varroa, we've upped the ante--all commercial beeswax is now contaminated with residues of beekeeper-applied synthetic miticides. The three most prevalent synthetic chemicals found in combs today all get there by being applied by beekeepers for mite control.
Practical note: And although there is no reason to be concerned about the tainting of honey by the legal use of these miticides, the beekeeper/applicator should be aware that both amitraz and tau-fluvalinate make California's list of "chemicals known to the State to cause reproductive toxicity," and coumaphos is of concern because it is a "cholinesterase-inhibiting pesticide." No varroacide is harmless to bees [64]--but the benefits of mite control generally (but not always) outweigh the adverse effects due to the miticide residues.
We beekeepers have clearly shifted the baseline for pesticide contamination of combs, which increases the total toxic load even before the contribution by agricultural pesticides.
Stop Right There!
Although it is a very attractive hypothesis to blame our problems on miticide or pesticide residues, let's do a reality check. On good forage in good weather, plenty of beekeepers see their colonies thrive even on old, dark, seriously-contaminated combs; but under stressful conditions those same residues might contribute to poor colony performance or even mortality.
No study has yet found support for the hypothesis that miticide residues are the cause of our current bee problems (although one would have every reason to suspect that they may contribute). In fact, vanEngelsdorp [65] found that surprisingly, higher levels of coumaphos residues negatively correlated with colony survival. How could this be? One possible explanation is that those beekeepers who used it experienced better mite control. But there is also another intriguing possibility--hormetic effects.
Undetectable Levels And Hormesis
Is your head spinning yet? I've presented evidence that undetectable levels of some pesticides could harm bees, that "inert" adjuvants can do the same, and that combs are often chock full of all sorts of pesticide and varroacides residues. Criminy, it's a wonder that bees survive at all! Or is it?
Bees have long been exposed to all sorts of natural, and recently, manmade toxins, and survived. Toxicity is a complicated subject. The only thing that separates a medicine from a poison is the dose. In general, if a pesticide has been tested upon adult and larval bees and found to have no observable adverse effects at a certain concentration, we would not expect to see adverse effects at lower concentrations. However, there are exceptions to this general rule--toxicity may vary up or down depending upon the dose [66]!
I've previously mentioned the term hormesis [67]-- the paradoxical effect of toxins at low concentrations. The paradox is that although most chemicals are toxic at high concentrations, the majority are likely beneficial at low concentrations. For those interested in this fascinating phenomenon, I suggest Dr. Chris Cutler's excellent and thought-provoking review [68]. It is not only possible, but actually probable that lose doses of pesticides may exert a beneficial effect upon a colony! (Don't be ridiculous--I'm not suggesting that bees are better off for the presence of pesticides!).
Wrap Up
Toxins, whether natural or manmade, are clearly a potential issue in colony health. To what degree pesticides contribute to colony morbidity or mortality is dependent upon exposure, the dose, and a host of associated factors. Beekeepers have long noticed that their bees often do better if allowed to forage on pesticide-free land. But many beekeepers today tell me that their bees do just fine in the middle of intense agricultural areas--so this is not a black or white situation.
In recent years beekeepers themselves have greatly added to the degree of contamination of their combs. Introductions of novel pesticides and adjuvants keep changing the picture. And now we're finding that pesticides that we formerly assumed were harmless to bees (fungicides and herbicides) may actually be quite toxic to larvae! Then there is the scary finding that undetectable levels of some pesticides might cause health issues, countered by the fascinating subject of hormesis.
I certainly do not profess to understand all this, but I have come to the following conclusions:
That bees have had to deal with toxins for a long time,
That pesticides will be with us for the foreseeable future,
That varroacides have likely added to the problem,
That pesticides can cause lethal and long-term sublethal effects in the hive, but
That many beekeepers in agricultural areas no longer consider pesticides to be a serious issue, whereas,
That colonies may go downhill after being exposed to some agricultural chemicals, or combinations thereof,
That toxicology in the hive is complex, and that there are few simple answers,
That it is unlikely that any single pesticide is to blame for our current colony health issues,
That we still have a lot to learn!
Next month I will look at the distribution of both managed colonies and of pesticide applications in the United States, and their relationship to bee health problems.
Acknowledgements
As always, I could not research these articles without the assistance of my longtime collaborator Peter Loring Borst, to whom I am greatly indebted. I also wish to thank Drs. Jim and Maryann Frazier, Chris Mullin, David Fischer, Eric Mussen, Thomas Steeger, and Roger Simonds for their generosity in taking the time to discuss pesticide issues with me.
References
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[2](Broken Link) http://perc.org/articles/everyone-calm-down-there-no-bee-pocalypse
[3] vanEngelsdorp, D and MD Meixner (2010) A historical review of managed honey bee populations in Europe and the United States and the factors that may affect them. Journal of Invertebrate Pathology 103: S80-S95. http://www.sciencedirect.com/science/article/pii/S0022201109001827
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[5] vanEngelsdorp and Meixner (2010) op. cit.
[6] Rucker (2012) op. cit.
[7] https://scientificbeekeeping.com/sick-bees-part-18f-colony-collapse-revisited-pesticides/
[8] https://scientificbeekeeping.com/the-extinction-of-the-honey-bee/
[9] https://scientificbeekeeping.com/historical-pesticide-overview/
[10] https://scientificbeekeeping.com/sick-bees-part-2-a-model-of-colony-collapse/
[11] Thompson, HM (2012) Interaction between pesticides and other factors in effects on bees. http://www.efsa.europa.eu/en/supporting/doc/340e.pdf
[12] Frazier, J, et al (2011) Pesticides and their involvement in colony collapse disorder. http://www.extension.org/pages/60318/pesticides-and-their-involvement-in-colony-collapse-disorder#.UgO3zKyaucw A must read!
[13] http://www.ars.usda.gov/is/AR/archive/jul12/colony0712.htm
[14] For an explanation refer to https://scientificbeekeeping.com/sick-bees-part-18b-colony-collapse-revisited/
[15] https://scientificbeekeeping.com/what-happened-to-the-bees-this-spring/
[16] Wilson, WT and DM Menapace (1979) Disappearing disease of honey bees: A survey of the United States. ABJ March 1979: 185-186.
"Certainly with both pesticide-related and [Disappearing Disease]-caused bee losses, the adult population of a colony may be reduced rapidly to a "handful" of bees or, in some cases, the entire population may be lost.
"However, in the case of pesticide poisoning, there is usually evidence of pesticide application...the worker bees either die in the field or in or near the hive depending on the type of pesticide. When the field force is killed and they "disappear," many dead or dying bees may be seen on the ground in the field or on the ground between the treated field and the apiary...If the foraging bees bring poison into the hive, then the nurse bees either die in the hive or at the entrance so one can see many crawling and tumbling adults and large amounts of neglected brood. Exposure to pesticides over an extended period results in very weak colonies, and some die out.
"In the case of [Disappearing Disease], the situation is quite different. The colonies frequently have gone through a period o nectar and pollen collection with active brood rearing [as in typical CCD]. Then the weather has turned unseasonably cool and damp and remained adverse for from about 3 to 14 days...During the inclement weather, the bee populations dwindle because the worker bees disappear from the hive leaving a "handful" of bees and the queen. Often these small populations recover and increase in size during hot weather and a long nectar flow or, or occasionally, the entire population absconds..."
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[25] Wu JY, Smart MD, Anelli CM, Sheppard WS (2012) Honey bees (Apis mellifera) reared in brood combs containing high levels of pesticide residues exhibit increased susceptibility to Nosema (Microsporidia) infection. J Invert Path 109: 326-329
[26] Pettis JS, Lichtenberg EM, Andree M, Stitzinger J, Rose R, et al. (2013) Crop Pollination Exposes Honey Bees to Pesticides Which Alters Their Susceptibility to the Gut Pathogen Nosema ceranae. PLoS ONE 8(7): e70182. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0070182#pone.0070182-Chaimanee1
[27] Maisonnasse A, et al (2010) E-b-Ocimene, a volatile brood pheromone involved in social regulation in the honey bee colony (Apis mellifera). PLoS ONE 5(10): e13531. http://www.plosone.org/article/info:doi/10.1371/journal.pone.0013531 These researchers studied (E)-b-ocimene, a volatile terpene commonly produced by plants to attract predatory mites, but also a critical pheromone produced by the brood and the queen.
[28] Decourtye A, et al. (2005) Comparative sublethal toxicity of nine pesticides on olfactory learning performances of the honeybee Apis mellifera. Archives of Environmental Contamination and Toxicology 48: 242-250. http://www.environmental-expert.com/Files/6063/articles/4909/QM245Q254G1T6X0R.pdf
[20] Yang E-C, Chang H-C, Wu W-Y, Chen Y-W (2012) Impaired olfactory associative behavior of honeybee workers due to contamination of imidacloprid in the larval stage. PLoS ONE 7(11): e49472. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0049472
[30] Bee health in Europe -Facts & figures 2013. OPERA http://operaresearch.eu/files/repository/20130122162456_BEEHEALTHINEUROPE-Facts&Figures2013.pdf
[31] The study by Drs. Scott-Dupree and Cutler is yet unpublished, but a summary can be found at http://www.producer.com/daily/ontario-field-study-finds-no-link-between-seed-treatments-bee-deaths/
[32] Cutler, GC, CD Scott-Dupree, DM Drexler (2013) Honey bees, neonicotinoids, and bee incident reports: the Canadian situation. Pest Management Science http://onlinelibrary.wiley.com/doi/10.1002/ps.3613/abstract
[33] Goulson, Dave (2013) An overview of the environmental risks posed by neonicotinoid insecticides. Journal of Applied Ecology 50: 977-987. https://www.sussex.ac.uk/webteam/gateway/file.php?name=goulson-2013-jae.pdf&site=411
[34] Scott-Dupree, CD, et al (2009) Impact of currently used or potentially useful insecticides for canola agroecosystems on Bombus impatiens (Hymenoptera: Apidae), Megachile rotundata (Hymentoptera: Megachilidae), and Osmia lignaria (Hymenoptera: Megachilidae). J Econ Entomol 102(1):177-82.
[35] Blacquiere, et al (2012) Neonicotinoids in bees: a review on concentrations, side-effects and risk assessment http://www.gesundebiene.at/wp-content/uploads/2012/02/Neonicotinoide-in-bees.pdf
[36] Hobbs, GA (1967) Domestication of Alfalfa Leaf-cutter Bees. Canada Dept. of Agriculture. Ottawa: Queen's Printer and Controller of stationary.
[37] Dr. Jerry Bromenshenk, pers. com.
[38] Abbott, VA, et al (2008) Lethal and sublethal effects of imidacloprid on Osmia lignaria and clothianidin on Megachile rotundata (Hymenoptera: Megachilidae). J Econ Entomol 101(3):784-96.
[39] http://pfspbees.org/sites/pfspbees.org/files/resource-files/pnw591.pdf
[40] PMRA (2013) Evaluation of Canadian Bee Mortalities Coinciding with Corn Planting in Spring 2012.
[41] PMRA (2013) Action to Protect Bees from Exposure to Neonicotinoid Pesticides http://www.hc-sc.gc.ca/cps-spc/alt_formats/pdf/pest/part/consultations/_noi2013-01/noi2013-01-eng.pdf
[42] Mullin CA, et al. (2010) op. cit.
[43] Rennich, K, et. al (2012) 2011-2012 National Honey Bee Pests and Diseases Survey Report. http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
[44] Christensen, K.; Harper, B.; Luukinen, B.; Buhl, K.; Stone, D. 2009. Chlorpyrifos Technical Fact Sheet; National Pesticide Information Center, Oregon State University Extension Services. http://npic.orst.edu/factsheets/chlorptech.pdf.
[45] Rortais, A (2005) Modes of honeybees exposure to systemic insecticides: estimated amounts of contaminated pollen and nectar consumed by different categories of bees. Apidologie 36: 71-83.
[46] Cresswell, JE, et al (2012) Differential sensitivity of honey bees and bumble bees to a dietary insecticide (imidacloprid). Zoology 115: 365- 371.
[47] Frazier (2011) op. cit.
[48] Papaefthimiou, C, et al (2013) Biphasic responses of the honeybee heart to nanomolar concentrations of amitraz. Pesticide Biochemistry and Physiology 107(1): 132-137. http://www.sciencedirect.com/science/article/pii/S0048357513001120
[49] Frazier, et al (2011) Assessing the reduction of field populations in honey bee colonies pollinating nine different crops. ABRC 2011
[50] Tan K, Yang S, Wang Z, Menzel R (2013) Effect of flumethrin on survival and olfactory learning in honeybees. PLoS ONE 8(6): e66295. doi:10.1371/journal.pone.0066295. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0066295
[51] Mussen, et al (2004) op. cit.
[52] http://www.abfnet.org/associations/10537/files/Dr.%20Gloria%20DeGrandi%20Hoffman_GS.mp3
[53] Zhu, W., D. Schmehl & J. Frazier (2011) Measuring and predicting honey bee larval survival after chronic pesticide exposure http://www.extension.org/pages/58650/proceedings-of-the-american-bee-research-conference-2011#.UhDTZX-aucw
[54] Mullin, C.A., J. Chen, W. Zhu, M.T. Frazier & J.L. Frazier - The formulation makes the bee poison. ABRC 2013
[55] Ciarlo TJ, Mullin CA, Frazier JL, Schmehl DR (2012) Learning impairment in honey bees caused by agricultural spray adjuvants. PLoS ONE 7(7): e40848. doi:10.1371/journal.pone.0040848
[56] (Broken Link!) http://www2.basf.us/diols/bcdiolsnmp.html
[57] http://www.epa.gov/opprd001/inerts/methyl.pdf
[58] Zhu, et al (2011) op. cit.
[59] Blacquiere, T, et al (2012) Neonicotinoids in bees: a review on concentrations, side-effects and risk assessment. Ecotoxicology 21(4): 973-992. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3338325/
[60] Frazier, M.T., S. Ashcraft, W. Zhu & J. Frazier - Assessing the reduction of field populations in honey bee colonies pollinating nine different crops http://www.extension.org/pages/58650/proceedings-of-the-american-bee-research-conference-2011#.UhDTZX-aucw
[61] Pettis, et al (2013) op. cit.
[62] A recent study confirm that the neonic residues in corn, soy, and canola pollen are at very low concentrations. Henderson, C.B. a, J.J. Bromenshenka, D.L. Fischerb. Clothianidin exposure levels from bee-collected pollen and nectar in seed-treated corn and canola plantings. ABRC 2013 http://bees.msu.edu/wp-content/uploads/2013/01/ABRC-abstracts-2013.pdf
[63] Cousin M, Silva-Zacarin E, Kretzschmar A, El Maataoui M, Brunet J-L, et al. (2013) Size changes in honey bee larvae oenocytes induced by exposure to paraquat at very low concentrations. PLoS ONE 8(5): e65693. doi:10.1371/journal.pone.0065693 http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0065693
[64] Boncristiani, H., et. al. (2011) Direct effect of acaricides on pathogen loads and gene expression levels of honey bee Apis mellifera. Journal of Insect Physiology. 58:613-620.
[65] vanEngelsdorp, D, et al () Weighing risk factors associated with bee colony collapse disorder by classification and regression tree analysis. J. Econ. Entomol. 103(5): 1517-1523. (Broken Link!) http://www.eclecticparrot.com.au/research_papers/VanEngelsdorp%202010%20Weighing%20risk%20factors%20in%20Bee%20CCD.pdf
[66] Cutler GC, Ramanaidu K, Astatkie T, and Isman MB. (2009) Green peach aphid, Myzus persicae (Hemiptera: Aphididae), reproduction during exposure to sublethal concentrations of imidacloprid and azadirachtin. Pest Manag Sci 65:205-209
[67] https://scientificbeekeeping.com/sick-bees-part-18f2-colony-collapse-revisited-plant-allelochemicals/
[68] Cutler, GC (2013) Insects, insecticides and hormesis: evidence and considerations for study. Dose-Response 11:154-177 (Broken Link!) http://dose-response.metapress.com/app/home/contribution.asp?referrer=parent&backto=issue,2,11;journal,3,34;linkingpublicationresults,1:119866,1
Category: Colony Health - Diseases, Viruses, CCD
Tags: collapse, colony, pesticides, sick bees | sick bees Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/sick-bees/ |
Sick Bees - Part 18F7: Colony Collapse Revisited - Pesticide Exposure
First published in: American Bee Journal, October and November 2013
Pesticide Exposure
Oh No, Not Pesticides Again!
Reality Checks
The Two Worlds of Beekeeping
Pesticides and Bee-pocalypse
A Comparison To Some "Control Groups"
The Four Horsemen And The Tip Point
Could Pesticides Cause Colony Mortality And CCD?
Short Memories
The Heart Of The Hive - The Nursery
Industry's Arguments
But Don't We Already Know That It's The Neonicotinoids?
An "Acid Test" Of Neonic Seed Treatment
So Which Pesticides Are Actually To Blame?
The Evidence
Oh Boy, Let's Do Some Math!
And How About The "Inerts"?
Choosing To Ignore The Obvious
Blinded By Bias
No More Safe Home To Return To
A Historical Artifact
The Beekeeper Contribution To Shifting The Tip Point
Stop Right There!
Undetectable Levels And Hormesis
Wrap Up
Acknowledgements
References
Sick Bees Part 18f7: Colony Collapse Revisited
Pesticide Exposure
Randy Oliver
ScientificBeekeeping.com
Originally published in ABJ Oct and Nov 2013
Oh No, Not Pesticides Again!
Some readers may wonder why I am spending so much time on the issue of pesticides, since to many (if not most) beekeepers, pesticides are a non issue. In answer, the main reason is that the public (and our lawmakers) are being hammered by the twin messages that the honey bee is on the verge of extinction, and that the reason is pesticides. In my writings, I'm attempting to address the validity of both of those claims. Let's start with the first.
Reality Checks
Honey bees have clearly (and deservedly) become one of today's most charismatic environmental poster children, and as such are a useful bioindicator that our human activities are having a negative impact upon pollinators, and wildlife in general.
But I also feel that we take care to not overstate or exaggerate our case. One of my greatest concerns is that beekeepers are allowing the media to scare the public with all the hue and cry of an impending bee-pocalypse (and that it is due to a certain type of pesticide). Our complicity in this message (as we enjoy the luxury of basking in the warmth of all the public support) may backfire on us one of these days--putting us into the position of the little boy who cried wolf. Some in the media are starting to notice that the facts don't support the claim that bees are disappearing (Fig. 1).
Figure 1. It's true that it's more difficult to keep bees healthy these days, but it doesn't look like bee-pocalypse is imminent (as evidenced by this recently-published chart). Whenever honey and pollination prices are high enough to make beekeeping profitable, resourceful beekeepers somehow manage to recover their colony losses [[i]]. Chart courtesy Shawn Regan [[ii]].
[i] Rucker, RR and WN Thurman (2012) Colony collapse disorder: the market response to bee disease. http://perc.org/sites/default/files/ps50.pdf
[ii] (Broken Link) http://perc.org/articles/everyone-calm-down-there-no-bee-pocalypse
In the rest of the world, the number of managed hives has actually been increasing [3]. And as far as claims that pesticides are driving bees to extinction, Hannah Nordhaus, the author of the excellent book The Beekeeper's Lament writes:
Reflexively blaming pesticides for all of the honey bee's problems may in fact slow the search for solutions. Honey bees have enough to do without having to serve as our exoskeletal canaries in a coalmine. Dying bees have become symbols of environmental sin, of faceless corporations out to ransack nature. Such is the story environmental journalism tells all too often. But it's not always the story that best helps us understand how we live in this world of nearly seven billion hungry people, or how we might square our ecological concerns and commitments with that reality. By engaging in simplistic and sometimes misleading environmental narratives -- by exaggerating the stakes and brushing over the inconvenient facts that stand in the way of foregone conclusions -- we do our field, and our subjects, a disservice [4].
Further reading: for a detailed and sober analysis of the factors that affect managed bee populations, I highly recommend the review by Drs. vanEngelsdorp and Meixner [5].
The reality is that it is not the honey bee that is being driven to extinction--it is instead the commercial beekeeper who is finding that his traditional business model is becoming less profitable due to today's greater degree of colony losses and the decreasing availability of good summer forage.
The question is, to what extent are pesticides involved in those problems?
The Two Worlds Of Beekeeping
There are two very different worlds of beekeeping--small scale (hobbyists, who constitute the vast majority of beekeepers by number) and large scale (commercialized professionals, who manage the vast majority of hives), with a small continuum of sideliners bridging the gap.
Hobby beekeeping is currently enjoying a bubble of resurgence, but in the Big Picture in the U.S., hobbyists manage an insignificant number of hives. And those small-scale beekeepers tend to keep their hives close to home, largely avoiding serious exposure to pesticides. But that's not to say that small-scale beekeepers are immune to pesticide kills; I've heard of several this season, and what with all the spraying for West Nile virus and the citrus psyllid, we can expect more of the same. And since there are far more small-scale beekeepers to put pressure on regulators and legislators, I feel that it is a good idea for them to be informed about pesticide issues.
Large-scale beekeepers, on the other hand, typically run migratory operations--moving their hives to almond pollination, and then to other agricultural areas (it's problematic to keep apiaries of hundreds of hives in the suburbs). The fate of those bees (and their keepers) is largely determined by agricultural land use practices and their degree of exposure to agricultural pesticides.
It is some of those large-scale beekeepers for whom extinction is a valid concern. The reason (as with any other enterprise) is financial--they can only survive so long unless their businesses continue to be profitable [6]. In recent years, they've had two things going for them--sky-high honey prices and elevated pollination fees. But all is not rosy--there are reasons for those prices going up; these days it's simply more costly to produce honey or to provide bees for pollination.
Today's breathtakingly-high high almond rental rates typically don't even cover operating costs--even if most of one's colonies make it through the winter! Today's 30% average winter loss rate is bleeding profitability from many operations. Not only does the beekeeper need to rebuild his numbers after almonds, but to stay in the black he must also make additional income from paid pollinations or a decent honey crop. And that may no longer be as easy as it used to be for various reasons:
Formerly bee-friendly farmland has been turned into agri-deserts devoid of any bee forage.
Honey producers on field crops (such as alfalfa, sunflowers, or cotton) get hammered time and again by pesticide spraying, sometimes watching whole yards of colonies dwindle or go queenless weeks afterwards.
Paid summer pollination contracts (such as for vine crops) may leave colonies in poor shape for the winter, due to the heavy stocking, the lack of nutritious pollen, and the exposure to multiple pesticides.
These days, the sad fact is that many good beekeepers are barely keeping their heads above water. So the beekeeper's lament continues--varroa, high winter mortality, and lack of good forage are driving a number of operations into the red.
Practical application: although the "extinction of the honey bee" makes for a good rallying cry, the real concern is the possible extinction of the migratory beekeeper who supplies necessary pollination services to agriculture. So far, the almond industry has been economically propping up the bee industry, but I'm not sure how long that arrangement will be sustainable.
Pestcides And Bee-Pocalypse
For some beekeepers, "bee-pocalypse" has already occurred. New York beekeeper Jim Doan, whose case I detailed in a previous article [7], sadly gave it up this year. Here is a beekeeper whose apiaries had been in the same locations for many years without noticeable pesticide problems, but who apparently suffered from devastating spray or dust kills this season and last, as evidenced by piles of fresh dead bees in front of his hives in spring.
Residue analysis of those dead bees clearly showed that they had been exposed to several pesticides, but none of the detects were at levels that would be expected to cause such carnage--so we don't even know which pesticides or practices to point the finger at! To my scientific mind, this is very frustrating--that our "system" was not able to identify the cause of Jim's bee kills, to change anything to keep them from recurring, nor compensate an innocent beekeeper for the loss of his livestock and livelihood.
As unlucky as Jim has been, his case is not necessarily the norm. Overall, the issue of environmental toxins is improving. In my own lifetime I've seen us clean up our pollution of the air and water, cease atmospheric testing of nuclear weapons, ban DDT, fluorocarbons, and PCB's, phase out the worst pesticides, and raise the general environmental consciousness. Humans still inflict far too damaging an environmental footprint on Earth, but we are moving in the right direction, and should give ourselves some credit for that!
There is no doubt that pesticides are often involved in bee health issues, but can we blame them for all our problems? That question is best answered by considering the health of those colonies that are not exposed to pesticides:
A Comparison To Some "Control Groups"
There are plenty of beekeepers in non agricultural areas whose apiaries are not exposed to pesticides to any extent. Those hives serve as a "control group," whose health we can compare to those colonies that do have to deal with pesticides.
For instance, in my own operation of about a thousand hives, their only exposure to pesticides is to the fungicides in the almond orchards (from which they don't appear to suffer to any serious extent). I haven't used synthetic miticides in over a decade, rotate my combs, and rarely feed syrup.
Yet, I've experienced CCD firsthand, see more queenlessness, unsuccessful supersedure, and experience somewhat higher winter losses than in the old days (meaning before varroa). I hear the same from many others in the pesticide-free control group. The simple fact is that these days it requires better husbandry to maintain productive colonies. Yet we in the "control group" can hardly blame pesticides to be the cause.
And then there are the stationary "treatment free" beekeepers in the middle of intense agriculture who suffer no higher colony loss rates than the norm, despite their apiaries being surrounded by corn and soy [8]. How the heck do we reconcile their success to the problems that the commercial guys experience in the same areas?
Do they owe their success to keeping fewer hives in a yard? To keeping locally-adapted survivor stock? To their placement within flight range of patches of undisturbed forage? To the fact that they don't move to multiple crops? Or is it because they aren't contaminating their combs with miticides? Believe me, if I knew the answer, I'd tell you!
As (the very successful) beekeeper Dave Mendes observes, colonies just seem to be more "fragile" these days. It's no surprise then that the addition of toxins of any sort can help to tip a colony over. The Ericksons [9] put it this way:
Pesticides and their residues in the hive stress bees as do other factors such as weather extremes, food shortages, pests, predators, and disease. Conversely, stress induced by other factors undoubtedly has a significant impact on the level of damage that a pesticide inflicts on a colony.
Note that the above words were written prior to our colonies having to deal with varroa, the varroa-vectored viruses, Nosema ceranae, our evolving brood diseases, GMO's, neonicotinoids, or Roundup Ready corn.
The Four Horsemen And The Tip Point
Colony growth is a function of the recruitment rate via successful broodrearing vs. the attrition rate of workers due to age, disease, the altruistic departure of sick bees, or the loss of foragers in the field. When recruitment exceeds attrition, colonies grow; when attrition exceeds recruitment, the colony population shrinks. Environmental factors, including toxins, can shift the tip point for colony growth (Fig. 2).
Figure 2. Any colony with a good laying queen has the potential to grow rapidly--the greater the rate of recruitment (successful broodrearing), the steeper the slope of the growth curve. In the real world, such potential growth is often held back by the lack of nutritious pollen, or by the stresses of toxins, chilling, or pathogens (especially the mite-associated viruses, nosema, or EFB). Any of those can strongly shift the tip point, slowing, or even reversing, the rate of colony growth.
In the last decade, something appears to have shifted that tip point--colonies today seem to more readily go into a downhill spiral and queens no longer hold up as well. Could it be due to pesticides?
Could Pesticides Cause Colony Mortality And CCD?
Of course they could! In 2010, after closely observing the progression of experimentally-induced CCD with my collaborator Dr. Eric Mussen, I published the flow chart below (Fig. 3) to detail the interactions and feedback loops involved in the step-by-step collapse of a colony [10]. At the time, I fully intended to further elaborate upon the contribution of toxins, but didn't get around to it until now.
Figure 3. The positive feedback loops that can lead to colony dwindling and/or sudden depopulation. I've since observed this process take place in sick colonies time and again.
In the above chart, I called out toxins (which would include pesticides) as one of the "Four Horsemen of Bee Apocolypse" (the four factors at top left). Below I've indicated in red those points at which toxins may exacerbate the downhill process (Fig. 4).
Figure 4. Note that toxins can exert lethal or sublethal effects (red bubbles) at every step in the process of colony dwindling or collapse. Pesticides may in some cases be the prime cause of colony mortality; more frequently they might be "contributory factors," especially due the prolonged sublethal effects of residues in the beebread or wax.
Please note that in these charts I'm referring to toxins generically, not specifically to manmade pesticides. Such toxins would include natural plant allelochemicals, industrial pollutants, metals such as arsenic or selenium in soil and dust, fungal and bacterial toxins (which may be altered in beebread by the presence of pesticide residues), beekeeper-applied varroacides, HMF in overheated corn syrup, all in addition to any agricultural pesticides. In the words of ecotoxicologist Dr. Helen Thompson, we must pay attention to the total toxin load of the hive, plus any interactions between those chemicals, as well as other contributory factors [11]--a sentiment also echoed by the Fraziers at Penn State [12]. So, back to our original question: Can toxins, including synthetic pesticides, cause colony morbidity or mortality?
Verdict #1: clearly, synthetic pesticides and varroacides may constitute the most serious toxin load for managed bees in agricultural areas, and have the potential kill a colony outright, or to exacerbate positive feedback loops that can result in dwindling, poor overwintering, or collapse.
But does any pesticide specifically cause CCD--"the disappearance of most, if not all, of the adult honey bees in a colony, leaving behind honey and brood but no dead bee bodies" [13] (and no sign of brood diseases or varroa-induced DWV collapse).
Analysis: The most direct way to answer that question is to see whether we can fulfill Koch's third postulate [14]: can we experimentally create the symptoms of CCD by treating a healthy hive with the pesticide in question?
Verdict #2: to the best of my knowledge, no one has yet duplicated the symptoms of CCD by treating a colony with any pesticide (the most obvious difference being that there are generally plenty of dead bees present in the case of pesticide toxicity). This is notably true for the neonicotinoids, for which any number of researchers have attempted to duplicate CCD symptoms by continually feeding colonies neonic-tainted syrup or pollen.
Hold on--drop those stones! I am not saying that pesticides cannot contributeto CCD or colony morbidity or mortality in general--my chart above clearly illustrates that they have the potential to do so. Yet even those beekeepers who manage to completely avoid pesticides may still experience sudden colony depopulations, dwindling, or excessive winter losses due to some combination the Four Horseman (as in the perfect storm detailed at [15]).
I feel that it is a serious error for us to try to link CCD to pesticides. Pesticides have always been an issue to beekeepers, but CCD-like events have historically come and gone (as in Disappearing Disease--read the description at [16]). Pesticides will remain an issue long after the term "CCD" is forgotten.
Bottom line: Despite the fact that the evidence at hand does not support the case that CCD is directly caused by any pesticide, that fact certainly does not mean that we should ignore pesticide issues. If anything, we beekeepers ourselves have helped to make pesticides even more of an issue these days.
Short Memories
There is a popular myth going around that pesticides only started to become an issue to honey bee colony survival in 2007. In fact, the sublethal effects of pesticides were well known to beekeepers and researchers long before then. If we review the older literature [17], we find that it was already well known that contaminated pollen was a more serious issue to colony health than the in-field kill of foragers. We knew that colonies might collect such tainted pollen from miles away, that dusts were worse than sprays, that young bees may be more susceptible than older bees, and that temperature and humidity had a great deal to do with pesticide toxicity. Pesticide issues were actually far worse in the 1960's and '70's than they are today, and have generally improved since then (not to say that some new issues haven't arisen).
On the other hand, the overall contamination of combs with pesticides has increased in recent years due to the direct contribution by we beekeepers ourselves. In virtually any residue analysis of beebread or beeswax these days in any country with varroa, the most prevalent toxins are the beekeeper-applied varroacides [18]-you may wish to refer back to my chart of the "toxicological eras of honey bee evolution [19].
So one question is, To what degree we have shifted the tip point of colony health by contaminating our brood combs with miticides? Let's explore the broodnest...
The Heart Of The Hive - The Nursery
The insidious, long-term effects of total toxin load (including pesticide and varroacide residues) would be from those that made it into the heart of the hive--the critical stored beebread and the wax of the brood combs (Fig. 5). Note: Dr. David Fischer of Bayer brings to my attention that in the case of imidacloprid, the results of his testing indicates that bees in the hive are more affected by residues in the nectar than by those in the pollen.
Figure 5. Long after a pesticide-sprayed field force has been replaced by newly-recruited foragers, the colony may still need to deal with the lingering effects of pesticide residues in the combs, and especially in the all-important stores of beebread. It is here that such persistent residues can affect colony health and buildup for many months after the initial exposure, and exactly where we should focus our attention.
Here's some food for thought: a toxin need not actually kill a single bee to mess up a colony. There are many ways in which sublethal levels of toxins can negatively affect the colony population curve. A few examples would be:
By decreasing the survival rate of larvae (as from residues of varroacides [20, 21], or fungicides [22]) , or by increasing their development time (as effected by various pollutants, plant alleleochemicals, pesticides, or miticides).
By affecting the proper fermentation of beebread (fungicides).
By affecting the sensitive nurse bees that must digest that beebread and produce the critical jelly used to feed the brood, queen, and other workers (natural plant toxins, pollutants, or pesticides).
By affecting the normal behavioral progression of the workers. E.g., if workers initiate foraging prematurely, this greatly reduces their overall longevity, and results in severe depression of colony growth [23] (much more research is crying to be done, but many chemicals would be suspect).
By requiring bees to allocate precious resources toward the detoxification of the poisons (as per my leaky boat analogy [24]).
By increasing the virulence of varroa, nosema, or viruses (any number of pesticides and miticides have been implicated [25, 26])
By affecting normal colony homeostasis, such as thermoregulation of the brood, which is dependent upon the proper assessment of temperature, and the ability to effectively generate heat by the vibration of the wing muscles (neurotoxins would be expected to affect this ability).
By affecting the longevity of the queen, the viability of spermatozoa, or the ability of a colony to successfully supersede (coumaphos notably had this effect)
By affecting the production of, or normal communication via pheromones (which include the recognition of brood and the queen) [27] (essential oils, formic acid, other pesticides?)
By affecting foragers' ability to communicate by dance, to navigate, to learn (a wide range of pesticides [28]), or to react properly to normal stimuli (neonics can clearly do this [29]; but similar effects could be due to any number of other pesticides).
Bottom line: the toxin load in the broodnest can greatly affect a colony in many ways, generally (but not necessarily always) negatively. The greater the total toxin load with which the colony is forced to deal, the more likely that it will suffer from the combined ill effects.
Industry's Arguments
In order to present an objective review of pesticide issues, we should also hear Industry's side of the argument. The industry-funded think tank OPERA [30] takes the position that:
Although, based on the facts outlined above, there does not appear to be any strong evidence that sublethal effects of pesticides play a key role as causative factors behind bee colony mortality (which is likewise supported by the fact that in several monitoring projects no correlation has been found between colony losses and pesticide exposure), sublethal effects are certainly a point where more fundamental research is needed to obtain a clearer picture of the nature of the issue.
The above statements are factually correct in that there is to date no compelling evidence that pesticides are at the root of the elevated rates of colony mortality seen in recent years, and that more fundamental research is clearly needed. But a long history of practical experience by beekeepers with the sublethal (as well as lethal) effects of pesticides leaves no doubt that pesticides certainly have the potential to cause colony health issues.
But Don't We Already Know That It's The Neonicotinoids?
The media have already tried and convicted the neonicotinoids as the cause of all bee problems, and it's currently fashionable to celebrate the restrictions recently imposed on them by the European Union. But it is rational? No one has ever shown convincing evidence that neonics are linked to colony collapse; conversely, there is abundant experimental and on-the-ground evidence that the residues from seed-treated plants do not appear to cause observable harm to colonies [31].
Planting dust, soil drenches, or foliar applications are a different story, but these are generally drift or misapplication issues, hitting individual apiaries, not the bee population as a whole. Our regulators are well aware of these issues, and working to fix the problems.
Regarding the completely unacceptable bee kills due to the dust from corn seeding, of interest is a recent paper by Drs. Chris Cutler and Cynthia Scott-Dupree [32]--environmental toxicologists from Canada's Dalhousie University--who analyzed the 110 pesticide incident reports received by Canada's PMRA since 2007. Ranking the reports by the degree of severity of the bee kill, they found that there were over five times as many "major incidents" due to non-neonicotinoid products (including carbofuran, chlorpyrifos, coumaphos, diazinon, dimethoate, fluvalinate, formic acid, permethrin, and phosmet) as there were due to neonics, yet that these incidents are largely ignored by the press and beekeepers, who for some reason single-mindedly focus upon the neonics.
Hey, I'm as concerned about pollinators and pesticides as anyone. A recent review by Goulson [33] points out the excessive use of neonics (actually all pesticides are greatly overused), and details the many environmental questions about this class of chemicals. But here's the thing--I can read studies all day long, but what I prefer to seek out are actual on-the-ground, real-life observations. Let me share one with you:
An "Acid Test" Of Neonic Seed Treatment
Activists are calling for a ban on clothianidin--the most common neonicotinoid seed treatment. Although honey bees appear to do just fine on seed-treated canola, their species has an advantage over solitary bees and other pollinators, due to their foraging on multiple plant species over a wide area, their social structure, and their processing of the pollen by nurse bees. So honey bees may not be the best indicator of neonic toxicity.
On the other hand, solitary bee species may be a better indicator as to whether neonic residues cause subtle adverse effects. Many solitary bees are "monovoltine," meaning that they only raise a single generation per year. Because of this, a negative effect on any single female bee could prevent the production of the next generation. It occurred to me that the Alfalfa Leafcutter Bee (Megachile rotundata), which is used to pollinate clothianidin-treated canola (Fig. 6), would provide an excellent "acid test" of clothianidin for several reasons:
Clothianidin has been shown to be highly toxic to leafcutter bees by topical application [34]. Since neonics are typically an order of magnitude more toxic by oral exposure [35], it is reasonable to expect that the leafcutter bee would be even more susceptible to residues consumed in food.
Leafcutter bees do all their foraging within a few hundred feet of the nest [36], so those placed in the middle of a canola field would forage solely upon treated canola.
Each individual female alone forages and provisions her nest, feeding upon the contaminated pollen and nectar as her sole protein and energy sources. If the insecticide negatively affected her behavior, navigational ability, health, or longevity she would be unable to reproduce effectively.
The male bees use canola nectar as their sole energy source, and if the insecticide residues interfered with their behavior or longevity, the female bees might not get properly mated.
The larvae consume a diet consisting solely of unprocessed contaminated pollen and nectar (rather than royal jelly), and thus every item in their diet would contain verified concentrations of clothianidin (approximately 1.7 ppb in the pollen; 0.8 ppb in the nectar [37]). Note: as with honey bees, neonicotinoids are virtually nontoxic to the larvae of the leafcutter bee [38].
The female constructs her nest by cutting (with her mouthparts) leaves from the treated canola plants, which contain even higher residues of clothianidin than the pollen, thus exposing her to even more of the chemical. The larva then develops surrounded by these contaminated leaves, and the pupa overwinters in them.
Figure 6. Tents covering Alfalfa Leafcutter bee nest boxes in a canola field.
In short, the leafcutter bees would constitute the most severe test case for clothianidin exposure from a seed-treated crop. So I phoned a commercial supplier of leafcutter bees in Ontario (who declined to be named) and asked him whether he had any problems with his bees reproducing or overwintering after being set in clothianidin seed-treated canola. He said that he had been rearing them on such fields for many years and did not observe any problem. I put a good deal of faith into such unbiased field experience by a commercial bee man. You can draw your own conclusions.
So Which Pesticides Are Actually To Blame?
It's pretty easy to diagnose an acute bee kill, what with piles of twitching bees in front of the hives (see "Signs and symptoms of bee poisoning" at [39]), and in many cases the responsible pesticide can be identified. To sidetrack briefly, remember when I mentioned a few articles back that the residues in Jim Doan's bee kills did not indicate that the bees contained lethal doses of the chemicals? This made me strongly suspect that we can't apply the LD50 data (in nanograms per bee) to the values obtained from actual field samples of dead bees. The recent report from Canada [40] confirms this. The highest residue level of clothianidin (from corn planting dust) found in any sample of dead bees from the entrances of a hive was 24 ppb, which works out to about a tenth of the theoretical amount necessary to kill a bee . This finding could be due to the metabolic degradation of the insecticide, but it certainly suggest that the LD50 value should be adjusted lower for samples of dead bees! I am greatly heartened that Canada is moving forward in addressing this issue of bee kills from corn planting dust [41].
Overt bee kills aside, more insidious are the residual effects due to contaminated dust, pollen, or nectar that foragers bring back into the broodnest. I'm told by beekeepers with far more experience with pesticides than I, that after exposure to certain pesticides, colony growth and production come to a standstill, sometimes for months, until the colony clears itself of residues and perhaps eventually recovers (or not). The problem is that few beekeepers (if any) can look inside a hive and diagnose which pesticide (or combination thereof) is causing the problem. He may notice spotty brood, poor buildup, winter dwindling, or queenlessness, but it is very hard to isolate the effect any particular pesticide residue, especially in today's stew of residues in combs. But that doesn't mean that we are completely blind...
The Evidence
Due to the rapid turnover of bees in a hive (other than the queen or "winter bees"), if a pesticide were indeed exerting a long-term effect upon colony health, then there would by necessity need to be residues of that pesticide or its degradation products persisting in the combs. With today's testing equipment, we can detect residues to the parts per billion level, and have quite a large database of residue analyses of beebread samples, which we can perhaps use to either finger or exonerate certain pesticides suspected of being involved in colony health issues.
In a court of law, all evidence would be laid out before the court to determine whether it was substantial enough to make a case against a particular suspect. We can do something similar by reviewing two large publicly-available datasets of actual pesticide analyses of beebread from across the country--one by the Penn State team , the other by the USDA (Tables 1 and 2). I've condensed their data to only those pesticide detects that were found in at least 10% (Penn State) or 5% (USDA) of the samples, following this reasoning:
If a pesticide isn't present in at least 10% of samples, then it isn't likely to be the cause of widespread problems.
I've also color-coded the results as to the type of pesticide, and included the median detection level (to help us to determine whether that dose would be expected to cause colony health problems, or whether it would be insignificant).
Pesticide
Present in percent of samples*
Median detection if positive for target (ppb)
Type of pesticide
Fluvalinate
88.3
40.2
Beekeeper-applied miticide
Coumaphos
75.1
13.1
Beekeeper-applied miticide
Chlorpyrifos
43.7
4.4
Insecticide
Chlorothalonil
52.9
35
Fungicide
Pendimethalin
45.7
13.4
Herbicide
Endosulfan I
28
4.2
Insecticide
Endosulfan sulfate
26.3
2.2
Insecticide
DMPF (amitraz)
31.2
75
Beekeeper-applied miticide
Atrazine
20.3
8.9
Herbicide
Endosulfan II
20
3.8
Insecticide
Fenpropathrin
18
7
Insecticide
Azoxystrobin
15.1
10.2
Fungicide
Metolachlor
14.9
8.1
Herbicide
THPI (Captan)
14.2
227
Fungicide
Captan
12.9
103
Fungicide
Esfenvalerate
11.7
3.3
Insecticide
Carbaryl
10.9
36.7
Insecticide
Cyhalothrin
10.9
1.7
Insecticide
Table 1. The 2010 survey by the Penn State team [42], based upon (depending upon the pesticide) either 350 or 247 samples. This study (plus numerous others worldwide) clearly point out that the predominant pesticide residues in brood combs are typically those from the beekeeper-applied miticides (yellow).
Table 2. This 2012 survey by the USDA [43] echoes the previous findings--the only pesticides found in at least 10% of the samples were from either beekeeper-applied miticides or chlorpyrifos. The 99 analyzed samples came from Alabama, California, Colorado, Florida, Idaho, Indiana, New York, South Dakota, Tennessee, Texas, and Wisconsin.
Keep in mind that the above surveys screen only for 174 chosen pesticides--compare this number to the roughly 1000 pesticide active ingredients and adjuvants registered for use in California. I've discussed the composition of this list with USDA's Roger Simonds, who runs the tests. It is prohibitively costly to test for every possible pesticide, so one must arbitrarily draw up a limited list of the chemicals of most concern. All are aware that this is a difficult task, since we don't even know which toxins with which we should be most concerned!
Note that in both surveys, the most common insecticide present was chlorpyrifos- an "old school" (introduced in 1965) organophosphate neurotoxin classified as being "highly toxic" to bees, and marketed as Dursban and Lorsban. Chlorpyrifos was previously widely used by homeowners and residential pest control companies. EPA has since restricted its use due to its toxicity to wildlife and aquatic organisms, and possible links to human health issues [44]--some of the reasons that EPA favors the neonicotinoids as "reduced risk" products.
Oh Boy, Let's Do Some Math!
But just because a pesticide is present, doesn't necessarily mean that it is causing measureable harm. A nurse bee may consume about 10 mg of beebread per day [45], so if she consumed that amount of pollen contaminated with chlorpyrifos at 6.5 ppb, then she would have been dosed with 0.065 ng (1 nanogram = 1 billionth of a gram) of the chemical. The question then is, how much chlorpyrifos does it take to actually harm a bee?
One commonly cited figure is that the LD50 for chlorpyrifos given orally is 360 ng/bee. Compare those figures (360 ng for toxicity vs. 0.065 in the daily diet)! Even though chlorpyrifos is a disturbingly common comb contaminant, it is unlikely that the median detected concentration (alone) would be causing colony health problems (not to say that higher doses don't hurt colonies).
But, you say, some of the neonics are even more toxic than chlorpyrifos. How about the mean 31 ppb found by the USDA in the few samples positive for imidacloprid? The typical nurse bee would consume 0.31 ng, compared to the oral LD50 of about 4-40 ng, so she'd be eating a tenth to a hundredth of the lethal dose. This would be cause for concern, tempered by the fact that a bee can easily metabolize that amount of imidacloprid a day [46]. Such consumption could legitimately be suspected of causing sublethal effects. However, keep in mind that that 31 ppb was an average, which was strongly skewed by a few samples with very high concentrations (which I'd fully expect to cause colony health problems). Plus this is not simply a matter of the average amount of contamination; one must also look at the percentage of positive detects. The Penn State team [47] puts it well:
Our residue results based on 1120 samples which include Mullin et al. (2010) and subsequently more than 230 additional samples do not support sufficient amounts and frequency of imidacloprid in pollen to broadly impact bees.
OK, so how about the varoacides fluvalinate at 40 ppb or the amitraz degradate DMPF at 100 ppb? Surprisingly, I can't find an oral LD50 for fluvalinate, so the contact toxicity figure (200 ng/bee) will need to suffice. Those residues work out to about 1/500th expected toxicity.
Amitraz scored a bit better, with the nurse bees consuming about 0.01 ng--far below the lethal dose. But a recent study found that an oral dose of 0.2 ng of amitraz causes more than a doubling of the heart rate of a bee [48]--that's at 1/20th of the average detect! The authors dryly state:
The above responses clearly show that the heart of the honeybee is extremely vulnerable to amitraz, which is nevertheless still used inside beehives, ostensibly to "protect" the honeybees against their main parasite, Varroa destructor.
How vulnerable? Frazier [49] observed that "Dead and dying bees collected around colonies in association with corn had only residues of 2,4-DMPF at 5,160 ppb." Looks like perhaps the beekeeper inadvertently killed his own bees with an off-label mite treatment that may have overworked their little hearts!
And if those miticide and insecticide residue weren't enough alone, some of the toxicity of these chemicals is additive or synergistic. The Penn State team again says it well:
[The] pyrethroids... were found in 79.4% of samples at 36-times higher amounts than the neonicotinoids, on average... The mean neonicotinoid residue was 37 ppb (scoring non-detects as 0 ppb), of which only 6.7 ppb was imidacloprid. Pyrethroids, by comparison, were present at a mean residue of 106 ppb and a frequency of 80.3% in pollen samples... Indeed, if a relative hazard to honey bees is calculated as the product of mean residue times frequency detected divided by the LD50, the hazard due to pyrethroid residues is three-times greater than that of neonicotinoids detected in pollen samples [emphasis mine].
The pyrethroids are popular because they are relatively nontoxic to humans. But they can sure kill honey bees. More so, they can cause sublethal effects, such as irreversible inhibition of olfactory learning ability [50].
Hey, we're only getting rolling! Mussen [51] pointed out a decade ago that fungicides could kill larvae; recent research from the Tucson lab [52] and elsewhere confirm that fungicide residues can mess up the colony (we sometimes observe this in almonds). Of note is that colonies treated with some fungicides were unsuccessful at requeening themselves! And recent research by Zhu [53] found that the relative toxicity of larvae to the commonly-detected fungicide chlorothalanil was almost 40 times higher than that of chlorpyrifos. Fungicides are frequently found at high concentrations in beebread.
I cannot help from returning to the refrain that instead of limiting our concern to any single pesticide, that we should be looking at the total toxin load that the colony is forced to deal with.
And How About The "Inerts"?
The pesticide detection analyses above do not look at the "inert" adjuvants in the pesticide "formulation." These chemicals not only help to disperse the pesticide over the waxy leaf surface, but also aid in its penetration through the insect cuticle, thus making the pesticide relatively more toxic to the bee!
Mullin and Ciarlo [54, 55] found that:
Formulations usually contain inerts at higher amounts than active ingredients, and these penetrating enhancers, surfactants and adjuvants can be more toxic on non-targets than the active ingredients. For example, we found that the miticide formulation Taktic®️ was four time more orally toxic to adult honey bees than the respective active ingredient amitraz. Impacts of 'inerts' in pollen and nectar alone or in combination with coincident pesticide residues on honey bee survival and behavior are unknown.
The researchers also found that:
Learning was [rapidly] impaired after ingestion of 20 ug of any of the four tested organosilicone adjuvants, indicating harmful effects on honey bees caused by agrochemicals previously believed to be innocuous.
One of the common adjuvants is a solvent NMP, described by BASF [56]:
NMP can be used as a solvent or co-solvent for the formulation of insecticides, fungicides, herbicides, seed treatment products and bioregulators where highly polar compounds are required. NMP is given preference over other highly polar solvents because it is exempt from the requirement of a tolerance when used as a solvent or co-solvent in pesticide formulations applied to growing crops, and it possesses a favorable toxicological and environmental profile.
The key words above are that these toxic solvents are "exempt from tolerance" [57], so they are sprayed all over crops along with the active ingredients of pesticides (including imidacloprid). Yet Zhu [58] recently reported that NMP can rapidly kill bee larvae. The authors conclude that:
Our study suggests that fungicide, the inert ingredient and pesticide interaction should be of high concern to honey bee larvae and overall colony health. None of these factors can be neglected in the pesticide risk assessment for honey bees.
Choosing To Ignore The Obvious
There is no doubt that neonics have the potential to harm bees, but the question is, do they really cause as much problem in the real world as we've been led to believe? This is not a matter of convincing the masses; this is an investigation of fact and evidence. For a pesticide to cause harm to a colony of bees, two necessary elements must occur:
The bees must be exposed to the pesticide. Evidence for this is best determined by chemical analysis of the pollen in the combs, since residues in the bodies of dead bees may be degraded, and because water-soluble insecticides such as the neonics are not absorbed into the wax (residues in the wax do document the history of exposure to lipophilic pesticides).
The pesticide must be present at a concentration above a trivial level.
When we take the time to determine which pesticides bees are actually found in the combs of hives, neonicotinoids are seldom present, or if detected are often at biologically irrelevant concentrations. Imidacloprid was detected in fewer than 3% of Mullin's 350 samples, and clothianidin not at all! Similarly, there were zero detects for clothianidin in the 99 USDA samples; imidacloprid was only present in 9%. Likewise, a number of European studies have shown similar results (reviewed in [59]).
In a recent study, the Fraziers [60] looked at hives placed in cotton, corn, alfalfa, apples, pumpkins, almonds, melons, blueberries, or wild flowers, and identified the residues in collected pollen, in returning foragers, and in dead or dying bees near the hives. Again, the only neonic noted was thiamethoxam in alfalfa (in which dying bees contained residues of ten different pesticides). However, there were alarmingly high detects of fungicides, the insecticide acephate, and the metabolite of the beekeeper-applied miticide amitraz.
The latest data comes from Dr. Jeff Pettis [61], whose group determined the pesticides in bee-collected pollen from six crops: apple, blueberry, cranberry, cucumber, pumpkin, and watermelon. Of the 35 pesticides detected, beekeeper-applied miticides and ag fungicides predominated (sometimes at alarming levels), followed by common organophosphate, pyrethroid, and cyclodiene insecticides (again sometimes at alarming levels). In the 17 samples tested, residues of neonics were only found in the samples from the apple orchards, and only one was found at a biologically-relevant concentration.
So my question is why the heck are so many activists pursuing the single-minded focus upon the neonics, when the clear evidence is that neonics are not commonly found in bee-collected pollen, and if present, are generally at levels that do not appear to negatively affect colony health [62]?
There is a lot more to pesticide issues than the neonics alone, and by focusing our attention solely upon them, we ignore the often far more serious effects of other pesticides.
Blinded By Bias
During the intense focus upon neonicotinoids the past few years, we've learned that exposure of bees to these insecticides can result in all sorts of sublethal effects. Unfortunately, many researchers appear to be wearing blinders as to the effects of other pesticides. The resulting narrowness of these studies skews our perspective--if we only look for effects from the neonics, we don't know how to rank the biological relevance of those effects relative to the effects of all the other toxins to which bees are exposed, generally to greater extent.
A practical complaint to researchers: if you are going to look for sublethal effects of neonics, please include positive controls of some other pesticides, so that we can learn whether the neonics are better or worse than the alternatives!
I commend one group that recently decided to take a look at the effects of a common herbicide upon the development of bee larvae [63]. The results of this straightforward and meticulous study are an eye opener!
The researchers found that exposing bee larvae to even infinitesimal amounts of the herbicide paraquat prevented them from fully developing their critical oenocyte cells (see box).
Oenocyte cells are not only involved in the production of lipids and lipoproteins, but they also appear to play a role in the constitution of external cuticle in both larvae and adults. In addition, they are involved in intermediary metabolism and synthesize hydrocarbons to waterproof cuticle or to make beeswax. Furthermore, oenocytes secrete hormones, especially those involved in larval and adult development. They are also described as the major cells expressing cytochrome P450 reductase, which is involved in detoxification of toxins [information paraphrased from the cited paper].
Exposure to even a part per trillion of paraquat suppressed the development of these extremely important cells. The authors conclude:
This study is the first which reports an effect of a pesticide at the very low concentration of 1 ng/kg, a concentration below the detection limits of the most efficient analytic methods. It shows that chemicals, including pesticides, are likely to have a potential impact at such exposure levels.
Who woulda thunk? Paraquat isn't included in the standard screening for pesticide residues, so we don't even know how prevalent it is in hives! The above findings should make it clear that we need to go back to the beginning if we are to understand the sublethal effects of pesticides (and adjuvants), even at perhaps undetectable levels.
We do know that here were 812,000 lbs of paraquat applied in California in 2010, as opposed to only 266,000 lbs of imidacloprid. Paraquat shows strong adverse effects upon bee larvae at a part per trillion, as compared to imidacloprid, which is so minimally toxic to bee larvae that no one has even been able to determine an LD50! So the amount of paraquat applied has far greater potential to cause problems to bees in agricultural areas (Fig. 7).
Figure 7. The herbicide paraquat appears to be harmful to bee larvae at levels as low as 1 part per trillion. Note the wide variety of crops, and the extensive areas to which it is applied.
So here we have clear scientific data from a well-designed laboratory experiment that a commonly-applied pesticide has the ability to cause immune suppression and other adverse effects in developing bees, yet these results have been virtually ignored by beekeepers and environmental groups. I just don't understand it!
No More Safe Home To Return To
Out of their protective hive, honey bees live in a hostile world, full of predators, deadly weather, and toxic agents (both natural and manmade). But the bees of old could generally return to a "safe" home, in which the transmission of natural toxins was largely minimized by the behavior of foragers, and by the processes of the conversion of nectar to honey, and of pollen into jelly (via the digestion of beebread by nurse bees). Both of these processes help to prevent the transmission of toxins from the foragers to the queen and the brood.
With the advent manmade pesticides, bees may no longer have that "safe" home to return to. Beebread and the wax combs nowadays are often contaminated with any number of pesticides (in addition to natural plant toxins and industrial pollutants). But this is not a "new" problem:
A Historical Artifact
Even before we had the ability to detect pesticide residues in combs to the parts per billion level, pesticide analyses often found easily-detectable levels of insecticides in bee hives. As a frame of reference, I sought out a historical artifact--the residues in the beeswax that had been rendered by beekeepers and reprocessed into a sheet of "clean" foundation. I was lucky enough to find that such a sample had recently been analyzed by the Tucson Bee Lab. Dr. Diana Sammataro forwarded me the results of the analysis of an undated "very old" piece of wax foundation from the Northeast (Table 3).
THIS IS THE TABLE !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!
Pesticides in an old piece of beeswax foundation.
Positive residue detect
ppb
Pendimethalin
13.1
Endrin
156
Dieldrin
160
Trifluralin
3.6
DDT p,p'
32.7
Heptachlor
35.1
Malathion
4.3
Chlorpyrifos
4.6
Dicofol
6.8
PCB's
8190
Chlorothalonil
84.6
Table 3. We can narrow down the foundation's date of manufacture by the residues present. Pendimethalin was first registered in 1972 (the same year that DDT was banned), and since there were no residues of fluvalinate, the foundation was clearly produced prior to the arrival of varroa around 1990. Thanks to Dr. Diana Sammataro and the Tucson Bee Lab.
Clearly, pesticide-contaminated combs are hardly a new phenomenon. In the above example, the beeswax batch used to produce the foundation came not from a single hive, but rather from the combined wax from many hives, likely from many beekeepers, and thus would represent an average sample of the degree of contamination somewhere in that 1972-1990 time frame. And that doesn't take into account whether the raw wax came mainly from cappings (which would have been minimally contaminated), or whether it went through the common practice of being filtered through activated carbon. But any colony started on such foundation purchased from a beekeeping supply house would clearly have had to deal with at least the residues of these lipophilic toxins from the get go!
An aside: perhaps of interest is something that I noticed years ago when I switched from dipping my own wax queen cell cups to using plastic cups. My "take" rate became better and more consistent. Was that because the beeswax at the time was contaminated with residues?
The Beekeeper Contribution To Shifting The Tip Point
One thing that is "new" is that since the arrival of varroa, we've upped the ante--all commercial beeswax is now contaminated with residues of beekeeper-applied synthetic miticides. The three most prevalent synthetic chemicals found in combs today all get there by being applied by beekeepers for mite control.
Practical note: And although there is no reason to be concerned about the tainting of honey by the legal use of these miticides, the beekeeper/applicator should be aware that both amitraz and tau-fluvalinate make California's list of "chemicals known to the State to cause reproductive toxicity," and coumaphos is of concern because it is a "cholinesterase-inhibiting pesticide." No varroacide is harmless to bees [64]--but the benefits of mite control generally (but not always) outweigh the adverse effects due to the miticide residues.
We beekeepers have clearly shifted the baseline for pesticide contamination of combs, which increases the total toxic load even before the contribution by agricultural pesticides.
Stop Right There!
Although it is a very attractive hypothesis to blame our problems on miticide or pesticide residues, let's do a reality check. On good forage in good weather, plenty of beekeepers see their colonies thrive even on old, dark, seriously-contaminated combs; but under stressful conditions those same residues might contribute to poor colony performance or even mortality.
No study has yet found support for the hypothesis that miticide residues are the cause of our current bee problems (although one would have every reason to suspect that they may contribute). In fact, vanEngelsdorp [65] found that surprisingly, higher levels of coumaphos residues negatively correlated with colony survival. How could this be? One possible explanation is that those beekeepers who used it experienced better mite control. But there is also another intriguing possibility--hormetic effects.
Undetectable Levels And Hormesis
Is your head spinning yet? I've presented evidence that undetectable levels of some pesticides could harm bees, that "inert" adjuvants can do the same, and that combs are often chock full of all sorts of pesticide and varroacides residues. Criminy, it's a wonder that bees survive at all! Or is it?
Bees have long been exposed to all sorts of natural, and recently, manmade toxins, and survived. Toxicity is a complicated subject. The only thing that separates a medicine from a poison is the dose. In general, if a pesticide has been tested upon adult and larval bees and found to have no observable adverse effects at a certain concentration, we would not expect to see adverse effects at lower concentrations. However, there are exceptions to this general rule--toxicity may vary up or down depending upon the dose [66]!
I've previously mentioned the term hormesis [67]-- the paradoxical effect of toxins at low concentrations. The paradox is that although most chemicals are toxic at high concentrations, the majority are likely beneficial at low concentrations. For those interested in this fascinating phenomenon, I suggest Dr. Chris Cutler's excellent and thought-provoking review [68]. It is not only possible, but actually probable that lose doses of pesticides may exert a beneficial effect upon a colony! (Don't be ridiculous--I'm not suggesting that bees are better off for the presence of pesticides!).
Wrap Up
Toxins, whether natural or manmade, are clearly a potential issue in colony health. To what degree pesticides contribute to colony morbidity or mortality is dependent upon exposure, the dose, and a host of associated factors. Beekeepers have long noticed that their bees often do better if allowed to forage on pesticide-free land. But many beekeepers today tell me that their bees do just fine in the middle of intense agricultural areas--so this is not a black or white situation.
In recent years beekeepers themselves have greatly added to the degree of contamination of their combs. Introductions of novel pesticides and adjuvants keep changing the picture. And now we're finding that pesticides that we formerly assumed were harmless to bees (fungicides and herbicides) may actually be quite toxic to larvae! Then there is the scary finding that undetectable levels of some pesticides might cause health issues, countered by the fascinating subject of hormesis.
I certainly do not profess to understand all this, but I have come to the following conclusions:
That bees have had to deal with toxins for a long time,
That pesticides will be with us for the foreseeable future,
That varroacides have likely added to the problem,
That pesticides can cause lethal and long-term sublethal effects in the hive, but
That many beekeepers in agricultural areas no longer consider pesticides to be a serious issue, whereas,
That colonies may go downhill after being exposed to some agricultural chemicals, or combinations thereof,
That toxicology in the hive is complex, and that there are few simple answers,
That it is unlikely that any single pesticide is to blame for our current colony health issues,
That we still have a lot to learn!
Next month I will look at the distribution of both managed colonies and of pesticide applications in the United States, and their relationship to bee health problems.
Acknowledgements
As always, I could not research these articles without the assistance of my longtime collaborator Peter Loring Borst, to whom I am greatly indebted. I also wish to thank Drs. Jim and Maryann Frazier, Chris Mullin, David Fischer, Eric Mussen, Thomas Steeger, and Roger Simonds for their generosity in taking the time to discuss pesticide issues with me.
References
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"Certainly with both pesticide-related and [Disappearing Disease]-caused bee losses, the adult population of a colony may be reduced rapidly to a "handful" of bees or, in some cases, the entire population may be lost.
"However, in the case of pesticide poisoning, there is usually evidence of pesticide application...the worker bees either die in the field or in or near the hive depending on the type of pesticide. When the field force is killed and they "disappear," many dead or dying bees may be seen on the ground in the field or on the ground between the treated field and the apiary...If the foraging bees bring poison into the hive, then the nurse bees either die in the hive or at the entrance so one can see many crawling and tumbling adults and large amounts of neglected brood. Exposure to pesticides over an extended period results in very weak colonies, and some die out.
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[53] Zhu, W., D. Schmehl & J. Frazier (2011) Measuring and predicting honey bee larval survival after chronic pesticide exposure http://www.extension.org/pages/58650/proceedings-of-the-american-bee-research-conference-2011#.UhDTZX-aucw
[54] Mullin, C.A., J. Chen, W. Zhu, M.T. Frazier & J.L. Frazier - The formulation makes the bee poison. ABRC 2013
[55] Ciarlo TJ, Mullin CA, Frazier JL, Schmehl DR (2012) Learning impairment in honey bees caused by agricultural spray adjuvants. PLoS ONE 7(7): e40848. doi:10.1371/journal.pone.0040848
[56] (Broken Link!) http://www2.basf.us/diols/bcdiolsnmp.html
[57] http://www.epa.gov/opprd001/inerts/methyl.pdf
[58] Zhu, et al (2011) op. cit.
[59] Blacquiere, T, et al (2012) Neonicotinoids in bees: a review on concentrations, side-effects and risk assessment. Ecotoxicology 21(4): 973-992. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3338325/
[60] Frazier, M.T., S. Ashcraft, W. Zhu & J. Frazier - Assessing the reduction of field populations in honey bee colonies pollinating nine different crops http://www.extension.org/pages/58650/proceedings-of-the-american-bee-research-conference-2011#.UhDTZX-aucw
[61] Pettis, et al (2013) op. cit.
[62] A recent study confirm that the neonic residues in corn, soy, and canola pollen are at very low concentrations. Henderson, C.B. a, J.J. Bromenshenka, D.L. Fischerb. Clothianidin exposure levels from bee-collected pollen and nectar in seed-treated corn and canola plantings. ABRC 2013 http://bees.msu.edu/wp-content/uploads/2013/01/ABRC-abstracts-2013.pdf
[63] Cousin M, Silva-Zacarin E, Kretzschmar A, El Maataoui M, Brunet J-L, et al. (2013) Size changes in honey bee larvae oenocytes induced by exposure to paraquat at very low concentrations. PLoS ONE 8(5): e65693. doi:10.1371/journal.pone.0065693 http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0065693
[64] Boncristiani, H., et. al. (2011) Direct effect of acaricides on pathogen loads and gene expression levels of honey bee Apis mellifera. Journal of Insect Physiology. 58:613-620.
[65] vanEngelsdorp, D, et al () Weighing risk factors associated with bee colony collapse disorder by classification and regression tree analysis. J. Econ. Entomol. 103(5): 1517-1523. (Broken Link!) http://www.eclecticparrot.com.au/research_papers/VanEngelsdorp%202010%20Weighing%20risk%20factors%20in%20Bee%20CCD.pdf
[66] Cutler GC, Ramanaidu K, Astatkie T, and Isman MB. (2009) Green peach aphid, Myzus persicae (Hemiptera: Aphididae), reproduction during exposure to sublethal concentrations of imidacloprid and azadirachtin. Pest Manag Sci 65:205-209
[67] https://scientificbeekeeping.com/sick-bees-part-18f2-colony-collapse-revisited-plant-allelochemicals/
[68] Cutler, GC (2013) Insects, insecticides and hormesis: evidence and considerations for study. Dose-Response 11:154-177 (Broken Link!) http://dose-response.metapress.com/app/home/contribution.asp?referrer=parent&backto=issue,2,11;journal,3,34;linkingpublicationresults,1:119866,1
Category: Colony Health - Diseases, Viruses, CCD
Tags: collapse, colony, pesticides, sick bees | colony Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/colony/ |
Sick Bees - Part 18F7: Colony Collapse Revisited - Pesticide Exposure
First published in: American Bee Journal, October and November 2013
Pesticide Exposure
Oh No, Not Pesticides Again!
Reality Checks
The Two Worlds of Beekeeping
Pesticides and Bee-pocalypse
A Comparison To Some "Control Groups"
The Four Horsemen And The Tip Point
Could Pesticides Cause Colony Mortality And CCD?
Short Memories
The Heart Of The Hive - The Nursery
Industry's Arguments
But Don't We Already Know That It's The Neonicotinoids?
An "Acid Test" Of Neonic Seed Treatment
So Which Pesticides Are Actually To Blame?
The Evidence
Oh Boy, Let's Do Some Math!
And How About The "Inerts"?
Choosing To Ignore The Obvious
Blinded By Bias
No More Safe Home To Return To
A Historical Artifact
The Beekeeper Contribution To Shifting The Tip Point
Stop Right There!
Undetectable Levels And Hormesis
Wrap Up
Acknowledgements
References
Sick Bees Part 18f7: Colony Collapse Revisited
Pesticide Exposure
Randy Oliver
ScientificBeekeeping.com
Originally published in ABJ Oct and Nov 2013
Oh No, Not Pesticides Again!
Some readers may wonder why I am spending so much time on the issue of pesticides, since to many (if not most) beekeepers, pesticides are a non issue. In answer, the main reason is that the public (and our lawmakers) are being hammered by the twin messages that the honey bee is on the verge of extinction, and that the reason is pesticides. In my writings, I'm attempting to address the validity of both of those claims. Let's start with the first.
Reality Checks
Honey bees have clearly (and deservedly) become one of today's most charismatic environmental poster children, and as such are a useful bioindicator that our human activities are having a negative impact upon pollinators, and wildlife in general.
But I also feel that we take care to not overstate or exaggerate our case. One of my greatest concerns is that beekeepers are allowing the media to scare the public with all the hue and cry of an impending bee-pocalypse (and that it is due to a certain type of pesticide). Our complicity in this message (as we enjoy the luxury of basking in the warmth of all the public support) may backfire on us one of these days--putting us into the position of the little boy who cried wolf. Some in the media are starting to notice that the facts don't support the claim that bees are disappearing (Fig. 1).
Figure 1. It's true that it's more difficult to keep bees healthy these days, but it doesn't look like bee-pocalypse is imminent (as evidenced by this recently-published chart). Whenever honey and pollination prices are high enough to make beekeeping profitable, resourceful beekeepers somehow manage to recover their colony losses [[i]]. Chart courtesy Shawn Regan [[ii]].
[i] Rucker, RR and WN Thurman (2012) Colony collapse disorder: the market response to bee disease. http://perc.org/sites/default/files/ps50.pdf
[ii] (Broken Link) http://perc.org/articles/everyone-calm-down-there-no-bee-pocalypse
In the rest of the world, the number of managed hives has actually been increasing [3]. And as far as claims that pesticides are driving bees to extinction, Hannah Nordhaus, the author of the excellent book The Beekeeper's Lament writes:
Reflexively blaming pesticides for all of the honey bee's problems may in fact slow the search for solutions. Honey bees have enough to do without having to serve as our exoskeletal canaries in a coalmine. Dying bees have become symbols of environmental sin, of faceless corporations out to ransack nature. Such is the story environmental journalism tells all too often. But it's not always the story that best helps us understand how we live in this world of nearly seven billion hungry people, or how we might square our ecological concerns and commitments with that reality. By engaging in simplistic and sometimes misleading environmental narratives -- by exaggerating the stakes and brushing over the inconvenient facts that stand in the way of foregone conclusions -- we do our field, and our subjects, a disservice [4].
Further reading: for a detailed and sober analysis of the factors that affect managed bee populations, I highly recommend the review by Drs. vanEngelsdorp and Meixner [5].
The reality is that it is not the honey bee that is being driven to extinction--it is instead the commercial beekeeper who is finding that his traditional business model is becoming less profitable due to today's greater degree of colony losses and the decreasing availability of good summer forage.
The question is, to what extent are pesticides involved in those problems?
The Two Worlds Of Beekeeping
There are two very different worlds of beekeeping--small scale (hobbyists, who constitute the vast majority of beekeepers by number) and large scale (commercialized professionals, who manage the vast majority of hives), with a small continuum of sideliners bridging the gap.
Hobby beekeeping is currently enjoying a bubble of resurgence, but in the Big Picture in the U.S., hobbyists manage an insignificant number of hives. And those small-scale beekeepers tend to keep their hives close to home, largely avoiding serious exposure to pesticides. But that's not to say that small-scale beekeepers are immune to pesticide kills; I've heard of several this season, and what with all the spraying for West Nile virus and the citrus psyllid, we can expect more of the same. And since there are far more small-scale beekeepers to put pressure on regulators and legislators, I feel that it is a good idea for them to be informed about pesticide issues.
Large-scale beekeepers, on the other hand, typically run migratory operations--moving their hives to almond pollination, and then to other agricultural areas (it's problematic to keep apiaries of hundreds of hives in the suburbs). The fate of those bees (and their keepers) is largely determined by agricultural land use practices and their degree of exposure to agricultural pesticides.
It is some of those large-scale beekeepers for whom extinction is a valid concern. The reason (as with any other enterprise) is financial--they can only survive so long unless their businesses continue to be profitable [6]. In recent years, they've had two things going for them--sky-high honey prices and elevated pollination fees. But all is not rosy--there are reasons for those prices going up; these days it's simply more costly to produce honey or to provide bees for pollination.
Today's breathtakingly-high high almond rental rates typically don't even cover operating costs--even if most of one's colonies make it through the winter! Today's 30% average winter loss rate is bleeding profitability from many operations. Not only does the beekeeper need to rebuild his numbers after almonds, but to stay in the black he must also make additional income from paid pollinations or a decent honey crop. And that may no longer be as easy as it used to be for various reasons:
Formerly bee-friendly farmland has been turned into agri-deserts devoid of any bee forage.
Honey producers on field crops (such as alfalfa, sunflowers, or cotton) get hammered time and again by pesticide spraying, sometimes watching whole yards of colonies dwindle or go queenless weeks afterwards.
Paid summer pollination contracts (such as for vine crops) may leave colonies in poor shape for the winter, due to the heavy stocking, the lack of nutritious pollen, and the exposure to multiple pesticides.
These days, the sad fact is that many good beekeepers are barely keeping their heads above water. So the beekeeper's lament continues--varroa, high winter mortality, and lack of good forage are driving a number of operations into the red.
Practical application: although the "extinction of the honey bee" makes for a good rallying cry, the real concern is the possible extinction of the migratory beekeeper who supplies necessary pollination services to agriculture. So far, the almond industry has been economically propping up the bee industry, but I'm not sure how long that arrangement will be sustainable.
Pestcides And Bee-Pocalypse
For some beekeepers, "bee-pocalypse" has already occurred. New York beekeeper Jim Doan, whose case I detailed in a previous article [7], sadly gave it up this year. Here is a beekeeper whose apiaries had been in the same locations for many years without noticeable pesticide problems, but who apparently suffered from devastating spray or dust kills this season and last, as evidenced by piles of fresh dead bees in front of his hives in spring.
Residue analysis of those dead bees clearly showed that they had been exposed to several pesticides, but none of the detects were at levels that would be expected to cause such carnage--so we don't even know which pesticides or practices to point the finger at! To my scientific mind, this is very frustrating--that our "system" was not able to identify the cause of Jim's bee kills, to change anything to keep them from recurring, nor compensate an innocent beekeeper for the loss of his livestock and livelihood.
As unlucky as Jim has been, his case is not necessarily the norm. Overall, the issue of environmental toxins is improving. In my own lifetime I've seen us clean up our pollution of the air and water, cease atmospheric testing of nuclear weapons, ban DDT, fluorocarbons, and PCB's, phase out the worst pesticides, and raise the general environmental consciousness. Humans still inflict far too damaging an environmental footprint on Earth, but we are moving in the right direction, and should give ourselves some credit for that!
There is no doubt that pesticides are often involved in bee health issues, but can we blame them for all our problems? That question is best answered by considering the health of those colonies that are not exposed to pesticides:
A Comparison To Some "Control Groups"
There are plenty of beekeepers in non agricultural areas whose apiaries are not exposed to pesticides to any extent. Those hives serve as a "control group," whose health we can compare to those colonies that do have to deal with pesticides.
For instance, in my own operation of about a thousand hives, their only exposure to pesticides is to the fungicides in the almond orchards (from which they don't appear to suffer to any serious extent). I haven't used synthetic miticides in over a decade, rotate my combs, and rarely feed syrup.
Yet, I've experienced CCD firsthand, see more queenlessness, unsuccessful supersedure, and experience somewhat higher winter losses than in the old days (meaning before varroa). I hear the same from many others in the pesticide-free control group. The simple fact is that these days it requires better husbandry to maintain productive colonies. Yet we in the "control group" can hardly blame pesticides to be the cause.
And then there are the stationary "treatment free" beekeepers in the middle of intense agriculture who suffer no higher colony loss rates than the norm, despite their apiaries being surrounded by corn and soy [8]. How the heck do we reconcile their success to the problems that the commercial guys experience in the same areas?
Do they owe their success to keeping fewer hives in a yard? To keeping locally-adapted survivor stock? To their placement within flight range of patches of undisturbed forage? To the fact that they don't move to multiple crops? Or is it because they aren't contaminating their combs with miticides? Believe me, if I knew the answer, I'd tell you!
As (the very successful) beekeeper Dave Mendes observes, colonies just seem to be more "fragile" these days. It's no surprise then that the addition of toxins of any sort can help to tip a colony over. The Ericksons [9] put it this way:
Pesticides and their residues in the hive stress bees as do other factors such as weather extremes, food shortages, pests, predators, and disease. Conversely, stress induced by other factors undoubtedly has a significant impact on the level of damage that a pesticide inflicts on a colony.
Note that the above words were written prior to our colonies having to deal with varroa, the varroa-vectored viruses, Nosema ceranae, our evolving brood diseases, GMO's, neonicotinoids, or Roundup Ready corn.
The Four Horsemen And The Tip Point
Colony growth is a function of the recruitment rate via successful broodrearing vs. the attrition rate of workers due to age, disease, the altruistic departure of sick bees, or the loss of foragers in the field. When recruitment exceeds attrition, colonies grow; when attrition exceeds recruitment, the colony population shrinks. Environmental factors, including toxins, can shift the tip point for colony growth (Fig. 2).
Figure 2. Any colony with a good laying queen has the potential to grow rapidly--the greater the rate of recruitment (successful broodrearing), the steeper the slope of the growth curve. In the real world, such potential growth is often held back by the lack of nutritious pollen, or by the stresses of toxins, chilling, or pathogens (especially the mite-associated viruses, nosema, or EFB). Any of those can strongly shift the tip point, slowing, or even reversing, the rate of colony growth.
In the last decade, something appears to have shifted that tip point--colonies today seem to more readily go into a downhill spiral and queens no longer hold up as well. Could it be due to pesticides?
Could Pesticides Cause Colony Mortality And CCD?
Of course they could! In 2010, after closely observing the progression of experimentally-induced CCD with my collaborator Dr. Eric Mussen, I published the flow chart below (Fig. 3) to detail the interactions and feedback loops involved in the step-by-step collapse of a colony [10]. At the time, I fully intended to further elaborate upon the contribution of toxins, but didn't get around to it until now.
Figure 3. The positive feedback loops that can lead to colony dwindling and/or sudden depopulation. I've since observed this process take place in sick colonies time and again.
In the above chart, I called out toxins (which would include pesticides) as one of the "Four Horsemen of Bee Apocolypse" (the four factors at top left). Below I've indicated in red those points at which toxins may exacerbate the downhill process (Fig. 4).
Figure 4. Note that toxins can exert lethal or sublethal effects (red bubbles) at every step in the process of colony dwindling or collapse. Pesticides may in some cases be the prime cause of colony mortality; more frequently they might be "contributory factors," especially due the prolonged sublethal effects of residues in the beebread or wax.
Please note that in these charts I'm referring to toxins generically, not specifically to manmade pesticides. Such toxins would include natural plant allelochemicals, industrial pollutants, metals such as arsenic or selenium in soil and dust, fungal and bacterial toxins (which may be altered in beebread by the presence of pesticide residues), beekeeper-applied varroacides, HMF in overheated corn syrup, all in addition to any agricultural pesticides. In the words of ecotoxicologist Dr. Helen Thompson, we must pay attention to the total toxin load of the hive, plus any interactions between those chemicals, as well as other contributory factors [11]--a sentiment also echoed by the Fraziers at Penn State [12]. So, back to our original question: Can toxins, including synthetic pesticides, cause colony morbidity or mortality?
Verdict #1: clearly, synthetic pesticides and varroacides may constitute the most serious toxin load for managed bees in agricultural areas, and have the potential kill a colony outright, or to exacerbate positive feedback loops that can result in dwindling, poor overwintering, or collapse.
But does any pesticide specifically cause CCD--"the disappearance of most, if not all, of the adult honey bees in a colony, leaving behind honey and brood but no dead bee bodies" [13] (and no sign of brood diseases or varroa-induced DWV collapse).
Analysis: The most direct way to answer that question is to see whether we can fulfill Koch's third postulate [14]: can we experimentally create the symptoms of CCD by treating a healthy hive with the pesticide in question?
Verdict #2: to the best of my knowledge, no one has yet duplicated the symptoms of CCD by treating a colony with any pesticide (the most obvious difference being that there are generally plenty of dead bees present in the case of pesticide toxicity). This is notably true for the neonicotinoids, for which any number of researchers have attempted to duplicate CCD symptoms by continually feeding colonies neonic-tainted syrup or pollen.
Hold on--drop those stones! I am not saying that pesticides cannot contributeto CCD or colony morbidity or mortality in general--my chart above clearly illustrates that they have the potential to do so. Yet even those beekeepers who manage to completely avoid pesticides may still experience sudden colony depopulations, dwindling, or excessive winter losses due to some combination the Four Horseman (as in the perfect storm detailed at [15]).
I feel that it is a serious error for us to try to link CCD to pesticides. Pesticides have always been an issue to beekeepers, but CCD-like events have historically come and gone (as in Disappearing Disease--read the description at [16]). Pesticides will remain an issue long after the term "CCD" is forgotten.
Bottom line: Despite the fact that the evidence at hand does not support the case that CCD is directly caused by any pesticide, that fact certainly does not mean that we should ignore pesticide issues. If anything, we beekeepers ourselves have helped to make pesticides even more of an issue these days.
Short Memories
There is a popular myth going around that pesticides only started to become an issue to honey bee colony survival in 2007. In fact, the sublethal effects of pesticides were well known to beekeepers and researchers long before then. If we review the older literature [17], we find that it was already well known that contaminated pollen was a more serious issue to colony health than the in-field kill of foragers. We knew that colonies might collect such tainted pollen from miles away, that dusts were worse than sprays, that young bees may be more susceptible than older bees, and that temperature and humidity had a great deal to do with pesticide toxicity. Pesticide issues were actually far worse in the 1960's and '70's than they are today, and have generally improved since then (not to say that some new issues haven't arisen).
On the other hand, the overall contamination of combs with pesticides has increased in recent years due to the direct contribution by we beekeepers ourselves. In virtually any residue analysis of beebread or beeswax these days in any country with varroa, the most prevalent toxins are the beekeeper-applied varroacides [18]-you may wish to refer back to my chart of the "toxicological eras of honey bee evolution [19].
So one question is, To what degree we have shifted the tip point of colony health by contaminating our brood combs with miticides? Let's explore the broodnest...
The Heart Of The Hive - The Nursery
The insidious, long-term effects of total toxin load (including pesticide and varroacide residues) would be from those that made it into the heart of the hive--the critical stored beebread and the wax of the brood combs (Fig. 5). Note: Dr. David Fischer of Bayer brings to my attention that in the case of imidacloprid, the results of his testing indicates that bees in the hive are more affected by residues in the nectar than by those in the pollen.
Figure 5. Long after a pesticide-sprayed field force has been replaced by newly-recruited foragers, the colony may still need to deal with the lingering effects of pesticide residues in the combs, and especially in the all-important stores of beebread. It is here that such persistent residues can affect colony health and buildup for many months after the initial exposure, and exactly where we should focus our attention.
Here's some food for thought: a toxin need not actually kill a single bee to mess up a colony. There are many ways in which sublethal levels of toxins can negatively affect the colony population curve. A few examples would be:
By decreasing the survival rate of larvae (as from residues of varroacides [20, 21], or fungicides [22]) , or by increasing their development time (as effected by various pollutants, plant alleleochemicals, pesticides, or miticides).
By affecting the proper fermentation of beebread (fungicides).
By affecting the sensitive nurse bees that must digest that beebread and produce the critical jelly used to feed the brood, queen, and other workers (natural plant toxins, pollutants, or pesticides).
By affecting the normal behavioral progression of the workers. E.g., if workers initiate foraging prematurely, this greatly reduces their overall longevity, and results in severe depression of colony growth [23] (much more research is crying to be done, but many chemicals would be suspect).
By requiring bees to allocate precious resources toward the detoxification of the poisons (as per my leaky boat analogy [24]).
By increasing the virulence of varroa, nosema, or viruses (any number of pesticides and miticides have been implicated [25, 26])
By affecting normal colony homeostasis, such as thermoregulation of the brood, which is dependent upon the proper assessment of temperature, and the ability to effectively generate heat by the vibration of the wing muscles (neurotoxins would be expected to affect this ability).
By affecting the longevity of the queen, the viability of spermatozoa, or the ability of a colony to successfully supersede (coumaphos notably had this effect)
By affecting the production of, or normal communication via pheromones (which include the recognition of brood and the queen) [27] (essential oils, formic acid, other pesticides?)
By affecting foragers' ability to communicate by dance, to navigate, to learn (a wide range of pesticides [28]), or to react properly to normal stimuli (neonics can clearly do this [29]; but similar effects could be due to any number of other pesticides).
Bottom line: the toxin load in the broodnest can greatly affect a colony in many ways, generally (but not necessarily always) negatively. The greater the total toxin load with which the colony is forced to deal, the more likely that it will suffer from the combined ill effects.
Industry's Arguments
In order to present an objective review of pesticide issues, we should also hear Industry's side of the argument. The industry-funded think tank OPERA [30] takes the position that:
Although, based on the facts outlined above, there does not appear to be any strong evidence that sublethal effects of pesticides play a key role as causative factors behind bee colony mortality (which is likewise supported by the fact that in several monitoring projects no correlation has been found between colony losses and pesticide exposure), sublethal effects are certainly a point where more fundamental research is needed to obtain a clearer picture of the nature of the issue.
The above statements are factually correct in that there is to date no compelling evidence that pesticides are at the root of the elevated rates of colony mortality seen in recent years, and that more fundamental research is clearly needed. But a long history of practical experience by beekeepers with the sublethal (as well as lethal) effects of pesticides leaves no doubt that pesticides certainly have the potential to cause colony health issues.
But Don't We Already Know That It's The Neonicotinoids?
The media have already tried and convicted the neonicotinoids as the cause of all bee problems, and it's currently fashionable to celebrate the restrictions recently imposed on them by the European Union. But it is rational? No one has ever shown convincing evidence that neonics are linked to colony collapse; conversely, there is abundant experimental and on-the-ground evidence that the residues from seed-treated plants do not appear to cause observable harm to colonies [31].
Planting dust, soil drenches, or foliar applications are a different story, but these are generally drift or misapplication issues, hitting individual apiaries, not the bee population as a whole. Our regulators are well aware of these issues, and working to fix the problems.
Regarding the completely unacceptable bee kills due to the dust from corn seeding, of interest is a recent paper by Drs. Chris Cutler and Cynthia Scott-Dupree [32]--environmental toxicologists from Canada's Dalhousie University--who analyzed the 110 pesticide incident reports received by Canada's PMRA since 2007. Ranking the reports by the degree of severity of the bee kill, they found that there were over five times as many "major incidents" due to non-neonicotinoid products (including carbofuran, chlorpyrifos, coumaphos, diazinon, dimethoate, fluvalinate, formic acid, permethrin, and phosmet) as there were due to neonics, yet that these incidents are largely ignored by the press and beekeepers, who for some reason single-mindedly focus upon the neonics.
Hey, I'm as concerned about pollinators and pesticides as anyone. A recent review by Goulson [33] points out the excessive use of neonics (actually all pesticides are greatly overused), and details the many environmental questions about this class of chemicals. But here's the thing--I can read studies all day long, but what I prefer to seek out are actual on-the-ground, real-life observations. Let me share one with you:
An "Acid Test" Of Neonic Seed Treatment
Activists are calling for a ban on clothianidin--the most common neonicotinoid seed treatment. Although honey bees appear to do just fine on seed-treated canola, their species has an advantage over solitary bees and other pollinators, due to their foraging on multiple plant species over a wide area, their social structure, and their processing of the pollen by nurse bees. So honey bees may not be the best indicator of neonic toxicity.
On the other hand, solitary bee species may be a better indicator as to whether neonic residues cause subtle adverse effects. Many solitary bees are "monovoltine," meaning that they only raise a single generation per year. Because of this, a negative effect on any single female bee could prevent the production of the next generation. It occurred to me that the Alfalfa Leafcutter Bee (Megachile rotundata), which is used to pollinate clothianidin-treated canola (Fig. 6), would provide an excellent "acid test" of clothianidin for several reasons:
Clothianidin has been shown to be highly toxic to leafcutter bees by topical application [34]. Since neonics are typically an order of magnitude more toxic by oral exposure [35], it is reasonable to expect that the leafcutter bee would be even more susceptible to residues consumed in food.
Leafcutter bees do all their foraging within a few hundred feet of the nest [36], so those placed in the middle of a canola field would forage solely upon treated canola.
Each individual female alone forages and provisions her nest, feeding upon the contaminated pollen and nectar as her sole protein and energy sources. If the insecticide negatively affected her behavior, navigational ability, health, or longevity she would be unable to reproduce effectively.
The male bees use canola nectar as their sole energy source, and if the insecticide residues interfered with their behavior or longevity, the female bees might not get properly mated.
The larvae consume a diet consisting solely of unprocessed contaminated pollen and nectar (rather than royal jelly), and thus every item in their diet would contain verified concentrations of clothianidin (approximately 1.7 ppb in the pollen; 0.8 ppb in the nectar [37]). Note: as with honey bees, neonicotinoids are virtually nontoxic to the larvae of the leafcutter bee [38].
The female constructs her nest by cutting (with her mouthparts) leaves from the treated canola plants, which contain even higher residues of clothianidin than the pollen, thus exposing her to even more of the chemical. The larva then develops surrounded by these contaminated leaves, and the pupa overwinters in them.
Figure 6. Tents covering Alfalfa Leafcutter bee nest boxes in a canola field.
In short, the leafcutter bees would constitute the most severe test case for clothianidin exposure from a seed-treated crop. So I phoned a commercial supplier of leafcutter bees in Ontario (who declined to be named) and asked him whether he had any problems with his bees reproducing or overwintering after being set in clothianidin seed-treated canola. He said that he had been rearing them on such fields for many years and did not observe any problem. I put a good deal of faith into such unbiased field experience by a commercial bee man. You can draw your own conclusions.
So Which Pesticides Are Actually To Blame?
It's pretty easy to diagnose an acute bee kill, what with piles of twitching bees in front of the hives (see "Signs and symptoms of bee poisoning" at [39]), and in many cases the responsible pesticide can be identified. To sidetrack briefly, remember when I mentioned a few articles back that the residues in Jim Doan's bee kills did not indicate that the bees contained lethal doses of the chemicals? This made me strongly suspect that we can't apply the LD50 data (in nanograms per bee) to the values obtained from actual field samples of dead bees. The recent report from Canada [40] confirms this. The highest residue level of clothianidin (from corn planting dust) found in any sample of dead bees from the entrances of a hive was 24 ppb, which works out to about a tenth of the theoretical amount necessary to kill a bee . This finding could be due to the metabolic degradation of the insecticide, but it certainly suggest that the LD50 value should be adjusted lower for samples of dead bees! I am greatly heartened that Canada is moving forward in addressing this issue of bee kills from corn planting dust [41].
Overt bee kills aside, more insidious are the residual effects due to contaminated dust, pollen, or nectar that foragers bring back into the broodnest. I'm told by beekeepers with far more experience with pesticides than I, that after exposure to certain pesticides, colony growth and production come to a standstill, sometimes for months, until the colony clears itself of residues and perhaps eventually recovers (or not). The problem is that few beekeepers (if any) can look inside a hive and diagnose which pesticide (or combination thereof) is causing the problem. He may notice spotty brood, poor buildup, winter dwindling, or queenlessness, but it is very hard to isolate the effect any particular pesticide residue, especially in today's stew of residues in combs. But that doesn't mean that we are completely blind...
The Evidence
Due to the rapid turnover of bees in a hive (other than the queen or "winter bees"), if a pesticide were indeed exerting a long-term effect upon colony health, then there would by necessity need to be residues of that pesticide or its degradation products persisting in the combs. With today's testing equipment, we can detect residues to the parts per billion level, and have quite a large database of residue analyses of beebread samples, which we can perhaps use to either finger or exonerate certain pesticides suspected of being involved in colony health issues.
In a court of law, all evidence would be laid out before the court to determine whether it was substantial enough to make a case against a particular suspect. We can do something similar by reviewing two large publicly-available datasets of actual pesticide analyses of beebread from across the country--one by the Penn State team , the other by the USDA (Tables 1 and 2). I've condensed their data to only those pesticide detects that were found in at least 10% (Penn State) or 5% (USDA) of the samples, following this reasoning:
If a pesticide isn't present in at least 10% of samples, then it isn't likely to be the cause of widespread problems.
I've also color-coded the results as to the type of pesticide, and included the median detection level (to help us to determine whether that dose would be expected to cause colony health problems, or whether it would be insignificant).
Pesticide
Present in percent of samples*
Median detection if positive for target (ppb)
Type of pesticide
Fluvalinate
88.3
40.2
Beekeeper-applied miticide
Coumaphos
75.1
13.1
Beekeeper-applied miticide
Chlorpyrifos
43.7
4.4
Insecticide
Chlorothalonil
52.9
35
Fungicide
Pendimethalin
45.7
13.4
Herbicide
Endosulfan I
28
4.2
Insecticide
Endosulfan sulfate
26.3
2.2
Insecticide
DMPF (amitraz)
31.2
75
Beekeeper-applied miticide
Atrazine
20.3
8.9
Herbicide
Endosulfan II
20
3.8
Insecticide
Fenpropathrin
18
7
Insecticide
Azoxystrobin
15.1
10.2
Fungicide
Metolachlor
14.9
8.1
Herbicide
THPI (Captan)
14.2
227
Fungicide
Captan
12.9
103
Fungicide
Esfenvalerate
11.7
3.3
Insecticide
Carbaryl
10.9
36.7
Insecticide
Cyhalothrin
10.9
1.7
Insecticide
Table 1. The 2010 survey by the Penn State team [42], based upon (depending upon the pesticide) either 350 or 247 samples. This study (plus numerous others worldwide) clearly point out that the predominant pesticide residues in brood combs are typically those from the beekeeper-applied miticides (yellow).
Table 2. This 2012 survey by the USDA [43] echoes the previous findings--the only pesticides found in at least 10% of the samples were from either beekeeper-applied miticides or chlorpyrifos. The 99 analyzed samples came from Alabama, California, Colorado, Florida, Idaho, Indiana, New York, South Dakota, Tennessee, Texas, and Wisconsin.
Keep in mind that the above surveys screen only for 174 chosen pesticides--compare this number to the roughly 1000 pesticide active ingredients and adjuvants registered for use in California. I've discussed the composition of this list with USDA's Roger Simonds, who runs the tests. It is prohibitively costly to test for every possible pesticide, so one must arbitrarily draw up a limited list of the chemicals of most concern. All are aware that this is a difficult task, since we don't even know which toxins with which we should be most concerned!
Note that in both surveys, the most common insecticide present was chlorpyrifos- an "old school" (introduced in 1965) organophosphate neurotoxin classified as being "highly toxic" to bees, and marketed as Dursban and Lorsban. Chlorpyrifos was previously widely used by homeowners and residential pest control companies. EPA has since restricted its use due to its toxicity to wildlife and aquatic organisms, and possible links to human health issues [44]--some of the reasons that EPA favors the neonicotinoids as "reduced risk" products.
Oh Boy, Let's Do Some Math!
But just because a pesticide is present, doesn't necessarily mean that it is causing measureable harm. A nurse bee may consume about 10 mg of beebread per day [45], so if she consumed that amount of pollen contaminated with chlorpyrifos at 6.5 ppb, then she would have been dosed with 0.065 ng (1 nanogram = 1 billionth of a gram) of the chemical. The question then is, how much chlorpyrifos does it take to actually harm a bee?
One commonly cited figure is that the LD50 for chlorpyrifos given orally is 360 ng/bee. Compare those figures (360 ng for toxicity vs. 0.065 in the daily diet)! Even though chlorpyrifos is a disturbingly common comb contaminant, it is unlikely that the median detected concentration (alone) would be causing colony health problems (not to say that higher doses don't hurt colonies).
But, you say, some of the neonics are even more toxic than chlorpyrifos. How about the mean 31 ppb found by the USDA in the few samples positive for imidacloprid? The typical nurse bee would consume 0.31 ng, compared to the oral LD50 of about 4-40 ng, so she'd be eating a tenth to a hundredth of the lethal dose. This would be cause for concern, tempered by the fact that a bee can easily metabolize that amount of imidacloprid a day [46]. Such consumption could legitimately be suspected of causing sublethal effects. However, keep in mind that that 31 ppb was an average, which was strongly skewed by a few samples with very high concentrations (which I'd fully expect to cause colony health problems). Plus this is not simply a matter of the average amount of contamination; one must also look at the percentage of positive detects. The Penn State team [47] puts it well:
Our residue results based on 1120 samples which include Mullin et al. (2010) and subsequently more than 230 additional samples do not support sufficient amounts and frequency of imidacloprid in pollen to broadly impact bees.
OK, so how about the varoacides fluvalinate at 40 ppb or the amitraz degradate DMPF at 100 ppb? Surprisingly, I can't find an oral LD50 for fluvalinate, so the contact toxicity figure (200 ng/bee) will need to suffice. Those residues work out to about 1/500th expected toxicity.
Amitraz scored a bit better, with the nurse bees consuming about 0.01 ng--far below the lethal dose. But a recent study found that an oral dose of 0.2 ng of amitraz causes more than a doubling of the heart rate of a bee [48]--that's at 1/20th of the average detect! The authors dryly state:
The above responses clearly show that the heart of the honeybee is extremely vulnerable to amitraz, which is nevertheless still used inside beehives, ostensibly to "protect" the honeybees against their main parasite, Varroa destructor.
How vulnerable? Frazier [49] observed that "Dead and dying bees collected around colonies in association with corn had only residues of 2,4-DMPF at 5,160 ppb." Looks like perhaps the beekeeper inadvertently killed his own bees with an off-label mite treatment that may have overworked their little hearts!
And if those miticide and insecticide residue weren't enough alone, some of the toxicity of these chemicals is additive or synergistic. The Penn State team again says it well:
[The] pyrethroids... were found in 79.4% of samples at 36-times higher amounts than the neonicotinoids, on average... The mean neonicotinoid residue was 37 ppb (scoring non-detects as 0 ppb), of which only 6.7 ppb was imidacloprid. Pyrethroids, by comparison, were present at a mean residue of 106 ppb and a frequency of 80.3% in pollen samples... Indeed, if a relative hazard to honey bees is calculated as the product of mean residue times frequency detected divided by the LD50, the hazard due to pyrethroid residues is three-times greater than that of neonicotinoids detected in pollen samples [emphasis mine].
The pyrethroids are popular because they are relatively nontoxic to humans. But they can sure kill honey bees. More so, they can cause sublethal effects, such as irreversible inhibition of olfactory learning ability [50].
Hey, we're only getting rolling! Mussen [51] pointed out a decade ago that fungicides could kill larvae; recent research from the Tucson lab [52] and elsewhere confirm that fungicide residues can mess up the colony (we sometimes observe this in almonds). Of note is that colonies treated with some fungicides were unsuccessful at requeening themselves! And recent research by Zhu [53] found that the relative toxicity of larvae to the commonly-detected fungicide chlorothalanil was almost 40 times higher than that of chlorpyrifos. Fungicides are frequently found at high concentrations in beebread.
I cannot help from returning to the refrain that instead of limiting our concern to any single pesticide, that we should be looking at the total toxin load that the colony is forced to deal with.
And How About The "Inerts"?
The pesticide detection analyses above do not look at the "inert" adjuvants in the pesticide "formulation." These chemicals not only help to disperse the pesticide over the waxy leaf surface, but also aid in its penetration through the insect cuticle, thus making the pesticide relatively more toxic to the bee!
Mullin and Ciarlo [54, 55] found that:
Formulations usually contain inerts at higher amounts than active ingredients, and these penetrating enhancers, surfactants and adjuvants can be more toxic on non-targets than the active ingredients. For example, we found that the miticide formulation Taktic®️ was four time more orally toxic to adult honey bees than the respective active ingredient amitraz. Impacts of 'inerts' in pollen and nectar alone or in combination with coincident pesticide residues on honey bee survival and behavior are unknown.
The researchers also found that:
Learning was [rapidly] impaired after ingestion of 20 ug of any of the four tested organosilicone adjuvants, indicating harmful effects on honey bees caused by agrochemicals previously believed to be innocuous.
One of the common adjuvants is a solvent NMP, described by BASF [56]:
NMP can be used as a solvent or co-solvent for the formulation of insecticides, fungicides, herbicides, seed treatment products and bioregulators where highly polar compounds are required. NMP is given preference over other highly polar solvents because it is exempt from the requirement of a tolerance when used as a solvent or co-solvent in pesticide formulations applied to growing crops, and it possesses a favorable toxicological and environmental profile.
The key words above are that these toxic solvents are "exempt from tolerance" [57], so they are sprayed all over crops along with the active ingredients of pesticides (including imidacloprid). Yet Zhu [58] recently reported that NMP can rapidly kill bee larvae. The authors conclude that:
Our study suggests that fungicide, the inert ingredient and pesticide interaction should be of high concern to honey bee larvae and overall colony health. None of these factors can be neglected in the pesticide risk assessment for honey bees.
Choosing To Ignore The Obvious
There is no doubt that neonics have the potential to harm bees, but the question is, do they really cause as much problem in the real world as we've been led to believe? This is not a matter of convincing the masses; this is an investigation of fact and evidence. For a pesticide to cause harm to a colony of bees, two necessary elements must occur:
The bees must be exposed to the pesticide. Evidence for this is best determined by chemical analysis of the pollen in the combs, since residues in the bodies of dead bees may be degraded, and because water-soluble insecticides such as the neonics are not absorbed into the wax (residues in the wax do document the history of exposure to lipophilic pesticides).
The pesticide must be present at a concentration above a trivial level.
When we take the time to determine which pesticides bees are actually found in the combs of hives, neonicotinoids are seldom present, or if detected are often at biologically irrelevant concentrations. Imidacloprid was detected in fewer than 3% of Mullin's 350 samples, and clothianidin not at all! Similarly, there were zero detects for clothianidin in the 99 USDA samples; imidacloprid was only present in 9%. Likewise, a number of European studies have shown similar results (reviewed in [59]).
In a recent study, the Fraziers [60] looked at hives placed in cotton, corn, alfalfa, apples, pumpkins, almonds, melons, blueberries, or wild flowers, and identified the residues in collected pollen, in returning foragers, and in dead or dying bees near the hives. Again, the only neonic noted was thiamethoxam in alfalfa (in which dying bees contained residues of ten different pesticides). However, there were alarmingly high detects of fungicides, the insecticide acephate, and the metabolite of the beekeeper-applied miticide amitraz.
The latest data comes from Dr. Jeff Pettis [61], whose group determined the pesticides in bee-collected pollen from six crops: apple, blueberry, cranberry, cucumber, pumpkin, and watermelon. Of the 35 pesticides detected, beekeeper-applied miticides and ag fungicides predominated (sometimes at alarming levels), followed by common organophosphate, pyrethroid, and cyclodiene insecticides (again sometimes at alarming levels). In the 17 samples tested, residues of neonics were only found in the samples from the apple orchards, and only one was found at a biologically-relevant concentration.
So my question is why the heck are so many activists pursuing the single-minded focus upon the neonics, when the clear evidence is that neonics are not commonly found in bee-collected pollen, and if present, are generally at levels that do not appear to negatively affect colony health [62]?
There is a lot more to pesticide issues than the neonics alone, and by focusing our attention solely upon them, we ignore the often far more serious effects of other pesticides.
Blinded By Bias
During the intense focus upon neonicotinoids the past few years, we've learned that exposure of bees to these insecticides can result in all sorts of sublethal effects. Unfortunately, many researchers appear to be wearing blinders as to the effects of other pesticides. The resulting narrowness of these studies skews our perspective--if we only look for effects from the neonics, we don't know how to rank the biological relevance of those effects relative to the effects of all the other toxins to which bees are exposed, generally to greater extent.
A practical complaint to researchers: if you are going to look for sublethal effects of neonics, please include positive controls of some other pesticides, so that we can learn whether the neonics are better or worse than the alternatives!
I commend one group that recently decided to take a look at the effects of a common herbicide upon the development of bee larvae [63]. The results of this straightforward and meticulous study are an eye opener!
The researchers found that exposing bee larvae to even infinitesimal amounts of the herbicide paraquat prevented them from fully developing their critical oenocyte cells (see box).
Oenocyte cells are not only involved in the production of lipids and lipoproteins, but they also appear to play a role in the constitution of external cuticle in both larvae and adults. In addition, they are involved in intermediary metabolism and synthesize hydrocarbons to waterproof cuticle or to make beeswax. Furthermore, oenocytes secrete hormones, especially those involved in larval and adult development. They are also described as the major cells expressing cytochrome P450 reductase, which is involved in detoxification of toxins [information paraphrased from the cited paper].
Exposure to even a part per trillion of paraquat suppressed the development of these extremely important cells. The authors conclude:
This study is the first which reports an effect of a pesticide at the very low concentration of 1 ng/kg, a concentration below the detection limits of the most efficient analytic methods. It shows that chemicals, including pesticides, are likely to have a potential impact at such exposure levels.
Who woulda thunk? Paraquat isn't included in the standard screening for pesticide residues, so we don't even know how prevalent it is in hives! The above findings should make it clear that we need to go back to the beginning if we are to understand the sublethal effects of pesticides (and adjuvants), even at perhaps undetectable levels.
We do know that here were 812,000 lbs of paraquat applied in California in 2010, as opposed to only 266,000 lbs of imidacloprid. Paraquat shows strong adverse effects upon bee larvae at a part per trillion, as compared to imidacloprid, which is so minimally toxic to bee larvae that no one has even been able to determine an LD50! So the amount of paraquat applied has far greater potential to cause problems to bees in agricultural areas (Fig. 7).
Figure 7. The herbicide paraquat appears to be harmful to bee larvae at levels as low as 1 part per trillion. Note the wide variety of crops, and the extensive areas to which it is applied.
So here we have clear scientific data from a well-designed laboratory experiment that a commonly-applied pesticide has the ability to cause immune suppression and other adverse effects in developing bees, yet these results have been virtually ignored by beekeepers and environmental groups. I just don't understand it!
No More Safe Home To Return To
Out of their protective hive, honey bees live in a hostile world, full of predators, deadly weather, and toxic agents (both natural and manmade). But the bees of old could generally return to a "safe" home, in which the transmission of natural toxins was largely minimized by the behavior of foragers, and by the processes of the conversion of nectar to honey, and of pollen into jelly (via the digestion of beebread by nurse bees). Both of these processes help to prevent the transmission of toxins from the foragers to the queen and the brood.
With the advent manmade pesticides, bees may no longer have that "safe" home to return to. Beebread and the wax combs nowadays are often contaminated with any number of pesticides (in addition to natural plant toxins and industrial pollutants). But this is not a "new" problem:
A Historical Artifact
Even before we had the ability to detect pesticide residues in combs to the parts per billion level, pesticide analyses often found easily-detectable levels of insecticides in bee hives. As a frame of reference, I sought out a historical artifact--the residues in the beeswax that had been rendered by beekeepers and reprocessed into a sheet of "clean" foundation. I was lucky enough to find that such a sample had recently been analyzed by the Tucson Bee Lab. Dr. Diana Sammataro forwarded me the results of the analysis of an undated "very old" piece of wax foundation from the Northeast (Table 3).
THIS IS THE TABLE !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!
Pesticides in an old piece of beeswax foundation.
Positive residue detect
ppb
Pendimethalin
13.1
Endrin
156
Dieldrin
160
Trifluralin
3.6
DDT p,p'
32.7
Heptachlor
35.1
Malathion
4.3
Chlorpyrifos
4.6
Dicofol
6.8
PCB's
8190
Chlorothalonil
84.6
Table 3. We can narrow down the foundation's date of manufacture by the residues present. Pendimethalin was first registered in 1972 (the same year that DDT was banned), and since there were no residues of fluvalinate, the foundation was clearly produced prior to the arrival of varroa around 1990. Thanks to Dr. Diana Sammataro and the Tucson Bee Lab.
Clearly, pesticide-contaminated combs are hardly a new phenomenon. In the above example, the beeswax batch used to produce the foundation came not from a single hive, but rather from the combined wax from many hives, likely from many beekeepers, and thus would represent an average sample of the degree of contamination somewhere in that 1972-1990 time frame. And that doesn't take into account whether the raw wax came mainly from cappings (which would have been minimally contaminated), or whether it went through the common practice of being filtered through activated carbon. But any colony started on such foundation purchased from a beekeeping supply house would clearly have had to deal with at least the residues of these lipophilic toxins from the get go!
An aside: perhaps of interest is something that I noticed years ago when I switched from dipping my own wax queen cell cups to using plastic cups. My "take" rate became better and more consistent. Was that because the beeswax at the time was contaminated with residues?
The Beekeeper Contribution To Shifting The Tip Point
One thing that is "new" is that since the arrival of varroa, we've upped the ante--all commercial beeswax is now contaminated with residues of beekeeper-applied synthetic miticides. The three most prevalent synthetic chemicals found in combs today all get there by being applied by beekeepers for mite control.
Practical note: And although there is no reason to be concerned about the tainting of honey by the legal use of these miticides, the beekeeper/applicator should be aware that both amitraz and tau-fluvalinate make California's list of "chemicals known to the State to cause reproductive toxicity," and coumaphos is of concern because it is a "cholinesterase-inhibiting pesticide." No varroacide is harmless to bees [64]--but the benefits of mite control generally (but not always) outweigh the adverse effects due to the miticide residues.
We beekeepers have clearly shifted the baseline for pesticide contamination of combs, which increases the total toxic load even before the contribution by agricultural pesticides.
Stop Right There!
Although it is a very attractive hypothesis to blame our problems on miticide or pesticide residues, let's do a reality check. On good forage in good weather, plenty of beekeepers see their colonies thrive even on old, dark, seriously-contaminated combs; but under stressful conditions those same residues might contribute to poor colony performance or even mortality.
No study has yet found support for the hypothesis that miticide residues are the cause of our current bee problems (although one would have every reason to suspect that they may contribute). In fact, vanEngelsdorp [65] found that surprisingly, higher levels of coumaphos residues negatively correlated with colony survival. How could this be? One possible explanation is that those beekeepers who used it experienced better mite control. But there is also another intriguing possibility--hormetic effects.
Undetectable Levels And Hormesis
Is your head spinning yet? I've presented evidence that undetectable levels of some pesticides could harm bees, that "inert" adjuvants can do the same, and that combs are often chock full of all sorts of pesticide and varroacides residues. Criminy, it's a wonder that bees survive at all! Or is it?
Bees have long been exposed to all sorts of natural, and recently, manmade toxins, and survived. Toxicity is a complicated subject. The only thing that separates a medicine from a poison is the dose. In general, if a pesticide has been tested upon adult and larval bees and found to have no observable adverse effects at a certain concentration, we would not expect to see adverse effects at lower concentrations. However, there are exceptions to this general rule--toxicity may vary up or down depending upon the dose [66]!
I've previously mentioned the term hormesis [67]-- the paradoxical effect of toxins at low concentrations. The paradox is that although most chemicals are toxic at high concentrations, the majority are likely beneficial at low concentrations. For those interested in this fascinating phenomenon, I suggest Dr. Chris Cutler's excellent and thought-provoking review [68]. It is not only possible, but actually probable that lose doses of pesticides may exert a beneficial effect upon a colony! (Don't be ridiculous--I'm not suggesting that bees are better off for the presence of pesticides!).
Wrap Up
Toxins, whether natural or manmade, are clearly a potential issue in colony health. To what degree pesticides contribute to colony morbidity or mortality is dependent upon exposure, the dose, and a host of associated factors. Beekeepers have long noticed that their bees often do better if allowed to forage on pesticide-free land. But many beekeepers today tell me that their bees do just fine in the middle of intense agricultural areas--so this is not a black or white situation.
In recent years beekeepers themselves have greatly added to the degree of contamination of their combs. Introductions of novel pesticides and adjuvants keep changing the picture. And now we're finding that pesticides that we formerly assumed were harmless to bees (fungicides and herbicides) may actually be quite toxic to larvae! Then there is the scary finding that undetectable levels of some pesticides might cause health issues, countered by the fascinating subject of hormesis.
I certainly do not profess to understand all this, but I have come to the following conclusions:
That bees have had to deal with toxins for a long time,
That pesticides will be with us for the foreseeable future,
That varroacides have likely added to the problem,
That pesticides can cause lethal and long-term sublethal effects in the hive, but
That many beekeepers in agricultural areas no longer consider pesticides to be a serious issue, whereas,
That colonies may go downhill after being exposed to some agricultural chemicals, or combinations thereof,
That toxicology in the hive is complex, and that there are few simple answers,
That it is unlikely that any single pesticide is to blame for our current colony health issues,
That we still have a lot to learn!
Next month I will look at the distribution of both managed colonies and of pesticide applications in the United States, and their relationship to bee health problems.
Acknowledgements
As always, I could not research these articles without the assistance of my longtime collaborator Peter Loring Borst, to whom I am greatly indebted. I also wish to thank Drs. Jim and Maryann Frazier, Chris Mullin, David Fischer, Eric Mussen, Thomas Steeger, and Roger Simonds for their generosity in taking the time to discuss pesticide issues with me.
References
[1] Rucker, RR and WN Thurman (2012) Colony collapse disorder: the market response to bee disease. http://perc.org/sites/default/files/ps50.pdf
[2](Broken Link) http://perc.org/articles/everyone-calm-down-there-no-bee-pocalypse
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[5] vanEngelsdorp and Meixner (2010) op. cit.
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"Certainly with both pesticide-related and [Disappearing Disease]-caused bee losses, the adult population of a colony may be reduced rapidly to a "handful" of bees or, in some cases, the entire population may be lost.
"However, in the case of pesticide poisoning, there is usually evidence of pesticide application...the worker bees either die in the field or in or near the hive depending on the type of pesticide. When the field force is killed and they "disappear," many dead or dying bees may be seen on the ground in the field or on the ground between the treated field and the apiary...If the foraging bees bring poison into the hive, then the nurse bees either die in the hive or at the entrance so one can see many crawling and tumbling adults and large amounts of neglected brood. Exposure to pesticides over an extended period results in very weak colonies, and some die out.
"In the case of [Disappearing Disease], the situation is quite different. The colonies frequently have gone through a period o nectar and pollen collection with active brood rearing [as in typical CCD]. Then the weather has turned unseasonably cool and damp and remained adverse for from about 3 to 14 days...During the inclement weather, the bee populations dwindle because the worker bees disappear from the hive leaving a "handful" of bees and the queen. Often these small populations recover and increase in size during hot weather and a long nectar flow or, or occasionally, the entire population absconds..."
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[20] Yang E-C, Chang H-C, Wu W-Y, Chen Y-W (2012) Impaired olfactory associative behavior of honeybee workers due to contamination of imidacloprid in the larval stage. PLoS ONE 7(11): e49472. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0049472
[30] Bee health in Europe -Facts & figures 2013. OPERA http://operaresearch.eu/files/repository/20130122162456_BEEHEALTHINEUROPE-Facts&Figures2013.pdf
[31] The study by Drs. Scott-Dupree and Cutler is yet unpublished, but a summary can be found at http://www.producer.com/daily/ontario-field-study-finds-no-link-between-seed-treatments-bee-deaths/
[32] Cutler, GC, CD Scott-Dupree, DM Drexler (2013) Honey bees, neonicotinoids, and bee incident reports: the Canadian situation. Pest Management Science http://onlinelibrary.wiley.com/doi/10.1002/ps.3613/abstract
[33] Goulson, Dave (2013) An overview of the environmental risks posed by neonicotinoid insecticides. Journal of Applied Ecology 50: 977-987. https://www.sussex.ac.uk/webteam/gateway/file.php?name=goulson-2013-jae.pdf&site=411
[34] Scott-Dupree, CD, et al (2009) Impact of currently used or potentially useful insecticides for canola agroecosystems on Bombus impatiens (Hymenoptera: Apidae), Megachile rotundata (Hymentoptera: Megachilidae), and Osmia lignaria (Hymenoptera: Megachilidae). J Econ Entomol 102(1):177-82.
[35] Blacquiere, et al (2012) Neonicotinoids in bees: a review on concentrations, side-effects and risk assessment http://www.gesundebiene.at/wp-content/uploads/2012/02/Neonicotinoide-in-bees.pdf
[36] Hobbs, GA (1967) Domestication of Alfalfa Leaf-cutter Bees. Canada Dept. of Agriculture. Ottawa: Queen's Printer and Controller of stationary.
[37] Dr. Jerry Bromenshenk, pers. com.
[38] Abbott, VA, et al (2008) Lethal and sublethal effects of imidacloprid on Osmia lignaria and clothianidin on Megachile rotundata (Hymenoptera: Megachilidae). J Econ Entomol 101(3):784-96.
[39] http://pfspbees.org/sites/pfspbees.org/files/resource-files/pnw591.pdf
[40] PMRA (2013) Evaluation of Canadian Bee Mortalities Coinciding with Corn Planting in Spring 2012.
[41] PMRA (2013) Action to Protect Bees from Exposure to Neonicotinoid Pesticides http://www.hc-sc.gc.ca/cps-spc/alt_formats/pdf/pest/part/consultations/_noi2013-01/noi2013-01-eng.pdf
[42] Mullin CA, et al. (2010) op. cit.
[43] Rennich, K, et. al (2012) 2011-2012 National Honey Bee Pests and Diseases Survey Report. http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
[44] Christensen, K.; Harper, B.; Luukinen, B.; Buhl, K.; Stone, D. 2009. Chlorpyrifos Technical Fact Sheet; National Pesticide Information Center, Oregon State University Extension Services. http://npic.orst.edu/factsheets/chlorptech.pdf.
[45] Rortais, A (2005) Modes of honeybees exposure to systemic insecticides: estimated amounts of contaminated pollen and nectar consumed by different categories of bees. Apidologie 36: 71-83.
[46] Cresswell, JE, et al (2012) Differential sensitivity of honey bees and bumble bees to a dietary insecticide (imidacloprid). Zoology 115: 365- 371.
[47] Frazier (2011) op. cit.
[48] Papaefthimiou, C, et al (2013) Biphasic responses of the honeybee heart to nanomolar concentrations of amitraz. Pesticide Biochemistry and Physiology 107(1): 132-137. http://www.sciencedirect.com/science/article/pii/S0048357513001120
[49] Frazier, et al (2011) Assessing the reduction of field populations in honey bee colonies pollinating nine different crops. ABRC 2011
[50] Tan K, Yang S, Wang Z, Menzel R (2013) Effect of flumethrin on survival and olfactory learning in honeybees. PLoS ONE 8(6): e66295. doi:10.1371/journal.pone.0066295. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0066295
[51] Mussen, et al (2004) op. cit.
[52] http://www.abfnet.org/associations/10537/files/Dr.%20Gloria%20DeGrandi%20Hoffman_GS.mp3
[53] Zhu, W., D. Schmehl & J. Frazier (2011) Measuring and predicting honey bee larval survival after chronic pesticide exposure http://www.extension.org/pages/58650/proceedings-of-the-american-bee-research-conference-2011#.UhDTZX-aucw
[54] Mullin, C.A., J. Chen, W. Zhu, M.T. Frazier & J.L. Frazier - The formulation makes the bee poison. ABRC 2013
[55] Ciarlo TJ, Mullin CA, Frazier JL, Schmehl DR (2012) Learning impairment in honey bees caused by agricultural spray adjuvants. PLoS ONE 7(7): e40848. doi:10.1371/journal.pone.0040848
[56] (Broken Link!) http://www2.basf.us/diols/bcdiolsnmp.html
[57] http://www.epa.gov/opprd001/inerts/methyl.pdf
[58] Zhu, et al (2011) op. cit.
[59] Blacquiere, T, et al (2012) Neonicotinoids in bees: a review on concentrations, side-effects and risk assessment. Ecotoxicology 21(4): 973-992. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3338325/
[60] Frazier, M.T., S. Ashcraft, W. Zhu & J. Frazier - Assessing the reduction of field populations in honey bee colonies pollinating nine different crops http://www.extension.org/pages/58650/proceedings-of-the-american-bee-research-conference-2011#.UhDTZX-aucw
[61] Pettis, et al (2013) op. cit.
[62] A recent study confirm that the neonic residues in corn, soy, and canola pollen are at very low concentrations. Henderson, C.B. a, J.J. Bromenshenka, D.L. Fischerb. Clothianidin exposure levels from bee-collected pollen and nectar in seed-treated corn and canola plantings. ABRC 2013 http://bees.msu.edu/wp-content/uploads/2013/01/ABRC-abstracts-2013.pdf
[63] Cousin M, Silva-Zacarin E, Kretzschmar A, El Maataoui M, Brunet J-L, et al. (2013) Size changes in honey bee larvae oenocytes induced by exposure to paraquat at very low concentrations. PLoS ONE 8(5): e65693. doi:10.1371/journal.pone.0065693 http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0065693
[64] Boncristiani, H., et. al. (2011) Direct effect of acaricides on pathogen loads and gene expression levels of honey bee Apis mellifera. Journal of Insect Physiology. 58:613-620.
[65] vanEngelsdorp, D, et al () Weighing risk factors associated with bee colony collapse disorder by classification and regression tree analysis. J. Econ. Entomol. 103(5): 1517-1523. (Broken Link!) http://www.eclecticparrot.com.au/research_papers/VanEngelsdorp%202010%20Weighing%20risk%20factors%20in%20Bee%20CCD.pdf
[66] Cutler GC, Ramanaidu K, Astatkie T, and Isman MB. (2009) Green peach aphid, Myzus persicae (Hemiptera: Aphididae), reproduction during exposure to sublethal concentrations of imidacloprid and azadirachtin. Pest Manag Sci 65:205-209
[67] https://scientificbeekeeping.com/sick-bees-part-18f2-colony-collapse-revisited-plant-allelochemicals/
[68] Cutler, GC (2013) Insects, insecticides and hormesis: evidence and considerations for study. Dose-Response 11:154-177 (Broken Link!) http://dose-response.metapress.com/app/home/contribution.asp?referrer=parent&backto=issue,2,11;journal,3,34;linkingpublicationresults,1:119866,1
Category: Colony Health - Diseases, Viruses, CCD
Tags: collapse, colony, pesticides, sick bees | pesticides Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/pesticides/ |
Testing of Bee Feed Syrups for Neonicotinoid Residues
First published in: American Bee Journal, August, 2012
Testing Of Bee Feed Syrups For Neonicotinoid Residues
Eric Mussen1 and Randy Oliver2
First Published in ABJ in August 2012
The widespread adoption of the systemic neonicotinoid insecticides has led a number of beekeepers to question whether the commercially available corn, beet, or cane sugar syrups might be contaminated with residues of those insecticides.
Introduction
Beekeepers often feed some form of sugar syrup to colonies for either buildup or winter stores. The raw materials for sugar production come mainly from three cultivated crops-traditionally sugar cane or sugar beets, from which sucrose is extracted; or from corn (maize), from which high fructose corn syrup (HFCS) is produced.
In recent years, growers have widely adopted the practice of treating corn and sugar beet seed with systemic neonicotinoid insecticides [1, 2, 3], and clothianidin may be used on sugar cane in some areas [4]. The understanding that these insecticides are "systemic" (transported throughout the plant tissues) has led some beekeepers to question whether residues may make it into the final sugar product.
We submitted samples of the bee feed syrups offered by two major U.S. suppliers for independent testing. Residues of neonicotinoid insecticides, as well as their degradation products, can be multiply-detected at as little as ppb levels by modern analytical instrumentation [5].
Materials And Methods
We solicited samples of syrups (Table 1) from Stuart Volby of Mann Lake Ltd. (Mann Lake, MN) and from Dadant (Chico, CA) branch manager John Gomez, which we reshipped for testing to Roger Simonds, Laboratory Manager of the USDA Agricultural Marketing Service lab. We requested analyses for neonicotinoid insecticides and their principal degradates.
Supplier Manufacturer Syrup Type
Mann Lake Ltd. Cargill Type 55 HFCS
Type 42 HFCS
Liquid sucrose (beet)
Liquid sucrose (cane)
Dadant & Sons, Inc. (Chico branch) Archer Daniels Midland (ADM) California blend:
50% Type 42 HFCS
50% Liquid sucrose (cane)
Table 1. Bee feed syrups submitted for analysis.
1 Extension Apiculturist, University of California, Davis, CA 95616
2 Proprietor, Golden West Apiaries, Grass Valley, CA 95945
Results
None of the tested samples contained detectable levels of either the neonicotinoid parent compounds or their degradates (Fig. 1).
Figure 1. Typical test results. The LOD is the "limit of detection," i.e., the lowest concentration in parts per billion (ppb) that the instrument can detect. The lab tested for both parent compounds (e.g., imidacloprid) as well as for the degradation products of the insecticides, which may also exhibit toxicity.
Discussion
Although no residues were detected in the syrup samples submitted for testing, the possibility exists that there were residues below the limit of detection (1 ppb for most of the parent compounds). However, levels below 1 ppb are generally accepted as being well below the no observable adverse effects concentration (NOAEC) [6].
These results are not surprising for HFCS, given that when the USDA tested 655 samples of corn grain in 2007 [7], no residues of neonicotinoid insecticides were detected. Although the tolerance level for clothianidin in sugar beets is 20 ppb [8], there are often no detectable residues from beets in the field [9]. Similarly, there were no detectable residues in the sample of beet sugar that we submitted.
Although this was a very limited sampling, it gave no evidence that beekeepers need to be concerned about neonicotinoid insecticide residues in feed syrups from the major suppliers.
Acknowledgements
Thanks to the cooperation of Stuart Volby and John Gomez for supplying samples, Roger Simonds for expediting the analyses, and to the U.C. Davis Extension Apiculture Program for providing funds for sample analyses.
References
[1] Anon (2012) 2012 Corn Insect Control Recommendations. http://eppserver.ag.utk.edu/redbook/pdf/corninsects.pdf
[2] Valent (2011) Valent USA Announces NipsIt™️ SUITE Sugar Beet Seed Treatment System. http://www.seedtoday.com/info/ST_articles.html?ID=113940
[3] Syngenta (2012) CRUISER FORCE sugar beet seed - the UK's number one choice. http://www.syngenta-crop.co.uk/pdfs/products/CruiserSB_uk_technical_update.pdf#view=fit
[4] APVMA (2010) Trade Advice Notice on clothianidin in the product Sumitomo Shield systemic insecticide http://www.apvma.gov.au/registration/assessment/docs/tan_clothianidin_60689.pdf
[5] http://quechers.cvua-stuttgart.de/
[6] Decourtye, A (2003) Learning performances of honeybees (Apis mellifera L) are differentially affected by imidacloprid according to the season. Pest Manag Sci 59: 269-278.
[7] USDA (2008) Pesticide Data Program Annual Summary, Calendar Year 2007, Appendix F Distribution of Residues by Pesticide in Corn Grain http://www.ams.usda.gov/AMSv1.0/getfile?dDocName=STELPRDC5074338
[8] Federal Register (2008) Clothianidin; Pesticide Tolerance. https://www.federalregister.gov/articles/2008/02/06/E8-1784/clothianidin-pesticide-tolerance
[9] FAO (2005) Clothianidin, Table 103. http://www.fao.org/fileadmin/templates/agphome/documents/Pests_Pesticides/JMPR/Evaluation10/Chlotiahinidin.pdf
Category: Pesticide Issues
Tags: bee feed syrups, insecticides, neonicotinoid, residues | neonicotinoid Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/neonicotinoid/ |
Sick Bees - Part 18F7: Colony Collapse Revisited - Pesticide Exposure
First published in: American Bee Journal, October and November 2013
Pesticide Exposure
Oh No, Not Pesticides Again!
Reality Checks
The Two Worlds of Beekeeping
Pesticides and Bee-pocalypse
A Comparison To Some "Control Groups"
The Four Horsemen And The Tip Point
Could Pesticides Cause Colony Mortality And CCD?
Short Memories
The Heart Of The Hive - The Nursery
Industry's Arguments
But Don't We Already Know That It's The Neonicotinoids?
An "Acid Test" Of Neonic Seed Treatment
So Which Pesticides Are Actually To Blame?
The Evidence
Oh Boy, Let's Do Some Math!
And How About The "Inerts"?
Choosing To Ignore The Obvious
Blinded By Bias
No More Safe Home To Return To
A Historical Artifact
The Beekeeper Contribution To Shifting The Tip Point
Stop Right There!
Undetectable Levels And Hormesis
Wrap Up
Acknowledgements
References
Sick Bees Part 18f7: Colony Collapse Revisited
Pesticide Exposure
Randy Oliver
ScientificBeekeeping.com
Originally published in ABJ Oct and Nov 2013
Oh No, Not Pesticides Again!
Some readers may wonder why I am spending so much time on the issue of pesticides, since to many (if not most) beekeepers, pesticides are a non issue. In answer, the main reason is that the public (and our lawmakers) are being hammered by the twin messages that the honey bee is on the verge of extinction, and that the reason is pesticides. In my writings, I'm attempting to address the validity of both of those claims. Let's start with the first.
Reality Checks
Honey bees have clearly (and deservedly) become one of today's most charismatic environmental poster children, and as such are a useful bioindicator that our human activities are having a negative impact upon pollinators, and wildlife in general.
But I also feel that we take care to not overstate or exaggerate our case. One of my greatest concerns is that beekeepers are allowing the media to scare the public with all the hue and cry of an impending bee-pocalypse (and that it is due to a certain type of pesticide). Our complicity in this message (as we enjoy the luxury of basking in the warmth of all the public support) may backfire on us one of these days--putting us into the position of the little boy who cried wolf. Some in the media are starting to notice that the facts don't support the claim that bees are disappearing (Fig. 1).
Figure 1. It's true that it's more difficult to keep bees healthy these days, but it doesn't look like bee-pocalypse is imminent (as evidenced by this recently-published chart). Whenever honey and pollination prices are high enough to make beekeeping profitable, resourceful beekeepers somehow manage to recover their colony losses [[i]]. Chart courtesy Shawn Regan [[ii]].
[i] Rucker, RR and WN Thurman (2012) Colony collapse disorder: the market response to bee disease. http://perc.org/sites/default/files/ps50.pdf
[ii] (Broken Link) http://perc.org/articles/everyone-calm-down-there-no-bee-pocalypse
In the rest of the world, the number of managed hives has actually been increasing [3]. And as far as claims that pesticides are driving bees to extinction, Hannah Nordhaus, the author of the excellent book The Beekeeper's Lament writes:
Reflexively blaming pesticides for all of the honey bee's problems may in fact slow the search for solutions. Honey bees have enough to do without having to serve as our exoskeletal canaries in a coalmine. Dying bees have become symbols of environmental sin, of faceless corporations out to ransack nature. Such is the story environmental journalism tells all too often. But it's not always the story that best helps us understand how we live in this world of nearly seven billion hungry people, or how we might square our ecological concerns and commitments with that reality. By engaging in simplistic and sometimes misleading environmental narratives -- by exaggerating the stakes and brushing over the inconvenient facts that stand in the way of foregone conclusions -- we do our field, and our subjects, a disservice [4].
Further reading: for a detailed and sober analysis of the factors that affect managed bee populations, I highly recommend the review by Drs. vanEngelsdorp and Meixner [5].
The reality is that it is not the honey bee that is being driven to extinction--it is instead the commercial beekeeper who is finding that his traditional business model is becoming less profitable due to today's greater degree of colony losses and the decreasing availability of good summer forage.
The question is, to what extent are pesticides involved in those problems?
The Two Worlds Of Beekeeping
There are two very different worlds of beekeeping--small scale (hobbyists, who constitute the vast majority of beekeepers by number) and large scale (commercialized professionals, who manage the vast majority of hives), with a small continuum of sideliners bridging the gap.
Hobby beekeeping is currently enjoying a bubble of resurgence, but in the Big Picture in the U.S., hobbyists manage an insignificant number of hives. And those small-scale beekeepers tend to keep their hives close to home, largely avoiding serious exposure to pesticides. But that's not to say that small-scale beekeepers are immune to pesticide kills; I've heard of several this season, and what with all the spraying for West Nile virus and the citrus psyllid, we can expect more of the same. And since there are far more small-scale beekeepers to put pressure on regulators and legislators, I feel that it is a good idea for them to be informed about pesticide issues.
Large-scale beekeepers, on the other hand, typically run migratory operations--moving their hives to almond pollination, and then to other agricultural areas (it's problematic to keep apiaries of hundreds of hives in the suburbs). The fate of those bees (and their keepers) is largely determined by agricultural land use practices and their degree of exposure to agricultural pesticides.
It is some of those large-scale beekeepers for whom extinction is a valid concern. The reason (as with any other enterprise) is financial--they can only survive so long unless their businesses continue to be profitable [6]. In recent years, they've had two things going for them--sky-high honey prices and elevated pollination fees. But all is not rosy--there are reasons for those prices going up; these days it's simply more costly to produce honey or to provide bees for pollination.
Today's breathtakingly-high high almond rental rates typically don't even cover operating costs--even if most of one's colonies make it through the winter! Today's 30% average winter loss rate is bleeding profitability from many operations. Not only does the beekeeper need to rebuild his numbers after almonds, but to stay in the black he must also make additional income from paid pollinations or a decent honey crop. And that may no longer be as easy as it used to be for various reasons:
Formerly bee-friendly farmland has been turned into agri-deserts devoid of any bee forage.
Honey producers on field crops (such as alfalfa, sunflowers, or cotton) get hammered time and again by pesticide spraying, sometimes watching whole yards of colonies dwindle or go queenless weeks afterwards.
Paid summer pollination contracts (such as for vine crops) may leave colonies in poor shape for the winter, due to the heavy stocking, the lack of nutritious pollen, and the exposure to multiple pesticides.
These days, the sad fact is that many good beekeepers are barely keeping their heads above water. So the beekeeper's lament continues--varroa, high winter mortality, and lack of good forage are driving a number of operations into the red.
Practical application: although the "extinction of the honey bee" makes for a good rallying cry, the real concern is the possible extinction of the migratory beekeeper who supplies necessary pollination services to agriculture. So far, the almond industry has been economically propping up the bee industry, but I'm not sure how long that arrangement will be sustainable.
Pestcides And Bee-Pocalypse
For some beekeepers, "bee-pocalypse" has already occurred. New York beekeeper Jim Doan, whose case I detailed in a previous article [7], sadly gave it up this year. Here is a beekeeper whose apiaries had been in the same locations for many years without noticeable pesticide problems, but who apparently suffered from devastating spray or dust kills this season and last, as evidenced by piles of fresh dead bees in front of his hives in spring.
Residue analysis of those dead bees clearly showed that they had been exposed to several pesticides, but none of the detects were at levels that would be expected to cause such carnage--so we don't even know which pesticides or practices to point the finger at! To my scientific mind, this is very frustrating--that our "system" was not able to identify the cause of Jim's bee kills, to change anything to keep them from recurring, nor compensate an innocent beekeeper for the loss of his livestock and livelihood.
As unlucky as Jim has been, his case is not necessarily the norm. Overall, the issue of environmental toxins is improving. In my own lifetime I've seen us clean up our pollution of the air and water, cease atmospheric testing of nuclear weapons, ban DDT, fluorocarbons, and PCB's, phase out the worst pesticides, and raise the general environmental consciousness. Humans still inflict far too damaging an environmental footprint on Earth, but we are moving in the right direction, and should give ourselves some credit for that!
There is no doubt that pesticides are often involved in bee health issues, but can we blame them for all our problems? That question is best answered by considering the health of those colonies that are not exposed to pesticides:
A Comparison To Some "Control Groups"
There are plenty of beekeepers in non agricultural areas whose apiaries are not exposed to pesticides to any extent. Those hives serve as a "control group," whose health we can compare to those colonies that do have to deal with pesticides.
For instance, in my own operation of about a thousand hives, their only exposure to pesticides is to the fungicides in the almond orchards (from which they don't appear to suffer to any serious extent). I haven't used synthetic miticides in over a decade, rotate my combs, and rarely feed syrup.
Yet, I've experienced CCD firsthand, see more queenlessness, unsuccessful supersedure, and experience somewhat higher winter losses than in the old days (meaning before varroa). I hear the same from many others in the pesticide-free control group. The simple fact is that these days it requires better husbandry to maintain productive colonies. Yet we in the "control group" can hardly blame pesticides to be the cause.
And then there are the stationary "treatment free" beekeepers in the middle of intense agriculture who suffer no higher colony loss rates than the norm, despite their apiaries being surrounded by corn and soy [8]. How the heck do we reconcile their success to the problems that the commercial guys experience in the same areas?
Do they owe their success to keeping fewer hives in a yard? To keeping locally-adapted survivor stock? To their placement within flight range of patches of undisturbed forage? To the fact that they don't move to multiple crops? Or is it because they aren't contaminating their combs with miticides? Believe me, if I knew the answer, I'd tell you!
As (the very successful) beekeeper Dave Mendes observes, colonies just seem to be more "fragile" these days. It's no surprise then that the addition of toxins of any sort can help to tip a colony over. The Ericksons [9] put it this way:
Pesticides and their residues in the hive stress bees as do other factors such as weather extremes, food shortages, pests, predators, and disease. Conversely, stress induced by other factors undoubtedly has a significant impact on the level of damage that a pesticide inflicts on a colony.
Note that the above words were written prior to our colonies having to deal with varroa, the varroa-vectored viruses, Nosema ceranae, our evolving brood diseases, GMO's, neonicotinoids, or Roundup Ready corn.
The Four Horsemen And The Tip Point
Colony growth is a function of the recruitment rate via successful broodrearing vs. the attrition rate of workers due to age, disease, the altruistic departure of sick bees, or the loss of foragers in the field. When recruitment exceeds attrition, colonies grow; when attrition exceeds recruitment, the colony population shrinks. Environmental factors, including toxins, can shift the tip point for colony growth (Fig. 2).
Figure 2. Any colony with a good laying queen has the potential to grow rapidly--the greater the rate of recruitment (successful broodrearing), the steeper the slope of the growth curve. In the real world, such potential growth is often held back by the lack of nutritious pollen, or by the stresses of toxins, chilling, or pathogens (especially the mite-associated viruses, nosema, or EFB). Any of those can strongly shift the tip point, slowing, or even reversing, the rate of colony growth.
In the last decade, something appears to have shifted that tip point--colonies today seem to more readily go into a downhill spiral and queens no longer hold up as well. Could it be due to pesticides?
Could Pesticides Cause Colony Mortality And CCD?
Of course they could! In 2010, after closely observing the progression of experimentally-induced CCD with my collaborator Dr. Eric Mussen, I published the flow chart below (Fig. 3) to detail the interactions and feedback loops involved in the step-by-step collapse of a colony [10]. At the time, I fully intended to further elaborate upon the contribution of toxins, but didn't get around to it until now.
Figure 3. The positive feedback loops that can lead to colony dwindling and/or sudden depopulation. I've since observed this process take place in sick colonies time and again.
In the above chart, I called out toxins (which would include pesticides) as one of the "Four Horsemen of Bee Apocolypse" (the four factors at top left). Below I've indicated in red those points at which toxins may exacerbate the downhill process (Fig. 4).
Figure 4. Note that toxins can exert lethal or sublethal effects (red bubbles) at every step in the process of colony dwindling or collapse. Pesticides may in some cases be the prime cause of colony mortality; more frequently they might be "contributory factors," especially due the prolonged sublethal effects of residues in the beebread or wax.
Please note that in these charts I'm referring to toxins generically, not specifically to manmade pesticides. Such toxins would include natural plant allelochemicals, industrial pollutants, metals such as arsenic or selenium in soil and dust, fungal and bacterial toxins (which may be altered in beebread by the presence of pesticide residues), beekeeper-applied varroacides, HMF in overheated corn syrup, all in addition to any agricultural pesticides. In the words of ecotoxicologist Dr. Helen Thompson, we must pay attention to the total toxin load of the hive, plus any interactions between those chemicals, as well as other contributory factors [11]--a sentiment also echoed by the Fraziers at Penn State [12]. So, back to our original question: Can toxins, including synthetic pesticides, cause colony morbidity or mortality?
Verdict #1: clearly, synthetic pesticides and varroacides may constitute the most serious toxin load for managed bees in agricultural areas, and have the potential kill a colony outright, or to exacerbate positive feedback loops that can result in dwindling, poor overwintering, or collapse.
But does any pesticide specifically cause CCD--"the disappearance of most, if not all, of the adult honey bees in a colony, leaving behind honey and brood but no dead bee bodies" [13] (and no sign of brood diseases or varroa-induced DWV collapse).
Analysis: The most direct way to answer that question is to see whether we can fulfill Koch's third postulate [14]: can we experimentally create the symptoms of CCD by treating a healthy hive with the pesticide in question?
Verdict #2: to the best of my knowledge, no one has yet duplicated the symptoms of CCD by treating a colony with any pesticide (the most obvious difference being that there are generally plenty of dead bees present in the case of pesticide toxicity). This is notably true for the neonicotinoids, for which any number of researchers have attempted to duplicate CCD symptoms by continually feeding colonies neonic-tainted syrup or pollen.
Hold on--drop those stones! I am not saying that pesticides cannot contributeto CCD or colony morbidity or mortality in general--my chart above clearly illustrates that they have the potential to do so. Yet even those beekeepers who manage to completely avoid pesticides may still experience sudden colony depopulations, dwindling, or excessive winter losses due to some combination the Four Horseman (as in the perfect storm detailed at [15]).
I feel that it is a serious error for us to try to link CCD to pesticides. Pesticides have always been an issue to beekeepers, but CCD-like events have historically come and gone (as in Disappearing Disease--read the description at [16]). Pesticides will remain an issue long after the term "CCD" is forgotten.
Bottom line: Despite the fact that the evidence at hand does not support the case that CCD is directly caused by any pesticide, that fact certainly does not mean that we should ignore pesticide issues. If anything, we beekeepers ourselves have helped to make pesticides even more of an issue these days.
Short Memories
There is a popular myth going around that pesticides only started to become an issue to honey bee colony survival in 2007. In fact, the sublethal effects of pesticides were well known to beekeepers and researchers long before then. If we review the older literature [17], we find that it was already well known that contaminated pollen was a more serious issue to colony health than the in-field kill of foragers. We knew that colonies might collect such tainted pollen from miles away, that dusts were worse than sprays, that young bees may be more susceptible than older bees, and that temperature and humidity had a great deal to do with pesticide toxicity. Pesticide issues were actually far worse in the 1960's and '70's than they are today, and have generally improved since then (not to say that some new issues haven't arisen).
On the other hand, the overall contamination of combs with pesticides has increased in recent years due to the direct contribution by we beekeepers ourselves. In virtually any residue analysis of beebread or beeswax these days in any country with varroa, the most prevalent toxins are the beekeeper-applied varroacides [18]-you may wish to refer back to my chart of the "toxicological eras of honey bee evolution [19].
So one question is, To what degree we have shifted the tip point of colony health by contaminating our brood combs with miticides? Let's explore the broodnest...
The Heart Of The Hive - The Nursery
The insidious, long-term effects of total toxin load (including pesticide and varroacide residues) would be from those that made it into the heart of the hive--the critical stored beebread and the wax of the brood combs (Fig. 5). Note: Dr. David Fischer of Bayer brings to my attention that in the case of imidacloprid, the results of his testing indicates that bees in the hive are more affected by residues in the nectar than by those in the pollen.
Figure 5. Long after a pesticide-sprayed field force has been replaced by newly-recruited foragers, the colony may still need to deal with the lingering effects of pesticide residues in the combs, and especially in the all-important stores of beebread. It is here that such persistent residues can affect colony health and buildup for many months after the initial exposure, and exactly where we should focus our attention.
Here's some food for thought: a toxin need not actually kill a single bee to mess up a colony. There are many ways in which sublethal levels of toxins can negatively affect the colony population curve. A few examples would be:
By decreasing the survival rate of larvae (as from residues of varroacides [20, 21], or fungicides [22]) , or by increasing their development time (as effected by various pollutants, plant alleleochemicals, pesticides, or miticides).
By affecting the proper fermentation of beebread (fungicides).
By affecting the sensitive nurse bees that must digest that beebread and produce the critical jelly used to feed the brood, queen, and other workers (natural plant toxins, pollutants, or pesticides).
By affecting the normal behavioral progression of the workers. E.g., if workers initiate foraging prematurely, this greatly reduces their overall longevity, and results in severe depression of colony growth [23] (much more research is crying to be done, but many chemicals would be suspect).
By requiring bees to allocate precious resources toward the detoxification of the poisons (as per my leaky boat analogy [24]).
By increasing the virulence of varroa, nosema, or viruses (any number of pesticides and miticides have been implicated [25, 26])
By affecting normal colony homeostasis, such as thermoregulation of the brood, which is dependent upon the proper assessment of temperature, and the ability to effectively generate heat by the vibration of the wing muscles (neurotoxins would be expected to affect this ability).
By affecting the longevity of the queen, the viability of spermatozoa, or the ability of a colony to successfully supersede (coumaphos notably had this effect)
By affecting the production of, or normal communication via pheromones (which include the recognition of brood and the queen) [27] (essential oils, formic acid, other pesticides?)
By affecting foragers' ability to communicate by dance, to navigate, to learn (a wide range of pesticides [28]), or to react properly to normal stimuli (neonics can clearly do this [29]; but similar effects could be due to any number of other pesticides).
Bottom line: the toxin load in the broodnest can greatly affect a colony in many ways, generally (but not necessarily always) negatively. The greater the total toxin load with which the colony is forced to deal, the more likely that it will suffer from the combined ill effects.
Industry's Arguments
In order to present an objective review of pesticide issues, we should also hear Industry's side of the argument. The industry-funded think tank OPERA [30] takes the position that:
Although, based on the facts outlined above, there does not appear to be any strong evidence that sublethal effects of pesticides play a key role as causative factors behind bee colony mortality (which is likewise supported by the fact that in several monitoring projects no correlation has been found between colony losses and pesticide exposure), sublethal effects are certainly a point where more fundamental research is needed to obtain a clearer picture of the nature of the issue.
The above statements are factually correct in that there is to date no compelling evidence that pesticides are at the root of the elevated rates of colony mortality seen in recent years, and that more fundamental research is clearly needed. But a long history of practical experience by beekeepers with the sublethal (as well as lethal) effects of pesticides leaves no doubt that pesticides certainly have the potential to cause colony health issues.
But Don't We Already Know That It's The Neonicotinoids?
The media have already tried and convicted the neonicotinoids as the cause of all bee problems, and it's currently fashionable to celebrate the restrictions recently imposed on them by the European Union. But it is rational? No one has ever shown convincing evidence that neonics are linked to colony collapse; conversely, there is abundant experimental and on-the-ground evidence that the residues from seed-treated plants do not appear to cause observable harm to colonies [31].
Planting dust, soil drenches, or foliar applications are a different story, but these are generally drift or misapplication issues, hitting individual apiaries, not the bee population as a whole. Our regulators are well aware of these issues, and working to fix the problems.
Regarding the completely unacceptable bee kills due to the dust from corn seeding, of interest is a recent paper by Drs. Chris Cutler and Cynthia Scott-Dupree [32]--environmental toxicologists from Canada's Dalhousie University--who analyzed the 110 pesticide incident reports received by Canada's PMRA since 2007. Ranking the reports by the degree of severity of the bee kill, they found that there were over five times as many "major incidents" due to non-neonicotinoid products (including carbofuran, chlorpyrifos, coumaphos, diazinon, dimethoate, fluvalinate, formic acid, permethrin, and phosmet) as there were due to neonics, yet that these incidents are largely ignored by the press and beekeepers, who for some reason single-mindedly focus upon the neonics.
Hey, I'm as concerned about pollinators and pesticides as anyone. A recent review by Goulson [33] points out the excessive use of neonics (actually all pesticides are greatly overused), and details the many environmental questions about this class of chemicals. But here's the thing--I can read studies all day long, but what I prefer to seek out are actual on-the-ground, real-life observations. Let me share one with you:
An "Acid Test" Of Neonic Seed Treatment
Activists are calling for a ban on clothianidin--the most common neonicotinoid seed treatment. Although honey bees appear to do just fine on seed-treated canola, their species has an advantage over solitary bees and other pollinators, due to their foraging on multiple plant species over a wide area, their social structure, and their processing of the pollen by nurse bees. So honey bees may not be the best indicator of neonic toxicity.
On the other hand, solitary bee species may be a better indicator as to whether neonic residues cause subtle adverse effects. Many solitary bees are "monovoltine," meaning that they only raise a single generation per year. Because of this, a negative effect on any single female bee could prevent the production of the next generation. It occurred to me that the Alfalfa Leafcutter Bee (Megachile rotundata), which is used to pollinate clothianidin-treated canola (Fig. 6), would provide an excellent "acid test" of clothianidin for several reasons:
Clothianidin has been shown to be highly toxic to leafcutter bees by topical application [34]. Since neonics are typically an order of magnitude more toxic by oral exposure [35], it is reasonable to expect that the leafcutter bee would be even more susceptible to residues consumed in food.
Leafcutter bees do all their foraging within a few hundred feet of the nest [36], so those placed in the middle of a canola field would forage solely upon treated canola.
Each individual female alone forages and provisions her nest, feeding upon the contaminated pollen and nectar as her sole protein and energy sources. If the insecticide negatively affected her behavior, navigational ability, health, or longevity she would be unable to reproduce effectively.
The male bees use canola nectar as their sole energy source, and if the insecticide residues interfered with their behavior or longevity, the female bees might not get properly mated.
The larvae consume a diet consisting solely of unprocessed contaminated pollen and nectar (rather than royal jelly), and thus every item in their diet would contain verified concentrations of clothianidin (approximately 1.7 ppb in the pollen; 0.8 ppb in the nectar [37]). Note: as with honey bees, neonicotinoids are virtually nontoxic to the larvae of the leafcutter bee [38].
The female constructs her nest by cutting (with her mouthparts) leaves from the treated canola plants, which contain even higher residues of clothianidin than the pollen, thus exposing her to even more of the chemical. The larva then develops surrounded by these contaminated leaves, and the pupa overwinters in them.
Figure 6. Tents covering Alfalfa Leafcutter bee nest boxes in a canola field.
In short, the leafcutter bees would constitute the most severe test case for clothianidin exposure from a seed-treated crop. So I phoned a commercial supplier of leafcutter bees in Ontario (who declined to be named) and asked him whether he had any problems with his bees reproducing or overwintering after being set in clothianidin seed-treated canola. He said that he had been rearing them on such fields for many years and did not observe any problem. I put a good deal of faith into such unbiased field experience by a commercial bee man. You can draw your own conclusions.
So Which Pesticides Are Actually To Blame?
It's pretty easy to diagnose an acute bee kill, what with piles of twitching bees in front of the hives (see "Signs and symptoms of bee poisoning" at [39]), and in many cases the responsible pesticide can be identified. To sidetrack briefly, remember when I mentioned a few articles back that the residues in Jim Doan's bee kills did not indicate that the bees contained lethal doses of the chemicals? This made me strongly suspect that we can't apply the LD50 data (in nanograms per bee) to the values obtained from actual field samples of dead bees. The recent report from Canada [40] confirms this. The highest residue level of clothianidin (from corn planting dust) found in any sample of dead bees from the entrances of a hive was 24 ppb, which works out to about a tenth of the theoretical amount necessary to kill a bee . This finding could be due to the metabolic degradation of the insecticide, but it certainly suggest that the LD50 value should be adjusted lower for samples of dead bees! I am greatly heartened that Canada is moving forward in addressing this issue of bee kills from corn planting dust [41].
Overt bee kills aside, more insidious are the residual effects due to contaminated dust, pollen, or nectar that foragers bring back into the broodnest. I'm told by beekeepers with far more experience with pesticides than I, that after exposure to certain pesticides, colony growth and production come to a standstill, sometimes for months, until the colony clears itself of residues and perhaps eventually recovers (or not). The problem is that few beekeepers (if any) can look inside a hive and diagnose which pesticide (or combination thereof) is causing the problem. He may notice spotty brood, poor buildup, winter dwindling, or queenlessness, but it is very hard to isolate the effect any particular pesticide residue, especially in today's stew of residues in combs. But that doesn't mean that we are completely blind...
The Evidence
Due to the rapid turnover of bees in a hive (other than the queen or "winter bees"), if a pesticide were indeed exerting a long-term effect upon colony health, then there would by necessity need to be residues of that pesticide or its degradation products persisting in the combs. With today's testing equipment, we can detect residues to the parts per billion level, and have quite a large database of residue analyses of beebread samples, which we can perhaps use to either finger or exonerate certain pesticides suspected of being involved in colony health issues.
In a court of law, all evidence would be laid out before the court to determine whether it was substantial enough to make a case against a particular suspect. We can do something similar by reviewing two large publicly-available datasets of actual pesticide analyses of beebread from across the country--one by the Penn State team , the other by the USDA (Tables 1 and 2). I've condensed their data to only those pesticide detects that were found in at least 10% (Penn State) or 5% (USDA) of the samples, following this reasoning:
If a pesticide isn't present in at least 10% of samples, then it isn't likely to be the cause of widespread problems.
I've also color-coded the results as to the type of pesticide, and included the median detection level (to help us to determine whether that dose would be expected to cause colony health problems, or whether it would be insignificant).
Pesticide
Present in percent of samples*
Median detection if positive for target (ppb)
Type of pesticide
Fluvalinate
88.3
40.2
Beekeeper-applied miticide
Coumaphos
75.1
13.1
Beekeeper-applied miticide
Chlorpyrifos
43.7
4.4
Insecticide
Chlorothalonil
52.9
35
Fungicide
Pendimethalin
45.7
13.4
Herbicide
Endosulfan I
28
4.2
Insecticide
Endosulfan sulfate
26.3
2.2
Insecticide
DMPF (amitraz)
31.2
75
Beekeeper-applied miticide
Atrazine
20.3
8.9
Herbicide
Endosulfan II
20
3.8
Insecticide
Fenpropathrin
18
7
Insecticide
Azoxystrobin
15.1
10.2
Fungicide
Metolachlor
14.9
8.1
Herbicide
THPI (Captan)
14.2
227
Fungicide
Captan
12.9
103
Fungicide
Esfenvalerate
11.7
3.3
Insecticide
Carbaryl
10.9
36.7
Insecticide
Cyhalothrin
10.9
1.7
Insecticide
Table 1. The 2010 survey by the Penn State team [42], based upon (depending upon the pesticide) either 350 or 247 samples. This study (plus numerous others worldwide) clearly point out that the predominant pesticide residues in brood combs are typically those from the beekeeper-applied miticides (yellow).
Table 2. This 2012 survey by the USDA [43] echoes the previous findings--the only pesticides found in at least 10% of the samples were from either beekeeper-applied miticides or chlorpyrifos. The 99 analyzed samples came from Alabama, California, Colorado, Florida, Idaho, Indiana, New York, South Dakota, Tennessee, Texas, and Wisconsin.
Keep in mind that the above surveys screen only for 174 chosen pesticides--compare this number to the roughly 1000 pesticide active ingredients and adjuvants registered for use in California. I've discussed the composition of this list with USDA's Roger Simonds, who runs the tests. It is prohibitively costly to test for every possible pesticide, so one must arbitrarily draw up a limited list of the chemicals of most concern. All are aware that this is a difficult task, since we don't even know which toxins with which we should be most concerned!
Note that in both surveys, the most common insecticide present was chlorpyrifos- an "old school" (introduced in 1965) organophosphate neurotoxin classified as being "highly toxic" to bees, and marketed as Dursban and Lorsban. Chlorpyrifos was previously widely used by homeowners and residential pest control companies. EPA has since restricted its use due to its toxicity to wildlife and aquatic organisms, and possible links to human health issues [44]--some of the reasons that EPA favors the neonicotinoids as "reduced risk" products.
Oh Boy, Let's Do Some Math!
But just because a pesticide is present, doesn't necessarily mean that it is causing measureable harm. A nurse bee may consume about 10 mg of beebread per day [45], so if she consumed that amount of pollen contaminated with chlorpyrifos at 6.5 ppb, then she would have been dosed with 0.065 ng (1 nanogram = 1 billionth of a gram) of the chemical. The question then is, how much chlorpyrifos does it take to actually harm a bee?
One commonly cited figure is that the LD50 for chlorpyrifos given orally is 360 ng/bee. Compare those figures (360 ng for toxicity vs. 0.065 in the daily diet)! Even though chlorpyrifos is a disturbingly common comb contaminant, it is unlikely that the median detected concentration (alone) would be causing colony health problems (not to say that higher doses don't hurt colonies).
But, you say, some of the neonics are even more toxic than chlorpyrifos. How about the mean 31 ppb found by the USDA in the few samples positive for imidacloprid? The typical nurse bee would consume 0.31 ng, compared to the oral LD50 of about 4-40 ng, so she'd be eating a tenth to a hundredth of the lethal dose. This would be cause for concern, tempered by the fact that a bee can easily metabolize that amount of imidacloprid a day [46]. Such consumption could legitimately be suspected of causing sublethal effects. However, keep in mind that that 31 ppb was an average, which was strongly skewed by a few samples with very high concentrations (which I'd fully expect to cause colony health problems). Plus this is not simply a matter of the average amount of contamination; one must also look at the percentage of positive detects. The Penn State team [47] puts it well:
Our residue results based on 1120 samples which include Mullin et al. (2010) and subsequently more than 230 additional samples do not support sufficient amounts and frequency of imidacloprid in pollen to broadly impact bees.
OK, so how about the varoacides fluvalinate at 40 ppb or the amitraz degradate DMPF at 100 ppb? Surprisingly, I can't find an oral LD50 for fluvalinate, so the contact toxicity figure (200 ng/bee) will need to suffice. Those residues work out to about 1/500th expected toxicity.
Amitraz scored a bit better, with the nurse bees consuming about 0.01 ng--far below the lethal dose. But a recent study found that an oral dose of 0.2 ng of amitraz causes more than a doubling of the heart rate of a bee [48]--that's at 1/20th of the average detect! The authors dryly state:
The above responses clearly show that the heart of the honeybee is extremely vulnerable to amitraz, which is nevertheless still used inside beehives, ostensibly to "protect" the honeybees against their main parasite, Varroa destructor.
How vulnerable? Frazier [49] observed that "Dead and dying bees collected around colonies in association with corn had only residues of 2,4-DMPF at 5,160 ppb." Looks like perhaps the beekeeper inadvertently killed his own bees with an off-label mite treatment that may have overworked their little hearts!
And if those miticide and insecticide residue weren't enough alone, some of the toxicity of these chemicals is additive or synergistic. The Penn State team again says it well:
[The] pyrethroids... were found in 79.4% of samples at 36-times higher amounts than the neonicotinoids, on average... The mean neonicotinoid residue was 37 ppb (scoring non-detects as 0 ppb), of which only 6.7 ppb was imidacloprid. Pyrethroids, by comparison, were present at a mean residue of 106 ppb and a frequency of 80.3% in pollen samples... Indeed, if a relative hazard to honey bees is calculated as the product of mean residue times frequency detected divided by the LD50, the hazard due to pyrethroid residues is three-times greater than that of neonicotinoids detected in pollen samples [emphasis mine].
The pyrethroids are popular because they are relatively nontoxic to humans. But they can sure kill honey bees. More so, they can cause sublethal effects, such as irreversible inhibition of olfactory learning ability [50].
Hey, we're only getting rolling! Mussen [51] pointed out a decade ago that fungicides could kill larvae; recent research from the Tucson lab [52] and elsewhere confirm that fungicide residues can mess up the colony (we sometimes observe this in almonds). Of note is that colonies treated with some fungicides were unsuccessful at requeening themselves! And recent research by Zhu [53] found that the relative toxicity of larvae to the commonly-detected fungicide chlorothalanil was almost 40 times higher than that of chlorpyrifos. Fungicides are frequently found at high concentrations in beebread.
I cannot help from returning to the refrain that instead of limiting our concern to any single pesticide, that we should be looking at the total toxin load that the colony is forced to deal with.
And How About The "Inerts"?
The pesticide detection analyses above do not look at the "inert" adjuvants in the pesticide "formulation." These chemicals not only help to disperse the pesticide over the waxy leaf surface, but also aid in its penetration through the insect cuticle, thus making the pesticide relatively more toxic to the bee!
Mullin and Ciarlo [54, 55] found that:
Formulations usually contain inerts at higher amounts than active ingredients, and these penetrating enhancers, surfactants and adjuvants can be more toxic on non-targets than the active ingredients. For example, we found that the miticide formulation Taktic®️ was four time more orally toxic to adult honey bees than the respective active ingredient amitraz. Impacts of 'inerts' in pollen and nectar alone or in combination with coincident pesticide residues on honey bee survival and behavior are unknown.
The researchers also found that:
Learning was [rapidly] impaired after ingestion of 20 ug of any of the four tested organosilicone adjuvants, indicating harmful effects on honey bees caused by agrochemicals previously believed to be innocuous.
One of the common adjuvants is a solvent NMP, described by BASF [56]:
NMP can be used as a solvent or co-solvent for the formulation of insecticides, fungicides, herbicides, seed treatment products and bioregulators where highly polar compounds are required. NMP is given preference over other highly polar solvents because it is exempt from the requirement of a tolerance when used as a solvent or co-solvent in pesticide formulations applied to growing crops, and it possesses a favorable toxicological and environmental profile.
The key words above are that these toxic solvents are "exempt from tolerance" [57], so they are sprayed all over crops along with the active ingredients of pesticides (including imidacloprid). Yet Zhu [58] recently reported that NMP can rapidly kill bee larvae. The authors conclude that:
Our study suggests that fungicide, the inert ingredient and pesticide interaction should be of high concern to honey bee larvae and overall colony health. None of these factors can be neglected in the pesticide risk assessment for honey bees.
Choosing To Ignore The Obvious
There is no doubt that neonics have the potential to harm bees, but the question is, do they really cause as much problem in the real world as we've been led to believe? This is not a matter of convincing the masses; this is an investigation of fact and evidence. For a pesticide to cause harm to a colony of bees, two necessary elements must occur:
The bees must be exposed to the pesticide. Evidence for this is best determined by chemical analysis of the pollen in the combs, since residues in the bodies of dead bees may be degraded, and because water-soluble insecticides such as the neonics are not absorbed into the wax (residues in the wax do document the history of exposure to lipophilic pesticides).
The pesticide must be present at a concentration above a trivial level.
When we take the time to determine which pesticides bees are actually found in the combs of hives, neonicotinoids are seldom present, or if detected are often at biologically irrelevant concentrations. Imidacloprid was detected in fewer than 3% of Mullin's 350 samples, and clothianidin not at all! Similarly, there were zero detects for clothianidin in the 99 USDA samples; imidacloprid was only present in 9%. Likewise, a number of European studies have shown similar results (reviewed in [59]).
In a recent study, the Fraziers [60] looked at hives placed in cotton, corn, alfalfa, apples, pumpkins, almonds, melons, blueberries, or wild flowers, and identified the residues in collected pollen, in returning foragers, and in dead or dying bees near the hives. Again, the only neonic noted was thiamethoxam in alfalfa (in which dying bees contained residues of ten different pesticides). However, there were alarmingly high detects of fungicides, the insecticide acephate, and the metabolite of the beekeeper-applied miticide amitraz.
The latest data comes from Dr. Jeff Pettis [61], whose group determined the pesticides in bee-collected pollen from six crops: apple, blueberry, cranberry, cucumber, pumpkin, and watermelon. Of the 35 pesticides detected, beekeeper-applied miticides and ag fungicides predominated (sometimes at alarming levels), followed by common organophosphate, pyrethroid, and cyclodiene insecticides (again sometimes at alarming levels). In the 17 samples tested, residues of neonics were only found in the samples from the apple orchards, and only one was found at a biologically-relevant concentration.
So my question is why the heck are so many activists pursuing the single-minded focus upon the neonics, when the clear evidence is that neonics are not commonly found in bee-collected pollen, and if present, are generally at levels that do not appear to negatively affect colony health [62]?
There is a lot more to pesticide issues than the neonics alone, and by focusing our attention solely upon them, we ignore the often far more serious effects of other pesticides.
Blinded By Bias
During the intense focus upon neonicotinoids the past few years, we've learned that exposure of bees to these insecticides can result in all sorts of sublethal effects. Unfortunately, many researchers appear to be wearing blinders as to the effects of other pesticides. The resulting narrowness of these studies skews our perspective--if we only look for effects from the neonics, we don't know how to rank the biological relevance of those effects relative to the effects of all the other toxins to which bees are exposed, generally to greater extent.
A practical complaint to researchers: if you are going to look for sublethal effects of neonics, please include positive controls of some other pesticides, so that we can learn whether the neonics are better or worse than the alternatives!
I commend one group that recently decided to take a look at the effects of a common herbicide upon the development of bee larvae [63]. The results of this straightforward and meticulous study are an eye opener!
The researchers found that exposing bee larvae to even infinitesimal amounts of the herbicide paraquat prevented them from fully developing their critical oenocyte cells (see box).
Oenocyte cells are not only involved in the production of lipids and lipoproteins, but they also appear to play a role in the constitution of external cuticle in both larvae and adults. In addition, they are involved in intermediary metabolism and synthesize hydrocarbons to waterproof cuticle or to make beeswax. Furthermore, oenocytes secrete hormones, especially those involved in larval and adult development. They are also described as the major cells expressing cytochrome P450 reductase, which is involved in detoxification of toxins [information paraphrased from the cited paper].
Exposure to even a part per trillion of paraquat suppressed the development of these extremely important cells. The authors conclude:
This study is the first which reports an effect of a pesticide at the very low concentration of 1 ng/kg, a concentration below the detection limits of the most efficient analytic methods. It shows that chemicals, including pesticides, are likely to have a potential impact at such exposure levels.
Who woulda thunk? Paraquat isn't included in the standard screening for pesticide residues, so we don't even know how prevalent it is in hives! The above findings should make it clear that we need to go back to the beginning if we are to understand the sublethal effects of pesticides (and adjuvants), even at perhaps undetectable levels.
We do know that here were 812,000 lbs of paraquat applied in California in 2010, as opposed to only 266,000 lbs of imidacloprid. Paraquat shows strong adverse effects upon bee larvae at a part per trillion, as compared to imidacloprid, which is so minimally toxic to bee larvae that no one has even been able to determine an LD50! So the amount of paraquat applied has far greater potential to cause problems to bees in agricultural areas (Fig. 7).
Figure 7. The herbicide paraquat appears to be harmful to bee larvae at levels as low as 1 part per trillion. Note the wide variety of crops, and the extensive areas to which it is applied.
So here we have clear scientific data from a well-designed laboratory experiment that a commonly-applied pesticide has the ability to cause immune suppression and other adverse effects in developing bees, yet these results have been virtually ignored by beekeepers and environmental groups. I just don't understand it!
No More Safe Home To Return To
Out of their protective hive, honey bees live in a hostile world, full of predators, deadly weather, and toxic agents (both natural and manmade). But the bees of old could generally return to a "safe" home, in which the transmission of natural toxins was largely minimized by the behavior of foragers, and by the processes of the conversion of nectar to honey, and of pollen into jelly (via the digestion of beebread by nurse bees). Both of these processes help to prevent the transmission of toxins from the foragers to the queen and the brood.
With the advent manmade pesticides, bees may no longer have that "safe" home to return to. Beebread and the wax combs nowadays are often contaminated with any number of pesticides (in addition to natural plant toxins and industrial pollutants). But this is not a "new" problem:
A Historical Artifact
Even before we had the ability to detect pesticide residues in combs to the parts per billion level, pesticide analyses often found easily-detectable levels of insecticides in bee hives. As a frame of reference, I sought out a historical artifact--the residues in the beeswax that had been rendered by beekeepers and reprocessed into a sheet of "clean" foundation. I was lucky enough to find that such a sample had recently been analyzed by the Tucson Bee Lab. Dr. Diana Sammataro forwarded me the results of the analysis of an undated "very old" piece of wax foundation from the Northeast (Table 3).
THIS IS THE TABLE !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!
Pesticides in an old piece of beeswax foundation.
Positive residue detect
ppb
Pendimethalin
13.1
Endrin
156
Dieldrin
160
Trifluralin
3.6
DDT p,p'
32.7
Heptachlor
35.1
Malathion
4.3
Chlorpyrifos
4.6
Dicofol
6.8
PCB's
8190
Chlorothalonil
84.6
Table 3. We can narrow down the foundation's date of manufacture by the residues present. Pendimethalin was first registered in 1972 (the same year that DDT was banned), and since there were no residues of fluvalinate, the foundation was clearly produced prior to the arrival of varroa around 1990. Thanks to Dr. Diana Sammataro and the Tucson Bee Lab.
Clearly, pesticide-contaminated combs are hardly a new phenomenon. In the above example, the beeswax batch used to produce the foundation came not from a single hive, but rather from the combined wax from many hives, likely from many beekeepers, and thus would represent an average sample of the degree of contamination somewhere in that 1972-1990 time frame. And that doesn't take into account whether the raw wax came mainly from cappings (which would have been minimally contaminated), or whether it went through the common practice of being filtered through activated carbon. But any colony started on such foundation purchased from a beekeeping supply house would clearly have had to deal with at least the residues of these lipophilic toxins from the get go!
An aside: perhaps of interest is something that I noticed years ago when I switched from dipping my own wax queen cell cups to using plastic cups. My "take" rate became better and more consistent. Was that because the beeswax at the time was contaminated with residues?
The Beekeeper Contribution To Shifting The Tip Point
One thing that is "new" is that since the arrival of varroa, we've upped the ante--all commercial beeswax is now contaminated with residues of beekeeper-applied synthetic miticides. The three most prevalent synthetic chemicals found in combs today all get there by being applied by beekeepers for mite control.
Practical note: And although there is no reason to be concerned about the tainting of honey by the legal use of these miticides, the beekeeper/applicator should be aware that both amitraz and tau-fluvalinate make California's list of "chemicals known to the State to cause reproductive toxicity," and coumaphos is of concern because it is a "cholinesterase-inhibiting pesticide." No varroacide is harmless to bees [64]--but the benefits of mite control generally (but not always) outweigh the adverse effects due to the miticide residues.
We beekeepers have clearly shifted the baseline for pesticide contamination of combs, which increases the total toxic load even before the contribution by agricultural pesticides.
Stop Right There!
Although it is a very attractive hypothesis to blame our problems on miticide or pesticide residues, let's do a reality check. On good forage in good weather, plenty of beekeepers see their colonies thrive even on old, dark, seriously-contaminated combs; but under stressful conditions those same residues might contribute to poor colony performance or even mortality.
No study has yet found support for the hypothesis that miticide residues are the cause of our current bee problems (although one would have every reason to suspect that they may contribute). In fact, vanEngelsdorp [65] found that surprisingly, higher levels of coumaphos residues negatively correlated with colony survival. How could this be? One possible explanation is that those beekeepers who used it experienced better mite control. But there is also another intriguing possibility--hormetic effects.
Undetectable Levels And Hormesis
Is your head spinning yet? I've presented evidence that undetectable levels of some pesticides could harm bees, that "inert" adjuvants can do the same, and that combs are often chock full of all sorts of pesticide and varroacides residues. Criminy, it's a wonder that bees survive at all! Or is it?
Bees have long been exposed to all sorts of natural, and recently, manmade toxins, and survived. Toxicity is a complicated subject. The only thing that separates a medicine from a poison is the dose. In general, if a pesticide has been tested upon adult and larval bees and found to have no observable adverse effects at a certain concentration, we would not expect to see adverse effects at lower concentrations. However, there are exceptions to this general rule--toxicity may vary up or down depending upon the dose [66]!
I've previously mentioned the term hormesis [67]-- the paradoxical effect of toxins at low concentrations. The paradox is that although most chemicals are toxic at high concentrations, the majority are likely beneficial at low concentrations. For those interested in this fascinating phenomenon, I suggest Dr. Chris Cutler's excellent and thought-provoking review [68]. It is not only possible, but actually probable that lose doses of pesticides may exert a beneficial effect upon a colony! (Don't be ridiculous--I'm not suggesting that bees are better off for the presence of pesticides!).
Wrap Up
Toxins, whether natural or manmade, are clearly a potential issue in colony health. To what degree pesticides contribute to colony morbidity or mortality is dependent upon exposure, the dose, and a host of associated factors. Beekeepers have long noticed that their bees often do better if allowed to forage on pesticide-free land. But many beekeepers today tell me that their bees do just fine in the middle of intense agricultural areas--so this is not a black or white situation.
In recent years beekeepers themselves have greatly added to the degree of contamination of their combs. Introductions of novel pesticides and adjuvants keep changing the picture. And now we're finding that pesticides that we formerly assumed were harmless to bees (fungicides and herbicides) may actually be quite toxic to larvae! Then there is the scary finding that undetectable levels of some pesticides might cause health issues, countered by the fascinating subject of hormesis.
I certainly do not profess to understand all this, but I have come to the following conclusions:
That bees have had to deal with toxins for a long time,
That pesticides will be with us for the foreseeable future,
That varroacides have likely added to the problem,
That pesticides can cause lethal and long-term sublethal effects in the hive, but
That many beekeepers in agricultural areas no longer consider pesticides to be a serious issue, whereas,
That colonies may go downhill after being exposed to some agricultural chemicals, or combinations thereof,
That toxicology in the hive is complex, and that there are few simple answers,
That it is unlikely that any single pesticide is to blame for our current colony health issues,
That we still have a lot to learn!
Next month I will look at the distribution of both managed colonies and of pesticide applications in the United States, and their relationship to bee health problems.
Acknowledgements
As always, I could not research these articles without the assistance of my longtime collaborator Peter Loring Borst, to whom I am greatly indebted. I also wish to thank Drs. Jim and Maryann Frazier, Chris Mullin, David Fischer, Eric Mussen, Thomas Steeger, and Roger Simonds for their generosity in taking the time to discuss pesticide issues with me.
References
[1] Rucker, RR and WN Thurman (2012) Colony collapse disorder: the market response to bee disease. http://perc.org/sites/default/files/ps50.pdf
[2](Broken Link) http://perc.org/articles/everyone-calm-down-there-no-bee-pocalypse
[3] vanEngelsdorp, D and MD Meixner (2010) A historical review of managed honey bee populations in Europe and the United States and the factors that may affect them. Journal of Invertebrate Pathology 103: S80-S95. http://www.sciencedirect.com/science/article/pii/S0022201109001827
[4] http://thebreakthrough.org/index.php/journal/past-issues/issue-1/an-environmental-journalists-lament/
[5] vanEngelsdorp and Meixner (2010) op. cit.
[6] Rucker (2012) op. cit.
[7] https://scientificbeekeeping.com/sick-bees-part-18f-colony-collapse-revisited-pesticides/
[8] https://scientificbeekeeping.com/the-extinction-of-the-honey-bee/
[9] https://scientificbeekeeping.com/historical-pesticide-overview/
[10] https://scientificbeekeeping.com/sick-bees-part-2-a-model-of-colony-collapse/
[11] Thompson, HM (2012) Interaction between pesticides and other factors in effects on bees. http://www.efsa.europa.eu/en/supporting/doc/340e.pdf
[12] Frazier, J, et al (2011) Pesticides and their involvement in colony collapse disorder. http://www.extension.org/pages/60318/pesticides-and-their-involvement-in-colony-collapse-disorder#.UgO3zKyaucw A must read!
[13] http://www.ars.usda.gov/is/AR/archive/jul12/colony0712.htm
[14] For an explanation refer to https://scientificbeekeeping.com/sick-bees-part-18b-colony-collapse-revisited/
[15] https://scientificbeekeeping.com/what-happened-to-the-bees-this-spring/
[16] Wilson, WT and DM Menapace (1979) Disappearing disease of honey bees: A survey of the United States. ABJ March 1979: 185-186.
"Certainly with both pesticide-related and [Disappearing Disease]-caused bee losses, the adult population of a colony may be reduced rapidly to a "handful" of bees or, in some cases, the entire population may be lost.
"However, in the case of pesticide poisoning, there is usually evidence of pesticide application...the worker bees either die in the field or in or near the hive depending on the type of pesticide. When the field force is killed and they "disappear," many dead or dying bees may be seen on the ground in the field or on the ground between the treated field and the apiary...If the foraging bees bring poison into the hive, then the nurse bees either die in the hive or at the entrance so one can see many crawling and tumbling adults and large amounts of neglected brood. Exposure to pesticides over an extended period results in very weak colonies, and some die out.
"In the case of [Disappearing Disease], the situation is quite different. The colonies frequently have gone through a period o nectar and pollen collection with active brood rearing [as in typical CCD]. Then the weather has turned unseasonably cool and damp and remained adverse for from about 3 to 14 days...During the inclement weather, the bee populations dwindle because the worker bees disappear from the hive leaving a "handful" of bees and the queen. Often these small populations recover and increase in size during hot weather and a long nectar flow or, or occasionally, the entire population absconds..."
[17] Johansen CA and DF Mayer (1990) Pollinator Protection: A Bee & Pesticide Handbook. Wicwas Press.
[18] Mullin CA, Frazier M, Frazier JL, Ashcraft S, Simonds R, et al. (2010) high levels of miticides and agrochemicals in North American apiaries: Implications for honey bee health. PLoS ONE 5(3): e9754. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0009754
[19] https://scientificbeekeeping.com/sick-bees-part-18f2-colony-collapse-revisited-plant-allelochemicals/
[20] Wu JY, CM Anelli, WS Sheppard (2011) Sub-lethal effects of pesticide residues in brood comb on worker honey bee (Apis mellifera) development and longevity. PLoS ONE 6: e14720 http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0014720
[21] Medici SK, Castro A, Sarlo EG, Marioli JM, Eguaras MJ (2012) The concentration effect of selected acaricides present in beeswax foundation on the survival of Apis mellifera colonies. J Apic Res 51: 164-168
[22] Eric C. Mussen, Julio E. Lopez, and Christine Y. S. Peng (2004) effects of selected fungicides on growth and development of larval honey bees, Apis mellifera L. (Hymenoptera: Apidae). Environmental Entomology 33(5):1151-1154.
[23] Frazier, J.L., M.T. Frazier, C.A. Mullin & W. Zhu - Does the reproductive ground plan hypothesis offer a mechanistic basis for understanding declining honey bee health? http://www.extension.org/pages/58650/proceedings-of-the-american-bee-research-conference-2011#.UhDTZX-aucw
[24] https://scientificbeekeeping.com/sick-bees-part-18f2-colony-collapse-revisited-keeping-a-leaky-boat-afloat/
[25] Wu JY, Smart MD, Anelli CM, Sheppard WS (2012) Honey bees (Apis mellifera) reared in brood combs containing high levels of pesticide residues exhibit increased susceptibility to Nosema (Microsporidia) infection. J Invert Path 109: 326-329
[26] Pettis JS, Lichtenberg EM, Andree M, Stitzinger J, Rose R, et al. (2013) Crop Pollination Exposes Honey Bees to Pesticides Which Alters Their Susceptibility to the Gut Pathogen Nosema ceranae. PLoS ONE 8(7): e70182. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0070182#pone.0070182-Chaimanee1
[27] Maisonnasse A, et al (2010) E-b-Ocimene, a volatile brood pheromone involved in social regulation in the honey bee colony (Apis mellifera). PLoS ONE 5(10): e13531. http://www.plosone.org/article/info:doi/10.1371/journal.pone.0013531 These researchers studied (E)-b-ocimene, a volatile terpene commonly produced by plants to attract predatory mites, but also a critical pheromone produced by the brood and the queen.
[28] Decourtye A, et al. (2005) Comparative sublethal toxicity of nine pesticides on olfactory learning performances of the honeybee Apis mellifera. Archives of Environmental Contamination and Toxicology 48: 242-250. http://www.environmental-expert.com/Files/6063/articles/4909/QM245Q254G1T6X0R.pdf
[20] Yang E-C, Chang H-C, Wu W-Y, Chen Y-W (2012) Impaired olfactory associative behavior of honeybee workers due to contamination of imidacloprid in the larval stage. PLoS ONE 7(11): e49472. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0049472
[30] Bee health in Europe -Facts & figures 2013. OPERA http://operaresearch.eu/files/repository/20130122162456_BEEHEALTHINEUROPE-Facts&Figures2013.pdf
[31] The study by Drs. Scott-Dupree and Cutler is yet unpublished, but a summary can be found at http://www.producer.com/daily/ontario-field-study-finds-no-link-between-seed-treatments-bee-deaths/
[32] Cutler, GC, CD Scott-Dupree, DM Drexler (2013) Honey bees, neonicotinoids, and bee incident reports: the Canadian situation. Pest Management Science http://onlinelibrary.wiley.com/doi/10.1002/ps.3613/abstract
[33] Goulson, Dave (2013) An overview of the environmental risks posed by neonicotinoid insecticides. Journal of Applied Ecology 50: 977-987. https://www.sussex.ac.uk/webteam/gateway/file.php?name=goulson-2013-jae.pdf&site=411
[34] Scott-Dupree, CD, et al (2009) Impact of currently used or potentially useful insecticides for canola agroecosystems on Bombus impatiens (Hymenoptera: Apidae), Megachile rotundata (Hymentoptera: Megachilidae), and Osmia lignaria (Hymenoptera: Megachilidae). J Econ Entomol 102(1):177-82.
[35] Blacquiere, et al (2012) Neonicotinoids in bees: a review on concentrations, side-effects and risk assessment http://www.gesundebiene.at/wp-content/uploads/2012/02/Neonicotinoide-in-bees.pdf
[36] Hobbs, GA (1967) Domestication of Alfalfa Leaf-cutter Bees. Canada Dept. of Agriculture. Ottawa: Queen's Printer and Controller of stationary.
[37] Dr. Jerry Bromenshenk, pers. com.
[38] Abbott, VA, et al (2008) Lethal and sublethal effects of imidacloprid on Osmia lignaria and clothianidin on Megachile rotundata (Hymenoptera: Megachilidae). J Econ Entomol 101(3):784-96.
[39] http://pfspbees.org/sites/pfspbees.org/files/resource-files/pnw591.pdf
[40] PMRA (2013) Evaluation of Canadian Bee Mortalities Coinciding with Corn Planting in Spring 2012.
[41] PMRA (2013) Action to Protect Bees from Exposure to Neonicotinoid Pesticides http://www.hc-sc.gc.ca/cps-spc/alt_formats/pdf/pest/part/consultations/_noi2013-01/noi2013-01-eng.pdf
[42] Mullin CA, et al. (2010) op. cit.
[43] Rennich, K, et. al (2012) 2011-2012 National Honey Bee Pests and Diseases Survey Report. http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
[44] Christensen, K.; Harper, B.; Luukinen, B.; Buhl, K.; Stone, D. 2009. Chlorpyrifos Technical Fact Sheet; National Pesticide Information Center, Oregon State University Extension Services. http://npic.orst.edu/factsheets/chlorptech.pdf.
[45] Rortais, A (2005) Modes of honeybees exposure to systemic insecticides: estimated amounts of contaminated pollen and nectar consumed by different categories of bees. Apidologie 36: 71-83.
[46] Cresswell, JE, et al (2012) Differential sensitivity of honey bees and bumble bees to a dietary insecticide (imidacloprid). Zoology 115: 365- 371.
[47] Frazier (2011) op. cit.
[48] Papaefthimiou, C, et al (2013) Biphasic responses of the honeybee heart to nanomolar concentrations of amitraz. Pesticide Biochemistry and Physiology 107(1): 132-137. http://www.sciencedirect.com/science/article/pii/S0048357513001120
[49] Frazier, et al (2011) Assessing the reduction of field populations in honey bee colonies pollinating nine different crops. ABRC 2011
[50] Tan K, Yang S, Wang Z, Menzel R (2013) Effect of flumethrin on survival and olfactory learning in honeybees. PLoS ONE 8(6): e66295. doi:10.1371/journal.pone.0066295. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0066295
[51] Mussen, et al (2004) op. cit.
[52] http://www.abfnet.org/associations/10537/files/Dr.%20Gloria%20DeGrandi%20Hoffman_GS.mp3
[53] Zhu, W., D. Schmehl & J. Frazier (2011) Measuring and predicting honey bee larval survival after chronic pesticide exposure http://www.extension.org/pages/58650/proceedings-of-the-american-bee-research-conference-2011#.UhDTZX-aucw
[54] Mullin, C.A., J. Chen, W. Zhu, M.T. Frazier & J.L. Frazier - The formulation makes the bee poison. ABRC 2013
[55] Ciarlo TJ, Mullin CA, Frazier JL, Schmehl DR (2012) Learning impairment in honey bees caused by agricultural spray adjuvants. PLoS ONE 7(7): e40848. doi:10.1371/journal.pone.0040848
[56] (Broken Link!) http://www2.basf.us/diols/bcdiolsnmp.html
[57] http://www.epa.gov/opprd001/inerts/methyl.pdf
[58] Zhu, et al (2011) op. cit.
[59] Blacquiere, T, et al (2012) Neonicotinoids in bees: a review on concentrations, side-effects and risk assessment. Ecotoxicology 21(4): 973-992. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3338325/
[60] Frazier, M.T., S. Ashcraft, W. Zhu & J. Frazier - Assessing the reduction of field populations in honey bee colonies pollinating nine different crops http://www.extension.org/pages/58650/proceedings-of-the-american-bee-research-conference-2011#.UhDTZX-aucw
[61] Pettis, et al (2013) op. cit.
[62] A recent study confirm that the neonic residues in corn, soy, and canola pollen are at very low concentrations. Henderson, C.B. a, J.J. Bromenshenka, D.L. Fischerb. Clothianidin exposure levels from bee-collected pollen and nectar in seed-treated corn and canola plantings. ABRC 2013 http://bees.msu.edu/wp-content/uploads/2013/01/ABRC-abstracts-2013.pdf
[63] Cousin M, Silva-Zacarin E, Kretzschmar A, El Maataoui M, Brunet J-L, et al. (2013) Size changes in honey bee larvae oenocytes induced by exposure to paraquat at very low concentrations. PLoS ONE 8(5): e65693. doi:10.1371/journal.pone.0065693 http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0065693
[64] Boncristiani, H., et. al. (2011) Direct effect of acaricides on pathogen loads and gene expression levels of honey bee Apis mellifera. Journal of Insect Physiology. 58:613-620.
[65] vanEngelsdorp, D, et al () Weighing risk factors associated with bee colony collapse disorder by classification and regression tree analysis. J. Econ. Entomol. 103(5): 1517-1523. (Broken Link!) http://www.eclecticparrot.com.au/research_papers/VanEngelsdorp%202010%20Weighing%20risk%20factors%20in%20Bee%20CCD.pdf
[66] Cutler GC, Ramanaidu K, Astatkie T, and Isman MB. (2009) Green peach aphid, Myzus persicae (Hemiptera: Aphididae), reproduction during exposure to sublethal concentrations of imidacloprid and azadirachtin. Pest Manag Sci 65:205-209
[67] https://scientificbeekeeping.com/sick-bees-part-18f2-colony-collapse-revisited-plant-allelochemicals/
[68] Cutler, GC (2013) Insects, insecticides and hormesis: evidence and considerations for study. Dose-Response 11:154-177 (Broken Link!) http://dose-response.metapress.com/app/home/contribution.asp?referrer=parent&backto=issue,2,11;journal,3,34;linkingpublicationresults,1:119866,1
Category: Colony Health - Diseases, Viruses, CCD
Tags: collapse, colony, pesticides, sick bees | collapse Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/collapse/ |
Does Oxalic Acid Treatment of Nucs Affect Honey Production?
First published in: American Bee Journal, December 2013
BEEKEEPER-FUNDED RESEARCH
Does Oxalic Acid Treatment Of Nucs Affect Honey Production?
Randy Oliver
ScientificBeekeeping.com
Originally published in ABJ Dec 2013
Last year I ran two trials to see whether I could take advantage of the brief window of opportunity which occurs 19 days after starting nucs with queen cells, during which the mites are forced out of the brood. I detailed the theory, timing, and procedure in a previous article [1]. The result was that treating nucs with an oxalic dribble was highly effective against varroa, and appeared to lead to increased colony strength. However, in one replicate, it appeared that the oxalic treatment may have reduced subsequent honey production. So I ran another trial this spring to confirm whether that was indeed the case.
Introduction
Varroa management is much easier if you begin the season with mites reduced to the lowest possible level. The problem is that colonies in the springtime are full of brood, which provides the mite with a place to hide from treatments. By inducing a period of broodlessness, the beekeeper can force all the mites out onto the adult bees, where they are exposed to the action of the mite treatment of your choice.
A very brief period of such broodlessness occurs when one makes up nucs using queen cells (as opposed to with a caged queen). With careful timing, one can obtain a high efficacy mite kill by applying a safe, inexpensive, and quick treatment of oxalic acid dribbled in sugar syrup. Although oxalic acid is considered to be a "natural" and "organic" treatment, a concentration high enough to kill mites is somewhat stressful to bees. The point of treatment, though, is that the short-term stress from the treatment should be more than compensated for by the long-term benefits to colony health and productivity by the knockback of the mite infestation rate.
This experiment was designed to test whether such an oxalic dribble of nucs would negatively affect the honey production of treated colonies in the ensuing months.
Materials And Methods/Trial Log
April 14, 2013 Made up a batch of 4-frame nucs, Italian stock, set in their own yard in the Sierra Foothills.
April 15 Installed 10-day queen cells from single mother.
May 2 Checked nucs for queenrightness; good take. Equalized the queenright nucs to 5 frames of bees using frames from the queenless nucs. Total count 37 colonies. There was some comb whitening from the spring honey flow and the colonies appeared healthy. I flipped a coin to randomly assign the hives to be treated (n = 19) and applied approx. 5 mL of 3.2% w:v oxalic syrup [2] applied by a garden sprayer set to a slow stream (field calibrated with a graduated cylinder).
May 10 Worked all colonies into singles, rechecking for queenrightness and brood health; added drawn brood combs and recorded starting weight of each hive. Most colonies were roughly equal in strength--a strong 5 frames of bees with 4 frames of brood. Colonies had been set back slightly by poor weather last week, but were showing a fair nectar shake this day. Good weather in forecast; the main honey flow about to begin.
May 11 In order to minimize the effect of any introduced nosema or EFB on the drawn comb, and to stimulate the colonies, I fed all 1/2 gal 1:1 sucrose syrup containing 95mg fumagillin and 100mg OTC per hive.
May 20 Blackberries (our main source of nectar) were coming into bloom, but disappointingly, there was only minimal nectar shake. Most colonies 6-10 frames strength. Weighed hives again (Fig. 1) and added a weighed deep second deep of foundation to all.
Figure 1. My sons Eric and Ian weighing a hive on a digital scale (placed under the empty package cage).
May 30 Unfortunately, it is clear that our expected main flow is not happening, apparently due to the winter drought. Fed 1/2 gal 1:1 syrup to stimulate the bees to forage.
June 10 Fed 1/2 gal 1:1 syrup
June 14 Blackberry bloom mostly over, minor nectar shake. Weighed all hives for the final time. Checked the two anomalous light-weight hives and censored both; one had gone queenless, and one had requeened itself.
Results
There was, as we typically observe, a wide colony-to-colony variation in weight gain (Fig. 2).
Figure 2. The amount of weight gain per hive (treated and controls combined) followed a normal distribution. Mean weight gain was 26 lbs (median 27 lbs). The highest producing colony was in the oxalic group. The three half gallons of fed syrup contained a total of 7.5 lbs of sugar per hive, which would be expected to have contributed to that amount of the weight gain. This was a very poor honey crop, but likely adequate to determine whether oxalic treatment substantially affected honey production.
At the first weighing (Day 25), the treated colonies, on average, put on slightly less weight, but the difference was not statistically significant (Fig. 3). At the second weighing (Day 59) the treated hives weighed slightly more on average, but again the difference was not statistically significant.
Figure 3. There was no significant difference in weight gain between groups at either time point.
Discussion
The typical great degree of colony variation, even in hives started with sister queens and kept in the same yard, often makes it difficult to tease out any minor effect of treatment. However, in particular trial there did not appear to be any substantial negative effect due to oxalic acid treatment.
The efficacy of treatment, as shown in the original trials, could be improved by blasting the parent hives with formic acid prior to making up the nucs. Any loss of the old queens would not be important, since the colonies were going to be nuked up anyway. I suspect that such a one-two combination of "natural" treatments would result in very low mite levels in the nucs.
Other treatments, such as Hopguard strips or powdered sugar dusting, might also be possibilities for working into this sort of mite management. All told, I find that this simple mite management method is safe and inexpensive, does not leave persistent residues in the combs, and does not appear to negatively affect honey production. In my own operation, we have now treated over 2000 nucs in this manner, and are pleased with the results.
Acknowledgements
Thanks to local beekeepers Fosten Wilson and Rick Blaski for their help in the field. Funding for this experiment came from beekeeper donations to ScientificBeekeeping.com, with special thanks to the Beekeepers Association of Southern California and to the beekeepers contracting with Scientific Ag Company. I am happy to share the raw data from any beekeeper-funded trials.
References
1 Simple Early Treatment of Nucs Against Varroa, ABJ April 2012
2 https://scientificbeekeeping.com/oxalic-acid-treatment-table/
Category: Varroa Management
Tags: honey production, nucs, oxalic acid treatment | honey production Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/honey-production/ |
Does Oxalic Acid Treatment of Nucs Affect Honey Production?
First published in: American Bee Journal, December 2013
BEEKEEPER-FUNDED RESEARCH
Does Oxalic Acid Treatment Of Nucs Affect Honey Production?
Randy Oliver
ScientificBeekeeping.com
Originally published in ABJ Dec 2013
Last year I ran two trials to see whether I could take advantage of the brief window of opportunity which occurs 19 days after starting nucs with queen cells, during which the mites are forced out of the brood. I detailed the theory, timing, and procedure in a previous article [1]. The result was that treating nucs with an oxalic dribble was highly effective against varroa, and appeared to lead to increased colony strength. However, in one replicate, it appeared that the oxalic treatment may have reduced subsequent honey production. So I ran another trial this spring to confirm whether that was indeed the case.
Introduction
Varroa management is much easier if you begin the season with mites reduced to the lowest possible level. The problem is that colonies in the springtime are full of brood, which provides the mite with a place to hide from treatments. By inducing a period of broodlessness, the beekeeper can force all the mites out onto the adult bees, where they are exposed to the action of the mite treatment of your choice.
A very brief period of such broodlessness occurs when one makes up nucs using queen cells (as opposed to with a caged queen). With careful timing, one can obtain a high efficacy mite kill by applying a safe, inexpensive, and quick treatment of oxalic acid dribbled in sugar syrup. Although oxalic acid is considered to be a "natural" and "organic" treatment, a concentration high enough to kill mites is somewhat stressful to bees. The point of treatment, though, is that the short-term stress from the treatment should be more than compensated for by the long-term benefits to colony health and productivity by the knockback of the mite infestation rate.
This experiment was designed to test whether such an oxalic dribble of nucs would negatively affect the honey production of treated colonies in the ensuing months.
Materials And Methods/Trial Log
April 14, 2013 Made up a batch of 4-frame nucs, Italian stock, set in their own yard in the Sierra Foothills.
April 15 Installed 10-day queen cells from single mother.
May 2 Checked nucs for queenrightness; good take. Equalized the queenright nucs to 5 frames of bees using frames from the queenless nucs. Total count 37 colonies. There was some comb whitening from the spring honey flow and the colonies appeared healthy. I flipped a coin to randomly assign the hives to be treated (n = 19) and applied approx. 5 mL of 3.2% w:v oxalic syrup [2] applied by a garden sprayer set to a slow stream (field calibrated with a graduated cylinder).
May 10 Worked all colonies into singles, rechecking for queenrightness and brood health; added drawn brood combs and recorded starting weight of each hive. Most colonies were roughly equal in strength--a strong 5 frames of bees with 4 frames of brood. Colonies had been set back slightly by poor weather last week, but were showing a fair nectar shake this day. Good weather in forecast; the main honey flow about to begin.
May 11 In order to minimize the effect of any introduced nosema or EFB on the drawn comb, and to stimulate the colonies, I fed all 1/2 gal 1:1 sucrose syrup containing 95mg fumagillin and 100mg OTC per hive.
May 20 Blackberries (our main source of nectar) were coming into bloom, but disappointingly, there was only minimal nectar shake. Most colonies 6-10 frames strength. Weighed hives again (Fig. 1) and added a weighed deep second deep of foundation to all.
Figure 1. My sons Eric and Ian weighing a hive on a digital scale (placed under the empty package cage).
May 30 Unfortunately, it is clear that our expected main flow is not happening, apparently due to the winter drought. Fed 1/2 gal 1:1 syrup to stimulate the bees to forage.
June 10 Fed 1/2 gal 1:1 syrup
June 14 Blackberry bloom mostly over, minor nectar shake. Weighed all hives for the final time. Checked the two anomalous light-weight hives and censored both; one had gone queenless, and one had requeened itself.
Results
There was, as we typically observe, a wide colony-to-colony variation in weight gain (Fig. 2).
Figure 2. The amount of weight gain per hive (treated and controls combined) followed a normal distribution. Mean weight gain was 26 lbs (median 27 lbs). The highest producing colony was in the oxalic group. The three half gallons of fed syrup contained a total of 7.5 lbs of sugar per hive, which would be expected to have contributed to that amount of the weight gain. This was a very poor honey crop, but likely adequate to determine whether oxalic treatment substantially affected honey production.
At the first weighing (Day 25), the treated colonies, on average, put on slightly less weight, but the difference was not statistically significant (Fig. 3). At the second weighing (Day 59) the treated hives weighed slightly more on average, but again the difference was not statistically significant.
Figure 3. There was no significant difference in weight gain between groups at either time point.
Discussion
The typical great degree of colony variation, even in hives started with sister queens and kept in the same yard, often makes it difficult to tease out any minor effect of treatment. However, in particular trial there did not appear to be any substantial negative effect due to oxalic acid treatment.
The efficacy of treatment, as shown in the original trials, could be improved by blasting the parent hives with formic acid prior to making up the nucs. Any loss of the old queens would not be important, since the colonies were going to be nuked up anyway. I suspect that such a one-two combination of "natural" treatments would result in very low mite levels in the nucs.
Other treatments, such as Hopguard strips or powdered sugar dusting, might also be possibilities for working into this sort of mite management. All told, I find that this simple mite management method is safe and inexpensive, does not leave persistent residues in the combs, and does not appear to negatively affect honey production. In my own operation, we have now treated over 2000 nucs in this manner, and are pleased with the results.
Acknowledgements
Thanks to local beekeepers Fosten Wilson and Rick Blaski for their help in the field. Funding for this experiment came from beekeeper donations to ScientificBeekeeping.com, with special thanks to the Beekeepers Association of Southern California and to the beekeepers contracting with Scientific Ag Company. I am happy to share the raw data from any beekeeper-funded trials.
References
1 Simple Early Treatment of Nucs Against Varroa, ABJ April 2012
2 https://scientificbeekeeping.com/oxalic-acid-treatment-table/
Category: Varroa Management
Tags: honey production, nucs, oxalic acid treatment | oxalic acid treatment Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/oxalic-acid-treatment/ |
Testing of Bee Feed Syrups for Neonicotinoid Residues
First published in: American Bee Journal, August, 2012
Testing Of Bee Feed Syrups For Neonicotinoid Residues
Eric Mussen1 and Randy Oliver2
First Published in ABJ in August 2012
The widespread adoption of the systemic neonicotinoid insecticides has led a number of beekeepers to question whether the commercially available corn, beet, or cane sugar syrups might be contaminated with residues of those insecticides.
Introduction
Beekeepers often feed some form of sugar syrup to colonies for either buildup or winter stores. The raw materials for sugar production come mainly from three cultivated crops-traditionally sugar cane or sugar beets, from which sucrose is extracted; or from corn (maize), from which high fructose corn syrup (HFCS) is produced.
In recent years, growers have widely adopted the practice of treating corn and sugar beet seed with systemic neonicotinoid insecticides [1, 2, 3], and clothianidin may be used on sugar cane in some areas [4]. The understanding that these insecticides are "systemic" (transported throughout the plant tissues) has led some beekeepers to question whether residues may make it into the final sugar product.
We submitted samples of the bee feed syrups offered by two major U.S. suppliers for independent testing. Residues of neonicotinoid insecticides, as well as their degradation products, can be multiply-detected at as little as ppb levels by modern analytical instrumentation [5].
Materials And Methods
We solicited samples of syrups (Table 1) from Stuart Volby of Mann Lake Ltd. (Mann Lake, MN) and from Dadant (Chico, CA) branch manager John Gomez, which we reshipped for testing to Roger Simonds, Laboratory Manager of the USDA Agricultural Marketing Service lab. We requested analyses for neonicotinoid insecticides and their principal degradates.
Supplier Manufacturer Syrup Type
Mann Lake Ltd. Cargill Type 55 HFCS
Type 42 HFCS
Liquid sucrose (beet)
Liquid sucrose (cane)
Dadant & Sons, Inc. (Chico branch) Archer Daniels Midland (ADM) California blend:
50% Type 42 HFCS
50% Liquid sucrose (cane)
Table 1. Bee feed syrups submitted for analysis.
1 Extension Apiculturist, University of California, Davis, CA 95616
2 Proprietor, Golden West Apiaries, Grass Valley, CA 95945
Results
None of the tested samples contained detectable levels of either the neonicotinoid parent compounds or their degradates (Fig. 1).
Figure 1. Typical test results. The LOD is the "limit of detection," i.e., the lowest concentration in parts per billion (ppb) that the instrument can detect. The lab tested for both parent compounds (e.g., imidacloprid) as well as for the degradation products of the insecticides, which may also exhibit toxicity.
Discussion
Although no residues were detected in the syrup samples submitted for testing, the possibility exists that there were residues below the limit of detection (1 ppb for most of the parent compounds). However, levels below 1 ppb are generally accepted as being well below the no observable adverse effects concentration (NOAEC) [6].
These results are not surprising for HFCS, given that when the USDA tested 655 samples of corn grain in 2007 [7], no residues of neonicotinoid insecticides were detected. Although the tolerance level for clothianidin in sugar beets is 20 ppb [8], there are often no detectable residues from beets in the field [9]. Similarly, there were no detectable residues in the sample of beet sugar that we submitted.
Although this was a very limited sampling, it gave no evidence that beekeepers need to be concerned about neonicotinoid insecticide residues in feed syrups from the major suppliers.
Acknowledgements
Thanks to the cooperation of Stuart Volby and John Gomez for supplying samples, Roger Simonds for expediting the analyses, and to the U.C. Davis Extension Apiculture Program for providing funds for sample analyses.
References
[1] Anon (2012) 2012 Corn Insect Control Recommendations. http://eppserver.ag.utk.edu/redbook/pdf/corninsects.pdf
[2] Valent (2011) Valent USA Announces NipsIt™️ SUITE Sugar Beet Seed Treatment System. http://www.seedtoday.com/info/ST_articles.html?ID=113940
[3] Syngenta (2012) CRUISER FORCE sugar beet seed - the UK's number one choice. http://www.syngenta-crop.co.uk/pdfs/products/CruiserSB_uk_technical_update.pdf#view=fit
[4] APVMA (2010) Trade Advice Notice on clothianidin in the product Sumitomo Shield systemic insecticide http://www.apvma.gov.au/registration/assessment/docs/tan_clothianidin_60689.pdf
[5] http://quechers.cvua-stuttgart.de/
[6] Decourtye, A (2003) Learning performances of honeybees (Apis mellifera L) are differentially affected by imidacloprid according to the season. Pest Manag Sci 59: 269-278.
[7] USDA (2008) Pesticide Data Program Annual Summary, Calendar Year 2007, Appendix F Distribution of Residues by Pesticide in Corn Grain http://www.ams.usda.gov/AMSv1.0/getfile?dDocName=STELPRDC5074338
[8] Federal Register (2008) Clothianidin; Pesticide Tolerance. https://www.federalregister.gov/articles/2008/02/06/E8-1784/clothianidin-pesticide-tolerance
[9] FAO (2005) Clothianidin, Table 103. http://www.fao.org/fileadmin/templates/agphome/documents/Pests_Pesticides/JMPR/Evaluation10/Chlotiahinidin.pdf
Category: Pesticide Issues
Tags: bee feed syrups, insecticides, neonicotinoid, residues | bee feed syrups Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/bee-feed-syrups/ |
What's Happening To The Bees? - Part 3
First published in: American Bee Journal, April 2014
CONTENTS
Setting The Stage: The Origins Of The Players
Early Changes in The Honey Bee Niche Due To Humans
The Human Deforestation Of Europe
Adaptation And Change In Business
The Creation Of A Niche For Bee-keeping
The Domestication Of The Honey Bee
The Price Of Domestication
Acknowledgements
Citations and Footnotes
What's Happening To The Bees?
Part 3
Originally published in ABJ April 2014
Randy Oliver
ScientificBeekeeping.com
In the last installment of this article I explored the limiting factors of the honey bee realized niche prior to the influence of humans. So let's now look at how the populating of Europe by modern humans affected the honey bee.
Setting The Stage: The Origins Of The Players
Let's first set the stage. The time frame of interest runs from about 10,000 years ago through about 400 years ago. This period spans the time from the last "ice age" (technically, the glacial period; during which it was too cold for bees to inhabit the area), covers the invasion and colonization of the warming continent by both bees and modern humans, and ends with when humans started transporting the honey bee across oceans.
Apis mellifera
The honey bee evolved long prior to the time frame of interest. Recent research [1] suggests that the genus Apis originally developed in Europe, and then spread into Asia (where it evolved into several different species), into North America (where it later went extinct), and into Africa (via Spain/Morocco). It was in Africa that the species Apis mellifera evolved, and then later migrated back into Europe and the Middle East, branching in various ecological habitats (realized niches) into locally-adapted subspecies.
Then came a prolonged Ice Age, during which there were periods of cold and dry glaciation interspersed by periods of warming (as we are currently enjoying). During the cold periods, ice covered northern Europe, and honey bees were forced to follow suitable habitat southward, retreating into warmer "refugia." During the warm (and wetter) periods, ice retreated and Europe could temporarily revegetate, allowing honey bees to expand their ranges back again northward. The current races of bees in Europe recolonized the region from such refugia as the climate warmed about 10,000 years ago [2]. I've shown the distribution of the named races (subspecies) of Apis mellifera in the map below (Fig. 1). The satellite image shows the differences in climate and vegetation in the various regions. Of note is that the first "keeping" of bees appears to have begun in the Fertile Crescent of the Middle East with A. m. jemenitica and syriaca.
Figure 1. Subspecies of Apis mellifera in Europe and the Mediterranean region. Our domesticated stocks in the U.S. primarily derive from the temperate-adapted ligustica (Italian), carnica (Carniolan), and perhaps caucasica. The feral population of bees in the U.S. also contains the mellifera (German dark) lineage [[i]]. Map by the author; satellite image from Google Earth; subspecies distribution from various sources [[ii]].
[i] Delaney, D (2008) Genetic characterization of U.S. honey bee populations. PhD Thesis http://www.dissertations.wsu.edu/Dissertations/Summer2008/d_delaney_070108.pdf
[ii] The classification of these races is rather arbitrary, and under debate by taxonomists, but gives a general idea. There are also discrete breeding populations within each of the subspecies. See:
Radloff, SE, and HR Hepburn (1998) The matter of sampling distance and confidence levels in the subspecific classification of honeybees, Apis mellifera L. Apidologie 29: 491-501. Open access.
Al-Ghamdi, AA, et al (2013) Geographical distribution and population variation of Apis mellifera jemenitica Ruttner. Journal of Apicultural Research 52(3): 124-133. Open access.
Practical application: each subspecies of honey bee is adapted to a specific habitat and climate. The "best" bee for any region is that which has already undergone countless generations of adaptation. Although the Italian bee is very popular among many beekeepers, it is certainly not the best adapted bee for non Mediterranean [5] conditions.
Homo sapiens
At the end of the last glacial period, modern humans also moved up into Europe from Africa, displacing the cold-adapted Neanderthals (as did the bees, modern humans also evolved into different races in the region). These hunter-gatherer human populations were at first not dense enough to exert an appreciable impact on the honey bee. This changed with the advent of pastoralism and agriculture--initially slash and burn, then later improved by the invention of the plow. The adoption of agricultural practices facilitated the niche of Homo sapiens--by greatly increasing the carrying capacity of the habitat (mainly by the farming of grain)-thus allowing the human population to begin its exponential growth (to be later limited by epidemics of infectious diseases).
Practical application: as we shall see, the factors of migration, locally-adapted races, displacement of existing populations, the farming of grain, and epidemics of infectious diseases will greatly affect the honey bee over the ensuing years.
Early Changes In The Honey Bee Niche Due To Humans
O.K., now that I've set the stage, let's take a look at how the early expansion of humanity into the native range of the honey bee affected the limiting factors of the bee's niche (I will cover more recent impacts later). Allow me to address each of the limiting factors that I've previously covered, in turn.
Limiting factor: The weather
Weather is the day-to-day expression of climate. For hundreds of thousands of years, the climate of Europe oscillated between periods of cold/dry and warmer/wetter, which of course greatly affected the local weather. The fundamental niche of the honey bee is limited by cold and prolonged winters, by extreme summer heat, and by lack of water and nectar-producing plants (especially forbs--herbaceous flowering plants other than grasses). For thousands of years at a time, parts of Europe simply did not provide conditions that met the requirements of the bees' fundamental niche, causing the extirpation of local populations or entire species. Keep in mind that any species has "edges" to its range, past which the species is stressed, or cannot successfully live. Slight changes in weather at the edges can temporarily make that habitat unsuitable for bee survival.
Practical application: for example, cold, wet summers in England may not allow bees to store enough honey to make it through the winter. Ditto for drought-prone California. And an unusually severe northern winter will challenge colonies of Italian bees.
We humans have little ability, other than by fervent rain dancing, of changing tomorrow's weather; however, we do have the ability to change the climate on a local basis, and likely even at the global scale. Climate then may affect the weather.
The burgeoning human population in Europe and the Mediterranean started grazing herds of domesticated mammals and cutting down the forests [6]. This loss of the shading forest cover likely resulted in the warming of central Europe, and the desertification of the Mediterranean region [7]. Such deforestation likely favored bees in central Europe (due to creating better conditions for forbs), but created drier (and less favorable) microclimates in the Mediterranean.
The Human Deforestation Of Europe
Let's look at the vegetation of Europe at the beginning of this period of time (Fig. 2):
Figure 2. The vegetation of Europe around 4,500 years ago, just before the main agricultural and deforestation phase by humanity in the region [[i]].
[i] Map from Adams, op. cit.
Note the extensive forest cover in the natural range of the honey bee in Europe and the Mediterranean at this time in geological history. Not shown is the range of the honey bee in the moister areas of the Middle East and northern Africa, which were also densely forested. Adams [9], by reviewing data on fossils of pollen, tracked the destruction of these forests by humans over the course of a few thousand years (accelerated about 3000 years ago by the invention of the iron axe and saw). The deforestation of the habitat brought about major changes in two limiting factors of the niche of the honey bee--the abundance of forage, and the availability of nest cavities.
Limiting factor: Carrying capacity of the habitat
Although some trees provide pollen in the spring, and a few, nectar, dense forest is not prime honey bee habitat, since the tree canopy shades out flowering low-growing forbs and shrubs. It was only in natural meadows and openings of such forest that there would have been suitable forage for bees over most of the season. However, such ancient trees would have furnished abundant nest cavities.
When humans invaded those areas, they practiced slash and burn agriculture, clearing the forests for pasture or crops, or cutting trees for structures, monuments, shipbuilding, or charcoal. These forests were largely devastated by the end of the Roman Empire. Although we abhor such devastation of virgin forests today, it was likely of benefit to the honey bee, as it allowed sunlight to hit the ground, favoring the growth of bee-friendly forage plants in the pastures and cropland (remember, herbicides had not yet been invented) (Fig. 3).
Figure 3. When I'm asked to give presentations to local groups interested in gardening for the benefit of pollinators, I like to open with this slide to illustrate a point-that by cutting down pine trees (which are of no value to honey bees), one allows sunlight to hit the understory of flowering plants. Since we have suppressed natural wildfires in California, formerly open land is being reclaimed by dense pine and oak forests. Such change has been detailed for my county at [[i]].
[i] Walker, PA, et al (2003) Landscape changes in Nevada County reflect social and ecological transitions. California Agriculture 57(4): 115-121.v
Thus, by clearing the forests (by approximately 75% in central Europe), humans improved (facilitated) one aspect of the realized niche of the honey bee, since such clearing favored the growth of a greater abundance of forage plants. But there was a flip side to this.
Limiting factor: Predation
Humans (by virtue of possessing a sweet tooth, climbing ability, and wood-cutting tools) are a formidable predator of the bee. This may well be one of the reasons that the Savannah Bee (Apis mellifera scutellata) so fiercely protect their nests (their long exposure to human predation would have selected for those colonies which were able to successfully deter human honey hunters).
Hunter-gatherers do not waste energy on hunting prey that does not give a positive return on investment. It takes a considerable investment in energy, pain, and risk of life and limb to harvest the combs from a small-entranced cavity high in a hollow tree (this may be one reason that European bees prefer to nest high in trees [11]. It was only once humans had their bellies full of grain that they had the luxury of satisfying their sweet tooth by making serious efforts to attack well-defended colonies high above ground.
As the human population became more dense, the pressure of predation on the honey bee would have increased greatly, favoring the survival of bees that possessed three traits--cryptic and inaccessible nesting, vigorous defense of that nest, and frequent swarming so that colony reproduction was greater than the loss due to human predation.
Limiting factor: Nesting cavities
The clearing of ancient forests affected another parameter of the honey bee niche. The falling of each hollow bee tree eliminated one available nest cavity. As hollow trees became rarer and rarer (and tended to remain rare in regrown managed forests), there would have been fewer and fewer places for honey bees to nest. The few remaining "bee trees" would have been targeted by honey hunters, who, with the use of steel axes and saws found it easier to simply fall a tree than to climb it. Each of these destructive predations by humans eliminated yet another increasingly rare nest cavity.
So by this time point in history, two major factors of the realized niche of honey bee had been altered by humans--there would have been more herbaceous and shrub forage available, but fewer nest sites. And such change created opportunity for humans to adapt from being honey hunters to honey farmers.
Adaptation And Change In Business
On two occasions in recent years, speakers [12] have suggested at conferences that those of us in the bee business read the motivational booklet Who Moved My Cheese? [13]. I recently did so. It's a cute little parable that can be read in minutes, but summarizes important lessons in recognizing business opportunities and adapting to changes in business niches. Two of these lessons are to:
Anticipate and Monitor Change, and then
Adapt To Change Quickly
Like it or not, things change. Niches, whether ecological or in business, change continually. Those who adapt may enjoy success; those who don't, go extinct. Both the honey bee and their keepers have learned to exploit various realized niches, and those niches change over the years. As I mentioned before, both bees and humans are highly adaptive species. Honey bees adapt by the process of genetic (and epigenetic) trial and error that we call evolution. Human beekeepers, generally blessed with larger brains, have the capacity to recognize upcoming changes in their niche, and the associated pitfalls and business opportunities.
However, human nature is such that many will waste their time lamenting about how difficult or impossible change is, rather than quickly adapting. On the other hand, those who are innovative and cognizant of business opportunities consistently make money.
Let me state emphatically that I do not consider myself to be any sort of great beekeeper or business guru. But what I have noticed over the years are inherent differences in the business attitudes of those beekeepers who always seem to be complaining, compared to those who are able to afford shiny new trucks. Throughout this article I will return to adaptations in the business of keeping bees made by successful beekeepers. So let's return to the change in the niche of traditional honey hunters in the homeland of the European honey bee.
The Creation Of A Niche For Bee-Keeping
Honey hunters would have put themselves out of business once they cut down all the hollow trees. That situation created a novel business opportunity, since there would now exist an insufficient number of natural nest sites for the number of colonies that could be supported by the local forage. All that a human entrepreneur needed to do would be to facilitate the bees' realized ecological niche by supplying them with what had now become the major limiting factor--the lack of suitable nest cavities. And voila, as the business niche of honey hunting dwindled, those skilled at plundering bee trees could adapt to become...bee-keepers! This supplying of nest cavities would have been especially successful in the Fertile Crescent once it lost its forests, and would also have allowed bee-keepers to expand the honey bee's range into arid areas naturally lacking trees or rock cavities.
This beekeeper in Yemen supplies his bees with nest cavities in a landscape lacking such naturally. Honey from Yemen fetches a high price--over $100 per pound by mail order [[i]]. The growing popularity of beekeeping in Yemen today suggests that the beekeepers there may soon reach the carrying capacity of the land [[ii]]. Photo by Gillian Duncan [[iii]].
[i] http://www.balqees.com/shop/yemeni/
[ii] http://www.yementimes.com/en/1633/business/1736/Liquid-pot-of-gold-Yemen's-honey-trade.htm
[iii] http://www.thenational.ae/business/industry-insights/the-life/sticky-patch-for-yemen-honey-exports
The honey bee, when kept as livestock, exhibited a trait that made them highly desirable to peasant farmers--a colony's ability to exploit floral resources over an area of at least 30 square miles (80 km2) [17]. This trait meant that the bee-keeper could exploit the production from land which he did not own (as beekeepers typically continue to do to this day).
Practical application: early "beekeepers" needed only to provide artificial nest cavities in areas where natural cavities had become scarce. The bees otherwise took care of themselves--foraging far and wide, and voluntarily returning home with the goods.
The practice of bee-keeping appears to have began in the Middle East, and then spread to other regions [18]. Early beekeepers, depending upon materials at hand, created all sorts of nest cavities (hives), such as horizontal or vertical hollow logs, clay pots or tubes, or straw skeps [19]. Horizontal hives were the norm in desert and Mediterranean climes; log gums, vertical hives, and skeps were often used in northerly (cold winter) regions. Once humans controlled the nest sites of the honey bee, thus began...
The Domestication Of The Honey Bee
Domestication: adaptation to intimate association with human beings.
Primitive beekeeping was not much different from predatory honey hunting, other than the hunters providing homes for their eventual prey within which to store the precious honey. So long as early bee-keepers practiced destructive harvesting (killing the colony in order to consume both brood and honey combs), little selective breeding would likely take place, due to the temptation to harvest the the most productive hives.
Clever beekeepers in the Mediterranean region (especially in the clay-rich Fertile Crescent) got around this problem by using horizontal clay tubes as hives, with the entrances to the front, and a removable plug in the back. Since bees tend to store honey away from the entrance, these beekeepers could harvest honey from the rear with a minimum of stinging by smoking the bees off the honey combs, without disturbing the broodnest. What a concept! Instead of killing the colony, one could "milk" it. (These tube hives were especially amenable to this practice, prior to the invention of movable frame hives. However, nondestructive harvest methods were also invented by "forest" and skep beekeepers [20] in northern regions).
The next thing they learned was how to propagate new colonies by transferring combs of brood and scoops of bees to new hives. They even learned how to transfer queen cells and virgin queens.
Practical application: this control of the queens meant that these beekeepers could then practice selective breeding, the foundation of the process of domesticating a species. I'm surprised by how few modern day beekeepers in this country selectively breed their own locally-adapted stock (since these "primitive" beekeepers were doing it 3000 years ago!).
Domestication is a sort of symbiotic mutualism, in which both the humans and the selected animals benefit. Beekeepers would certainly select for propagation those colonies that were most productive and amenable to being worked. Milner [21] explains:
The gentle behaviour of the major races of honey bee may be due, of course, to selection for this quality over many generations; even the "skep" beekeepers of former days would, no doubt, tend to destroy the worst tempered bees and retain the gentler colonies.
Not only would beekeepers select from local stock, but even import more desirable stock. Three thousand years ago, in the ancient city of Tel Rehov in Israel, commercial beekeeping was practiced [22] using a gentle, productive strain of bees imported from Turkey!
Limiting factor: Competition for food
Let's suppose that beekeepers have now increased the available supply of skeps, gums, or Langstroth hives until the bee population is no longer limited by the number of nesting sites, but by something else? And now we get to the meat of the issue--competition for food resources. There is a limit to the number of colonies of bees that any area, no matter how rich in flowering plants, can support. That limit is called the carrying capacity of the landscape, and is commonly used to calculate how many livestock a pasture can support.
Beekeepers in my neck of the woods would no more brag about how much honey they made in a particular location than would a fisherman brag about the location of his favorite fishing hole. Should one do so, he'd likely find hundreds of new hives sitting on top of him the next season. This would be a perfect example of Garret Hardin's influential concept of The Tragedy of the Commons [23], in which he points out that it may be to the individual herder's benefit to add yet one more head of livestock to the common pasture, but to the herder community's detriment once the addition of another animal exceeds the carrying capacity of the land (beekeepers today in some jurisdictions have wisely (and self-protectively) mitigated this inherent and inevitable problem by limiting commercial apiaries to registered locations, typically no closer than two miles apart) (Fig. 4).
Figure 4. The Tragedy of the Commons exemplified. Locations of registered apiaries (blue dots) in North Dakota [[i]]. I added a 2 1/2-mile-radius red circle in the center to indicate the area covered by the typical foraging range of a colony. Clearly, the forage areas of many of these locations overlap.
[i] https://apps.nd.gov/ndda/mapping/
And what sort of carrying capacities will various landscape types support? Studies have found natural colony densities of from 1-25 per square mile (the lesser density typical in temperate forests; the higher density in tropical areas, esp. with Africanized bees) [25]. Beekeepers of managed hives generally limit their apiary sizes so as not to exceed the carrying capacity of the land to produce a surplus honey crop.
Practical application: for example, in good forage areas of Montana and the Dakotas, beekeepers try to keep commercial apiaries a minimum of 2 miles apart. If such apiaries were placed on a 2-mi grid, that would allow 4 sq. mi. of forage area per apiary. Even at a high stocking rate of 48 hives per apiary, the stocking density would be only 12 managed hives per sq. mi. (6/mi2 at 24 hives per yard).
How does the density of managed hives in the European bee's native range compare? Eva Crane cites records of hive density in Hungary in the late 1700's of 30 to 460 per square mile! In the European Union today, in which beekeepers in some areas are complaining of poor colony performance, there are some 15 million reported managed hives, which works out to nearly 9 hives per square mile (perhaps exceeding the natural carrying capacity of the land).
By comparison, in the U.S. (which contains roughly the same percentage of arable land) the average density is only about 1 hive per square mile. Of course, average density over a continent does not reflect the actual hive loading of any particular area. Especially in the U.S., hives tend to be moved around, as opposed to the often stationary apiaries in Europe, and during summer, over half of all hives are located in only six states, accounting for only 16% of the U.S. land mass. However, even in those six states, the density of hives only starts to approach that of Europe as a whole!
Practical application: The Tragedy of the Commons definitely applies to beekeeping, since bees can't be fenced in. I was driven out of a very good area in Nevada by beekeepers who moved in thousands of hives to the extent that I could hit another apiary with a thrown stone from any of my long-time locations. California has also reached that point in many areas, as beekeepers step on each others' toes looking for any favorable place to place hives.
When I hear of all the bee problems in Europe, I wonder as to how much beekeepers there have contributed to the problem by overstocking hives on the available pasture. I'll return later to the impact of modern agricultural practices upon the carrying capacity of agricultural land for bees.
Limiting factor: Reproductive success rate
In the absence of natural nest cavities, the survival of the honey bee depended in many areas upon the provision of such nest sites by humans, in the form of some sort of managed "hives." And that fact gave beekeepers control over the reproductive success of any particular colony. By choosing which colonies were allowed to reproduce, beekeepers would rather quickly have been able to domesticate the bee by providing nest cavities only to those most amendable to husbandry. It would only have been in the scattered relict forests that wild, unmanaged populations of bees would have been able to survive. And this finally brings us to what I suspect is a major factor negatively affecting honey bees today:
The Price Of Domestication
Are honey bees truly a domesticated animal? And if so, how has that favored or hurt them? I'm out of space for now, but it gets more interesting...
A Note And Acknowledgements
Although I've spent considerable time in researching this article, my interpretation of the evidence is largely speculative. If anyone can add to this subject, please let me know.
As always, I am greatly indebted to my colleague Peter Borst, without whose research assistance I could not write these articles. And I cannot express how much I grateful I am for the words of appreciation from beekeepers worldwide, as well as their donations that support my research, writing, and website maintenance.
Citations And Footnotes
1 Ulrich Kotthoff, U, et al (2013) Greater past disparity and diversity hints at ancient migrations of European honey bee lineages into Africa and Asia. Journal of Biogeography 40: 1832-1838. Open access.
2 Adams, J (n.d.) Europe during the last 150,000 years. http://www.esd.ornl.gov/projects/qen/nercEUROPE.html This is a fascinating compilation of information and maps on the changes in climate and vegetation of Europe over time.
Ruttner, F (1988) Biogeography and taxonomy of honeybees. Springer-Verlag.
Miguel, I (2007) Gene flow within the M evolutionary lineage of Apis mellifera: role of the Pyrenees, isolation by distance and post-glacial re-colonization routes in the western Europe. Apidologie 38: 141-155. Open access.
Franck, P, et al (1998) The origin of West European subspecies of honeybees (Apis mellifera): New insights from microsatellite and mitochondrial data. Evolution 52(4): 1119-1134. Open access.
3 Delaney, D (2008) Genetic characterization of U.S. honey bee populations. PhD Thesis http://www.dissertations.wsu.edu/Dissertations/Summer2008/d_delaney_070108.pdf
4 The classification of these races is rather arbitrary, and under debate by taxonomists, but gives a general idea. There are also discrete breeding populations within each of the subspecies. See:
Radloff, SE, and HR Hepburn (1998) The matter of sampling distance and confidence levels in the subspecific classification of honeybees, Apis mellifera L. Apidologie 29: 491-501. Open access.
Al-Ghamdi, AA, et al (2013) Geographical distribution and population variation of Apis mellifera jemenitica Ruttner. Journal of Apicultural Research 52(3): 124-133. Open access.
5 http://en.wikipedia.org/wiki/Mediterranean_climate
6 Williams, M (2000) Dark ages and dark areas: global deforestation in the deep past. Journal of Historical Geography 26: 28-46. http://geography.fullerton.edu/taylor/ENST595T/darkages.pdf
http://www.fao.org/docrep/004/ab580e/AB580E02.htm
Oosthoek, KJW (n.d.) The Role of Wood in World History. http://www.eh-resources.org/wood.html
7 Milich, L (1997) Desertification. http://ag.arizona.edu/~lmilich/desclim.html.
8 Map from Adams, op. cit.
9 Adams, J, op. cit.
10 Walker, PA, et al (2003) Landscape changes in Nevada County reflect social and ecological transitions. California Agriculture 57(4): 115-121.
11 Seeley, TD and RA Morse (1978) Nest site selection by the honey bee, Apis mellifera. Insectes Sociaux 25(4): 323-337.
12 Thanks to Jay Miller and Darren Cox.
13 Johnson, S (1998) Who Moved My Cheese? G.P. Putnam's Sons.
14 http://www.balqees.com/shop/yemeni/
15 (Broken Link!) http://www.yementimes.com/en/1633/business/1736/Liquid-pot-of-gold-Yemen's-honey-trade.htm
16 http://www.thenational.ae/business/industry-insights/the-life/sticky-patch-for-yemen-honey-exports
17 Beekman, M and F Ratnieks (2000) Long-range foraging by the honey-bee, Apis mellifera. Functional Ecology 14(4): 490-496.
18 I've taken much of this historical information from Crane, Eva (1999) The World History of Beekeeping and Honey Hunting. Taylor and Francis Group.
19 I highly recommend the book The Quest for the Perfect Hive by Gene Kritsky (2010) Oxford University Press.
20 "Forest beekeeping" was practiced in Northern Europe, whereby beekeepers, would cut a recloseable door to a hollow high in a tree, allowing for repeated harvest without killing the colony.
21 Milner, A (2008) An introduction to understanding honeybees, their origins, evolution and diversity. http://www.bibba.com/origins_milner.php This is an excellent review of the domesticated races of the honey bee, and a well-thought plea for the breeding of locally-adapted stocks. See also:
(Broken Link!) http://www.aragriculture.org/insects/bees/races.htm
22 Mazar, A and N Panitz-Cohen (2007) It is the land of honey: Beekeeping at Tel Rehov. Published in Near Eastern Archaeology 70(4): 202-219. Open access.
Bloch, G, et al (2010) Industrial apiculture in the Jordan Valley during Biblical times with Anatolian bees. PNAS 107(25): 11240-11244. Open access.
23 Hardin, G (1968) The Tragedy of the Commons. Science 162(3859): 1243-1248. http://www.sciencemag.org/content/162/3859/1243.full
24 https://apps.nd.gov/ndda/mapping/
25 Ratnieks, FLW, et al (1991) The natural nest and nest density of the Africanized honey bee (Hymenoptera, Apidae) near Tapachula, Chiapas, Mexico. Can. Entomol. 123: 353-359.
Baum, KA, et al (2005) Spatial and Temporal Distribution and Nest Site Characteristics of Feral Honey Bee (Hymenoptera: Apidae) Colonies in a Coastal Prairie Landscape. Environmental Entomology 34(3):610-618.
Taber, S, III (1979) A population of feral honey bee colonies. Am. Bee J.ABJ 119: 842-847.
Category: Colony Health - Diseases, Viruses, CCD
Tags: ccd | ccd Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/ccd/ |
Sick Bees - Part 18A: Colony Collapse Revisited
First published in: ABJ May 2012
Gone, or Just Taking a Breather?
CCD in Retrospect?
The Anatomy of Colony Collapse
Relative Risk
The Holst Milk Test
Treating for Nosema
Pollen Supplement Patties
Yet Another Sign of Impending Collapse
Ag Exposure as a Risk Factor
Reliving History
Acknowledgements
References
[8] The Holst Milk Test
Randy Oliver
In my article on almond pollination last month I pointed out that beekeepers in the U.S. started experiencing increased colony mortality in the mid 2000's. What made the headlines was an unusual form of sudden colony mortality eventually given the name "Colony Collapse Disorder" (CCD). But this season CCD has sort of fallen off the radar. So perhaps it's time to look back at what we've learned.
Gone, Or Just Taking A Breather?
The question is, has CCD now gone the way of previous cases of "Disappearing Disease"--episodes in which some disease caused bouts of sudden mortality, and then disappeared before anyone could figure out what caused it? A number of researchers suspected that CCD would do the same, following the typical progression of a pathogen-induced plague. The surprise was that it stuck around as long as it did.
If CCD is indeed caused by one or more novel virulent pathogens, we'd expect that pathogen's virulence to be burning out by now. On the other hand, if CCD is caused by an extraneous environmental factor, such as cell phones, GMO's, or some pesticide, we would not expect to see a change until that factor was removed from the environment.
Or perhaps, CCD simply requires enough chilling of colonies to kick it into gear (figure 1):
Figure 1. . The unusually warm winter may have contributed to better colony survival this year. These maps show winter temperature "departures from normal" for December, January, and February. Red areas experienced higher than normal temperatures; blue areas colder. Each color step indicates an additional 2degF deviation. Colony mortality is often related to weather patterns. Source http://www.ncdc.noaa.gov/img/climate/research/cag3/asos-feb2012-nocities.gif.
Practical application: to minimize mortality, winter your colonies in the warmest possible locations--sunny southward slopes, out of cold pockets, or move them to warmer areas.
CCD In Retrospect?
I wish that I could have entitled this article "CCD in Retrospect," but I'm still seeing some colonies suffering sudden collapse! This winter when I moved my strong hives to almond pollination, I left the dinks behind in my bee yards in the foothills. The apparent reason for many of these colonies being dinks is that they are fighting a virus or nosema infection, which they may eventually get the better of. I've learned that if you simply leave them to their ways, they will often dwindle down to a couple of frames of bees, and then either ramp up their antiviral response or gain the upper hand over nosema, and turn around, vibrantly recovering with the first pollen flows as though nothing had happened!
I feel that in many cases in which the queen is blamed, the actual culprit is a virus or nosema infection of the workers, as these queens often show every indication of being able to lay vigorously, given a healthy cohort of foragers to bring home the bacon. In my neck of the woods, if the colony has "turned around" by late February, it will generally be fine. As it happened, late this February I enjoyed a visit by Bee Culture editor Kim Flottum, accompanied by photographer Kodua Galieti. I took them out to look at some of the recovering dinks (Fig. 2). Kodua snapped some photos, which she has generously granted me permission to use--see more of her photos at www.koduaphotography.com/.
Figure 2. A recovering dink in late February, building up on early alder pollen. This colony was a bit stronger than three frames of bees, but clearly is on the road to recovery! It does not appear that this colony being a dink was the fault of the queen. But note the barely adequate bee to brood ratio--this amount of bees will have a hard time keeping the brood warm in the event of a cold snap!
Practical application: I find that a low bee to brood ratio is a typical sign of a colony struggling with a virus or nosema infection--sick bees abandon the hive. Should the colony in the photo above manage to hatch out its brood before a cold snap, then it will then have a whole new crop of healthy young bees, and a good crack at complete recovery.
The Anatomy Of Colony Collapse
Unfortunately, one of the dinks in the same yard told a different story (Fig. 3). It had also built up similarly to the colony pictured above, but then had a relapse during a two-day cold snap--cold snaps being a common precursor to sudden colony collapse. If the bees and brood get chilled, the colony may go into a rapid downhill spiral. I've previously described in detail the progression of colony collapse-see https://scientificbeekeeping.com/sick-bees-part-2-a-model-of-colony-collapse/.
Figure 3. This colony is in the middle of a sudden collapse. You can easily see the outline of the brood area, delineated by the crescents of freshly-packed pollen, which must have been covered by bees a few days prior. This colony continued to collapse quickly, and finally died in a cold snap a week later--with only silver-dollar sized patch of dead bees remaining.
Note also the lack of stored nectar around the brood area--this is despite the fact that a nectar flow was on, and adjacent colonies were whitening comb. This is exactly what I observed when I inoculated colonies with IAPV--they would collapse hungry due to lack of foragers, even in the midst of plenty. Plus the bees in sick colonies seem to be unable to utilize honey stored in close proximity to the broodnest. Collapse can then come suddenly (Fig. 4) in the event of even a minor chill, although the sick bees leave the nest, rather than dying in the typical pathetic cluster indicative of starvation (Fig. 8).
Practical application: sudden collapse can happen seemingly overnight. But it is, in my experience, preceded by a low bee to brood ratio and lack of nectar foraging, which are signs to be aware of. Sick colonies may or may not take syrup.
Figure 4. Collapse came quickly, as evidenced by this fresh, white pupa outside the cluster. Abandoned larvae and pupae soon die and turn gray, and can be used to estimate the amount of time since bees were covering the brood.
The queen, however, had not given up (Fig. 5). This is typical in colony collapse--the disease does not appear to be directly attributable to the queen. It's just that the bees get sick and fly off to die!
Figure 5. The queen appeared healthy and robust, as evidenced by fresh eggs in nearly every single cell in the abandoned brood area (two eggs in some cells). Note the lack of signs of varroa (no guanine deposits, deformed wings, nor partially emerged adults). Also note the presence of "snotty brood."
Practical application: In deadouts, check to see whether varroa/DWV were the culprits. Inspect the remnants of the broodnest for white guanine deposits on the cell "ceilings," bees with deformed wings, and partially uncapped mature worker brood, often with deformed wings. However, DWV can also take down a colony with few of those signs present.
I'd like to draw your attention to the snotty brood. The diseased brood generally matched the signs of EFB, but was not quite typical. Dr. Jeff Pettis now uses the catchy term "Idiopathic Brood Disease Syndrome" for this atypical sick brood, which means "we haven't completely figured out what causes it yet".
So this poor colony looked like it was going to make it, but then lost its battle with the pathogens. Note that this yard was in a pesticide-free area, and there was no sign of mites.
Relative Risk
Relative Risk: the ratio of the chance of a disease developing among members of a population exposed to a factor compared with a similar population not exposed to the factor.
Dr. Dennis vanEngelsdorp and co researchers determined the "relative risk" of several factors often associated with colony collapse. A factor with a high relative risk doesn't necessarily mean that the factor will cause the collapse, but rather that it is associated with a higher incidence of collapse (for example cold weather has a high relative risk for colony mortality, even though it isn't necessarily directly responsible for their death). Determining relative risk is like setting the odds for eventual collapse--a relative risk of 2 doubles the odds that the colony will die.
Practical application: If snotty brood is present, the relative risk of that colony dying is nearly [redacted] times that of a colony without it.
Sorry, when I asked Dr. vanEngelsdorp how to cite the preliminary relative risk figures that he and Dr. Jeff Pettis presented at the major conventions this season, he asked me to hold off until they are more firm on the numbers--so I am respectfully deferring to his request. I find this line of research to be of great potential value to beekeepers, and I want to only publish accurate information!
I've currently got a number of colonies with spotty brood and signs of "EFB-like" snotty brood. I'm familiar with the classic symptoms of EFB--curled, twisted young larvae with white tracheal tubes standing out against a yellowish background, slight sour odor, minor ropiness, and drying to a removable rubbery scale. I'd occasionally see EFB in springtime; especially when strong colonies were deprived of pollen due to rain, and then the disease would spontaneously disappear with the advent of a good pollen flow.
But nowadays I'm seeing a great deal of "atypical" EFB. It may be associated with mites and viruses, since the signs are similar to those seen in sick brood in colonies suffering from Parasitic Mite Syndrome (PMS), but I now see it in colonies with low mite levels!
One odd thing is the smell, since this dead brood gets really putrid stinky! The scientist who first identified the bacterium responsible for EFB was G.F. White (yes, the same guy who identified Nosema apis). Dr. White stated that EFB "is characterized by the death of the brood during its uncapped stage...In advanced cases the disease may be accompanied by an odor, but in the writer's experience this never has been marked and never offensive" [1]. But other bacteria are commonly associated with EFB; perhaps these are causing the differences in smell and appearance. An excellent page on the diagnosis of EFB (with color photographs) can be found at Extension.org [2].
So I sent samples off to the USDA Bee Diagnostic Lab, and wish to thank Sam and Bart for helpful discussion and a speedy turnaround so that I could make deadline for this article. The samples came back positive for EFB.
In the past several years, I'm seeing what appear to be two different forms of atypical EFB-like brood disease:
Syndrome 1:
Larvae prior to propupal stage turning bright corn yellow, usually remaining in the "C" shape without much twisting. I've heard of this same symptom from many beekeepers across the country.
Syndrome 2:
A greater proportion of older, rather than younger, sick larvae in the combs, many of them capped over, and having sunken, perforated cappings. These older larvae often turn flaccid without twisting, and eventually melt down into strongly putrid-smelling goo (but with a very different odor than AFB).
The dead capped brood may melt down into a dark watery pool, rather than the translucent-opaque, slightly ropy goop typical of EFB. The liquid also really stinks with a putrid, rather than sour, odor!
Capped pupae dying in the same colonies. EFB should not kill pupae [3], since the larva sheds its infected gut lining when it pupates. However, these pupae may be infected by something else, such as a virus--they look very much like pupae dying from DWV.
The disease does not necessarily go away with a pollen flow.
Practical application: Some of these symptoms can be confused with those of AFB--I was surprised when I sent a very similar-looking sample to the lab last season and it came back positive for AFB! My quandary is that I wish to burn any AFB combs, whereas EFB responds well to the antibiotics oxytetracycline or tylosin (I hear anecdotally that OTC gives better control, plus has less chance of getting into the honey). A brood break, such as by making splits, may help as well.
The Holst Milk Test
While I was waiting for the lab results, I tried a diagnostic technique that I'd never done before--the Holst Milk Test for AFB [8]. This test detects the presence of the strong proteolytic enzyme that the sporulating AFB bacteria release in order to melt down the larval bodies in the last stage of infection. The enzyme will also break down milk protein--and "clarify" a weak solution of powdered milk within minutes. Luckily, I had a comb of obvious AFB on hand to show to my beginners classes, so I tested fully decomposed suspect EFB-like larvae against known AFB scale. The results were impressive (Fig. 6)! I highly recommend this test for beginners who suspect AFB in deadouts.
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I experimented with the test a bit. The more concentrated the milk solution, the longer it takes AFB to clear it--sometimes overnight (use less milk powder than in the photo above for a quicker field test). EFB will cause the milk to clump, but you don't get the clear "apple juice" look as with AFB.
Treating For Nosema
Speaking of treatments, since I recently found a correlation between weak colonies and the prevalence of nosema (percentage of bees infected), I tried treating all my dinks once a week from late January through early February with a drench of fumagillin (Fig. 7), 3-4 times total [4].
Figure 7. I find that using a garden watering can to apply medication by drench is very quick. Since I only apply 1/4 cup to small colonies, I stand little chance of contaminating my spring honey. Multiple weekly drenches spread the medication out over an entire brood cycle. Take caution if you add essential oil "feeding stimulants"--they can cause wetting and drowning of bees! Note the uneaten pollen supplement patty.
Because I had treated these dinks recently against nosema, I assumed that I could rule it out as the cause for the collapse. But beekeeping certainly has a way of making an ass of you when you assume anything! As I'm writing this article, it occurs to me that I should go back to the yard and grab a sample of the remaining dead bees to test for nosema...
O.K., I'm back now- Result: 8 out of 10 of them had their guts loaded with spores! And one contained amoeba cysts to boot. That was an eye opener!
Dr. vanEngelsdorp found that even a relatively low level of nosema (1M spores in the house bees) increases the odds of a colony collapsing by a factor of [redacted]. More to the point, having 8 bees out of 10 infected is a death sentence for a colony! Oh, and by the way, there was no sign of dysentery.
Disclaimer: Now please don't get me wrong--I'm not saying that Nosema ceranae is the cause of CCD! It is not necessarily present when colonies suffer sudden collapse--the viruses are quite capable of doing that on their own!
Practical application: The "spring turnover" of colony population, during which the aged winter bees must rear replacements, is a dicey time for weak or sick colonies. The old bees must not only fight parasite buildup and winter cold, but must also generate heat for the broodnest, and produce jelly in order to rear healthy young bees to take their places. If they don't pull this feat off, the colony can quickly crash! This colony collapsed during a mild California foothill winter, with a good nectar and pollen flow on, interspersed with occasional bouts of snowfall. The chill events appear to be the fatal factor.
Practical application: My guess as to why fumagillin did not clear the infection is that I was simply too late in applying it--the infection had already seriously taken hold, and this colony was simply unable to replace the infected bees with healthy ones in time. But remember, most of the dinks recovered quite handily!
As we looked through the dinks, we came upon some with yet another indicator of impending collapse--the presence of supersedure cells (Figures 8 and 9).
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I commonly see unexpected supersedure cells in heavily infected colonies--it doesn't really seem to matter what the pathogen or parasite is. I'm not sure whether the bees are blaming the queen for their misery, or whether the queen gets infected and puts out a pheromonal signal to replace her.
Figure 9. Here is yet another dink that died with supersedure cells (I'm pointing to two), despite the presence of an apparently healthy queen (see Figure 10). You can see that this colony had recently covered a fairly large brood area. Note also the remains of a pollen patty fed at an earlier date.
Of even more import is that some risk factors may synergize. If you multiply the relative risk due to a nosema infection times the relative risk due to the presence of supersedure cells, you then get a combined relative risk of [redacted; but much higher].
Practical application: the combination of a nosema infection plus supersedure cells does not bode well for a colony's survival!
Figure 10. A close up of the dead cluster--you can see the queen near the top center. In none of these deadouts were there any appreciable numbers of dead bees on the bottom boards. Note the absence of "heads in the cells" typical for starvation.
As I'm looking at this photo I realize that my readers would be curious as to whether this colony also tested positive for nosema, so off I go again back to the same yard (through the rain--what I do for my readers)...
O.K. I eventually found this exact same frame of dead bees, and squashed the abdomens of ten of them. Wanna guess? Nine of them were chock full of spores! So the infection had clearly moved into the last few young bees. Unfortunately, I had given the dead queen to Kodua to photograph, so couldn't test her (the queen) for spores.
Practical application: don't count on dysentery to be a reliable indicator of serious Nosema ceranae infection--it isn't, although I see it occasionally over the snow in front of infected colonies. If you're not testing your dinks and deadouts for nosema, you have no idea as to whether Nosema ceranae is causing winter/spring mortality!
Practical application caveat: over the past few years when I've tested the few remaining bees in collapsed deadouts, nosema was generally not evident (leading me to conclude that nosema was not a problem). In those cases, collapse was likely due to a virus infection. I'm not clear as to why this year is different, although my nosema levels have been ramping up each year (I hadn't been treating against nosema). Overall, my bees this year have not been at their best, although a strong majority went to almonds and look fine. I'll spot test them when they return (I'm typing these words in early March).
Pollen Supplement Patties
I haven't heard the researchers mention it, but I observe that yet another indicator of elevated risk for later collapse is that the colony does not consume pollen supplement in the fall. Beekeepers have long noticed that untouched protein patties are generally a sign of queenlessness, but I'm finding that they are also often a sign of a sick colony. Most all of my dinks had uneaten patties on the top bars in February (Figs. 7, 9, and 11).
Figure 11. It seems that I could largely predict which colonies would eventually dwindle or die by whether they consumed protein patties in fall (the size of this patty suggests that the cluster was much larger when we put it on--we only put patty over seams filled with bees). Healthy colonies gobble supplement up, leaving no scraps. We checked every colony that didn't consume their patty in the fall to confirm that they indeed had a laying queen; yet few that had patty remaining in February were strong enough to go to almonds.
Practical application: a good indicator that a colony is going downhill is that it doesn't consume protein patties. It might be a very good idea to quarantine those colonies to an isolated "sick yard" (like far away from my hives in the almonds!).
Yet Another Sign Of Impending Collapse
I thought that I was perhaps the only one who noticed this one, but in conversation with other beekeepers who suffered from CCD, I found that others also observed that the cappings over the brood sometimes turned a very dark reddish tint, and instead of being slightly rounded outwards, would be flat. The brood appeared to be perfectly healthy under the cappings. I found this to be a sign that a colony was in trouble. However, I didn't notice it when we later experimentally caused colony collapse with IAPV, nor do I notice it with colonies collapsing from Nosema ceranae.
Ag Exposure As A Risk Factor
Oh man, is this a touchy subject, with some very strong and adamant opinions out there! Beekeepers have long noticed that colonies set in certain agricultural areas go downhill, or may not make it through the following winter. Sometimes a certain pesticide is clearly to blame; other times it may simply be due to the lack, or poor nutritional quality, of the forage in the agricultural area, especially in this age of "clean farming" and wall to wall corn or soy.
When I first published my model for colony collapse, mentioning that some pesticides become more toxic to bees at cooler temperatures, Dr. Eric Mussen sent me this note:
"When Dr. Eric Erickson was employed at the USDA laboratory in Madison, WI, he conducted a small demonstration study based on observations reported by a number of nearby beekeepers. The beekeepers told him that when their hives were located near commercial corn fields and permethrin was applied to the crop during "bloom" (tassels producing pollen), the colonies did not survive over winter.
"Dr. Erickson had half the lab colonies moved into an area near a corn field and had an application of permethrin made during bloom. No noticeable bee loss was noted in the apiary at the time. The colonies were then returned to the lab apiary and all colonies were prepared for winter. During the winter all the permethrin-exposed colonies died, whereas all the stay-at-home colonies survived. It wasn't clear as to whether the mortality was due to the corn pollen, the pesticide, or something else, but the point is that colonies foraging upon sprayed corn fields in tassel exhibited a delayed effect of high winter mortality-greater than that of the colonies that were not exposed to the treated corn."
Practical application: in the registration process of pesticides, they are normally only tested on bees at about 80degF. We really have little idea as to the effect of pesticides upon bees at 45degF--the temperature of the bees in the outer shell of the winter cluster!
I recently attended a presentation in Oregon in which commercial beekeepers described the number of pollination contracts that they moved their bees to during the summer, and more to my interest, the sheer number of pesticide applications that the bees had to deal with. To my mind, it's a wonder that their bees survive at all!
Practical application: some ag crops in certain areas are the kiss of death to bees, but the effect may not be noticed until winter. This is a complex subject, having to do not only with pesticides, but also with colony population dynamics, parasite dynamics, nutrition, symbiotic fungi and bacteria, pesticide and miticide synergies, pesticide/pathogen synergies, and who knows what else! I doubt that the problem has a simple answer.
Dr. Mark Carroll of the ARS is currently engaged in a project called "The Costs of Following the Bloom-Nutrient Processing, Microbial Dynamics, and Colony Health in a Migratory Beekeeping Operation" [5]. I hope that his research can help to answer some of the above questions. In a recent presentation, he spoke of "overextended bees" in migratory operations, suffering from poor nutrition and parasite buildup. Perhaps he should also have spoken of "overextended beekeepers," who are simply trying to run more colonies than they can properly manage!
There is a raging debate as to whether the systemic neonicotinoid insecticides are causing CCD, fueled by a great deal of conjecture and hyperbole that is often confused with fact. I'll discuss this in my next article.
Reliving History
There is nothing new about the phenomenon of sudden colony collapse. In 1897 R.C. Aikin, from Colorado, described a similar phenomenon [6]:
"In [May] of 1891...I had been watching carefully the progress of brood rearing, and had the colonies quite strong in both bees and brood. ... Many colonies were so strong that they were clustering out, although we had not unpacked yet...While they were so, I had looked all over and equalized stores and brood, then was absent about ten days... [when] I went to the out-apiaries to again inspect as to stores... I was astonished at the very few bees in them. I went to some hives that I knew had been clustered out about ten days previously, and I found not enough bees to cover the brood. The weather was warm, the bees packed in chaff, and the few bees left were spread all through the hives caring for the brood.
"Some of the colonies were so depopulated that, when I lifted combs, I could lay my open palm on the face of a comb of brood and scarcely touch a bee. It was not what I understand as spring dwindling. The bees were mainly young, for bees had been hatching for weeks...
"The bees just vanished, and were nowhere to be seen. If they had died in or about the hive, possibly we might have found out what was the matter; but they seemed to evaporate, hence I have called it "evaporation." The loss of bees was so complete that many colonies had not half a teacupful of bees left, where, less than a week before, they covered brood In three combs and upward. The queens, it seems, were always left; but the workers so completely evaporated that the brood perished."
Beekeepers have always had to deal with episodes of colony collapse, sudden or not, and depending upon their fortitude and perseverance, use the bees' biological capacity for rapid increase to recover. This "get over it and get going" attitude is exemplified in a scene from the movie "The Last Beekeeper." While sitting at a diner, a woman commercial beekeeper is despairing about how CCD has financially ruined her operation; meanwhile, her companions, an older beekeeper couple, between bites of food, just keep saying "You gotta restock, you gotta restock." That scene to me was the archetype of the attitude necessary for successful beekeeping.
CCD was never actually a serious bee issue--there was little doubt (other than in the minds of fanatics) that the honey bee would survive. CCD was really about whether commercial beekeepers could financially survive such serious losses. And as I pointed out last month, were it not for the "generosity" of the almond growers, many of us would not have!
In my own beekeeping career, my operation has been devastated by collapse events four times: first by tracheal mite in the late 1980's (to which many beekeepers lost 70% of their colonies); then by varroa (I lost 97% around 1996); then again when Apistan strips failed in the late 1990's. And this dismal record doesn't even take into account those El Nino years in which I decimated my operation myself in order to fill my nuc orders! By the time I got hit by CCD in 2005, collapse events were old hat!
However, each of the above events was followed by seasons in which I could recover. But as we picked up each new parasite, recovery got a bit more difficult, due to increased levels of colony morbidity and mortality. Preceding, and concurrent with CCD, our colonies were already experiencing an elevated rate of winter loss over the norm. What the heck is the "norm"? Back in the "good old days," beekeepers expected to lose maybe 5% of colonies over the winter; perhaps 10% where winters were severe. Losses were mainly blamed upon starvation, queen failure, or Nosema apis.
After the arrival of varroa, the "normal" winter loss rate ramped up to the 15-20% range. CCD (and perhaps Nosema ceranae) notched that average rate up to above 30%-a level at which winter losses really started to hurt! The interesting thing is that about a quarter of commercial operations get hit disproportionately hard, and about a quarter have few problems. Beekeepers and researchers are pulling their hair out trying to find the causes for the difference!
What made CCD stand out was our inability to blame it on the "Usual Suspects." However, it also became an oh so handy scapegoat for absolving oneself from blame for losses due to mismanagement, poor timing, lack of varroa control, or anything else. I'm not depreciating the devastation and distress caused by CCD in some operations (the film "The Last Beekeeper" is heart wrenching), but most beekeepers found that given enough financial incentive, they could recover and figure out how to avoid major losses.
Practical application: those beekeepers who diligently keep mite and nosema levels down, ensure that their bees get good nutrition, and are not continuously exposed to commercial agriculture tend to have fewer problems with colony collapse (not that I expect you to take that as any sort of revelation!).
As you can see by the blow-by-blow account that I'm giving of my own learning curve, I personally sure haven't figured everything out--beekeeping presents new challenges every year! I like the recent quote from California beekeeper Henry Harlan [7]:
"If you meet a beekeeper who says he knows it all, his bees will probably be dead next year."
In any case, Colony Collapse Disorder has presented us with an opportunity to learn a great deal about bee health. I will follow this article with a critical analysis of the suspect causes of both CCD specifically, and increased colony mortality and morbidity in general, followed by a summary of experiments that actually tested various hypotheses.
Acknowledgements
As always, I am deeply indebted to Peter Borst for his help with research, and to my wife Stephanie for her critical reading of my manuscripts. And thanks to Dianne Behnke of Dadant for digging out and scanning old articles from ABJ for me! I am especially appreciative of the worldwide community of bee researchers, who take the time to discuss my questions at length.
References
[1] White, GF (1920) European foulbrood. USDA Bulletin No. 810.
[2] http://www.oie.int/fileadmin/Home/eng/Health_standards/tahm/2.02.03_EUROPEAN_FOULB.pdf
[3] http://www.extension.org/pages/23693/european-foulbrood:-a-bacterial-disease-affecting-honey-bee-brood
[4] The drench consisted of 2 Tbl Fumagilin-B (200mg fumagillin) per 1/2 gal of 1:1 syrup, which allowed me to mix up fresh batches as needed. At the rate of 1/4 cup of drench per dose, each dink received a dose of 12.5mg of active ingredient, which would be the recommended rate for a 3-frame dink to be given multiple treatments.
[5] http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=420102
[6] Aikin, RC (1897) Bees evaporated: a new malady. Glean. Bee Cult. 25(13):479-480.
[7] http://www.latimes.com/business/la-fi-california-bees-20120304,0,2026018,full.story
[8] The Holst Milk Test
Holst, EC (1946). A simple field test for American foulbrood. Am. Bee J., 86: 14-34.
The enzyme is produced by the bacteria only when the larvae reach the "ropy" stage or later, and persists in the dried "scale"--it won't work with larvae at an earlier stage of disease. It is often easiest to simply rip out the entire bottom of the cell with forceps and drop it all into the tube. You can also drop in the twig that you use to test for ropiness. The more diseased larval remains you add, the quicker the reaction; however, if you use only a partial scale, or a twig, then either use less solution, or dilute the milk even further.
The reaction can also be speeded up by warming the water to up to 165degF (as hot as you can hold your fingers in). I could get tubes of 1/2 tsp of weak milk solution inoculated with a single scale to clear in less than 5 minutes by incubating them in a cup of hot water.
It is easy to make up a field AFB test kit consisting of a pair of tweezers, a vial of milk powder, and some clear glass vials for running the tests. At home, you can use liquid milk (skim preferred) diluted 1:4, again at the ratio of 1 scale per 1/2 tsp of diluted milk. When first trying this test, I suggest that you run an uninoculated vial of milk solution side by side for comparison.
Note that the test is retarded if the combs have been stored with paradichlorobenzene for wax moth control.
Category: Colony Health - Diseases, Viruses, CCD | Sick Bees - Part 18A: Colony Collapse Revisited - Scientific Beekeeping | https://scientificbeekeeping.com/sick-bees-part-18a-colony-collapse-revisited/ |
What Happened To The Bees This Spring? (Part 1 & 2)
First published in: American Bee Journal, June 2013
Part 1: Environmental and Biotic Factors
Setting the Stage
The Lead Up
The Drought
Lack of Good Forage
Varroa
Diseases
Other Indicators of Impending Collapse
An Unexpected Chill
Feedback from Brokers
The Silent Majority
Beekeeper Management
Part 2: The Contribution From Pesticides
The Lynch Mob
Debunking The Myths
The Precautionary Principal
See For Yourself
Be Careful What You Ask For!
The Effect Of Drought
Actions To Take
Bottom Line
References
What Happened To The Bees This Spring?
Part 1: Environmental And Biotic Factors
Randy Oliver
ScientificBeekeeping.com
First published in ABJ June 2013
By now, most everyone has heard that honey bee colonies died in massive numbers this winter. Reporter Dan Rather, in his newscast Buzzkill [1], showed unfortunate beekeepers, some of whom had lost half or more of their colonies, predicting gloom and doom for the bee industry. What were the causes of this year's bee shortage? As Rather says, "Everyone has an opinion." The question is whether those opinions are based upon fact! So let's go over the events leading up to the bee supply debacle.
Setting The Stage
Nearly 800,000 acres of almond trees in California came into bloom this winter--the trees typically start flowering about Valentine's Day, and the bloom lasts for only about two weeks. Almonds require cross fertilization between adjacent rows of varieties (Fig. 1), and honey bees are trucked in from all over the country to do the job (roughly a million and a half colonies). Many large commercial beekeepers move their hives into California in November to overwinter in holding yards; others build them up on winter pollen flows in Florida or Texas, or hold them in temperature-controlled potato cellars until shortly before bloom. The hives are generally placed into the orchards about a week before the first flowers appear. There is virtually no forage in the orchards prior to, or after bloom in many areas.
Figure 1. An almond orchard in late February, showing the flowering of rows of different cultivars required for cross pollination. The bare "late" varieties have not yet bloomed; the green "early" pollenizers have finished bloom. Grading of colonies is normally done during the bloom of the main crop (usually Nonpareil).
The Lead Up
Two seasons ago there was also a shortage of bees in almonds, following the coldest January (2011) in 17 years (cold being a major stressor of wintering bee colonies). Beekeepers then replaced their deadouts with package bees and splits, thus starting a new generation of colonies, which tend to have lower varroa mite levels than established colonies. These colonies entered autumn 2011 in pretty good shape, and then enjoyed the fourth warmest January (2012) on record! As a result, there was the lowest rate of winter mortality in years, and plenty of bees for almonds in 2012 (Fig. 2).
Figure 2. Percent winter losses since the beginning of the national survey--the data is not yet in for 2012/13. Note that there has been a general downward trend, suggesting that whatever caused the high losses in 2007/8 has not been such a problem in recent years. Note also the cyclical nature of colony winter losses, with high losses in 2004/5, 2007/8, 2009/10, and 2012/13 (some data not shown) Data from [[i]].
[i] http://www.ars.usda.gov/is/pr/2012/120531.htm and California DPR.
I was curious as to whether the colony loss rate was linked to the use of neonicotinoid insecticides. There is no recent USDA data, so I went through the California Pesticide Use Reports (data available through 2010). I plotted the amount of imidacloprid applied to crops in California in the preceding year in red (the seed treatment clothianidin didn't even make the top 100 list of pesticides applied). Although there appears to be a possible correlation from 2006 through 2009, the trends were reversed for 2010. I will be curious to add the 2011 data when it becomes available.
In March of 2012 I received a phone call from a California queen producer who had a prescient insight as to a potential brewing disaster. He was receiving calls for queen bees from Northern beekeepers whose bees had already grown to swarming condition due to the unseasonably warm spring weather (Fig. 3).
Figure 3. Last year's warm spring in much of the country lead to early broodrearing, and as a result, early buildup of varroa levels. Note the record warm spring in the Midwest.
The queen producer noted that such early brood rearing also meant early mite buildup, and predicted that since most Midwestern beekeepers treat for mites by the calendar, that they would unknowingly allow mites to build to excessive levels before treatment. This was strike one against the bees.
The Drought
Then it didn't rain-by midsummer, it was clear that the continental U.S. was in serious drought, including California, whose beekeepers supply nearly half the bees for almond pollination. The only ways that we kept our colonies strong was to either feed expensive pollen supplement and sugar syrup, or to move them to elusive better pasture out of state. By late summer, 60% of the U.S. was in drought, meaning that unless your bees were next to soybeans or irrigated crops, there was little forage for them. This lack of good nutrition was strike two against the bees (Fig. 4).
Figure 4. The severe drought in the Midwest really put the hurt to bee pasture in those states in which the majority of commercial hives spend the summer. Source [[i]].
[i] http://www.ncdc.noaa.gov/temp-and-precip/maps.php
Drought not only dries up nectar and pollen sources, but also forces bees to fly further and more frequently for water. Plus it concentrates ag chemicals and pesticides in the few sources of surface water available to bees. The bees started to show the hurt.
Beekeepers tried to move their hives to areas of better forage, sometimes overstocking an area with too many hives, which led to excessive competition for resources, and the spreading of parasites. Others desperately chased less desirable crops such as sunflowers. Colonies in holding yards in California found little to eat, due to our record dry weather. Some beekeepers with winter eucalyptus locations found them crowded with other hives.
Lack Of Good Forage
In Buzzkill, Bret Adee brought up the fact that bee pasture in the Midwest is disappearing under the plow, largely due to our environmentally-irresponsible taxpayer-subsidized policies that encourage farmers to plant every square foot of land into corn (Fig. 5). Bee brokers told me that colonies coming to almonds from the Midwest were in generally poorer shape this year than those coming from the southern states.
Practical application: some Midwestern beekeepers split their operations, hauling some to the South to rebuild over winter, and the rest directly to California-there was a night and day difference as to how the colonies looked in February!
Figure 5. Grasslands and wetlands in the Corn Belt are rapidly being converted to monocultural, heavily herbicided corn/soy, which eliminates virtually all bee and wildlife forage. A new study found that between 2006 and 2011 there was a net loss of 1.3 million acres of grassland. This affects not only bees--the authors [[i]] state that "As a consequence, populations of grassland nesting birds are declining faster than any other group of birds in North America."
[i] Wright, CK & MC Wimberly (2013) Recent land use change in the Western Corn Belt threatens grasslands and wetlands. https://www.motherjones.com/files/pnas201215404_nwow5w1.pdf
To put this loss of bee pasture into perspective, I asked some Dakota beekeepers for estimates of how many acres of CRP grassland are needed to sustain a colony of bees. In recent years, the overall hive density in North Dakota has been more than 10 hives per square mile (less than 64 acres per hive, including wastelands).
Practical application: the best guess by those beekeepers was that each colony of bees requires about 5-15 acres of productive land for forage (late summer forage being the critical factor). If we use the figure of 10 acres per colony, then the conversion of 1.3 million acres of grassland to herbicided cropland suggests that forage for 130,000 colonies of bees has been eliminated in the past five years in the Corn Belt alone! This figure represents nearly 9% of all colonies needed for almond pollination.
Varroa
An excellent window into the causes of colony health problems is the USDA National Honey Bee Pests and Diseases Survey Report [5] (the latest data have not yet been released). It is worrisome that varroa levels appear to be steadily climbing year after year.
And if the drought and forage problems weren't enough, the favored miticide of commercial beekeepers became unavailable for a time last summer, and mite levels built to killing levels in a number of operations. By late July, some of us were already predicting a disaster for the upcoming almond pollination season. Although many beekeepers finally got mite levels down with late-season treatments, the damage had already been done, and there was no turning the colonies around. Strike three for the bees!
In November semi loads of hives started moving into California, or had been placed in potato cellars. Some of the colonies that arrived from the Midwest were in poor shape, or crawling with mites. Oddly, few beekeepers at the time owned up to having problems, despite the reports that I kept hearing of mite and forage issues! I'm not sure whether this was due to denial, wishful thinking, simple lack of lifting the lids, or something else.
Diseases
Nosema infection also runs rampant across the country--70% of colonies were infected in June of last year. The stressful factors leading up to almond bloom apparently put a lot of hives close to the "tip point" at which pathogens can overwhelm the colony immune system and start it going backwards, or initiate the slide into sudden depopulation (detailed at [6]). Few seem to be mentioning signs of CCD-it is unfortunate that the media keep using that term as a catch-all for all hive problems!
One should keep in mind that the winter collapse issue appears to be cyclical, similar to flu or other pathogen epidemics. I have strong reason to suspect that the constantly-evolving viruses are involved in these colony collapse epidemics.
There has also been a strong resurgence of European Foulbrood and other unidentified brood diseases [7] (Figs. 6, 7, and 8). Unlike EFB of old, the new forms don't go away with a nectar flow.
Figure 6. "Shot brood" due to EFB. Note the fat queen near the center. Despite her vigorous egglaying, this colony is unable to pull ahead due to excessive brood mortality. Lots of beekeepers reported EFB symptoms this winter.
Figure 7. You really have to look hard in some colonies with spotty brood to see the cause! Two larvae in this photo show signs of EFB infection.
Figure 8. Dying brood from one of my sick colonies this spring with EFB-like symptoms. Note the "shot" pattern, the twisted larvae, and the dried larval remains. There is also some AFB-like coloration, but lack of roping or AFB odor (this odor is distinct and sour), nor a positive Holst milk test. In this colony, even pupae were dying. I observe these symptoms independent of whether the hives went to almond pollination or not. Colonies with this (or similar) infection cannot grow. Treatment with oxytetracycline generally clears it up.
One thing that I noticed in Buzzkill was the uneaten pollen supplement patties in many of the crashed hives. I've mentioned before [8] that I've found a colony's failure to consume pollen supplement to be a reliable predictor that that colony will later collapse.
Another strong predictor of winter collapse is weak strength in fall (upcoming article), again strongly suggesting that those colonies already have some sort of health issue going into winter. I heard reports from all over the country that bees went into winter in poor condition.
An Unexpected Chill
The final blow to hives in California was a blast of icy weather (Fig. 9). This unexpected chilling compounded all the existing problems! I've previously pointed out that colony collapse often follows unseasonable chills, since it shifts the tip point for virus and nosema epidemics. Clusters that had expanded for broodrearing contracted, resulting in chilled brood and dead young bees on the ground. My own colonies simply shut down broodrearing completely, losing about two weeks of buildup.
Figure 9. Chilling events (blue arrows) in Modesto, California this winter (the dark blue lines represent normal highs and lows). The unusual chilling in late December and early January (hitting the '20's in a number of areas) came at the time when colonies normally begin to build up for almonds. This severe (for California) cold set the already-stressed colonies back hard, and may have allowed nosema and viruses to gain the upper hand. Graph from wunderground.com.
At the national convention in January, the first reports of beekeepers with collapsing operations were heard. But still, the industry was in denial, with an apparent glut of promised bees as late as the end of the month (two weeks before start of bloom)! But when the rubber finally hit the road in mid February, that illusory supply quickly evaporated, with desperate growers and brokers scrambling to obtain bees--some offering obscenely high prices for substandard colonies.
And then, due to the cool spring, the trees held off on blooming for an extra 10-14 days [9]-colonies placed in anticipation of normal start of bloom just sat there starving and shivering on the cold orchard floors.
Practical application: the biology here is that this is the time of the "spring turnover" in bee populations in California, during which the old overwintered adult bees must rear their replacements for the spring buildup of population. The conditions in the almond orchards prior to bloom are miserable for smaller colonies--it is warm enough to encourage them to break winter cluster and expand the broodnest, but overnight frosts on the Valley floor can cause serious chill stress. Furthermore, it is often warm enough to fly at midday, but there is virtually nothing to forage upon until the trees start blooming! Such fruitless foraging further wears out the workers, and allows sick bees to drift to adjacent hives. Worse yet, the desperate foragers rob out any dead or dying colonies in adjacent orchards, rapidly and effectively transmitting mites, nosema, viruses, and anything else harmful in the deadouts.
Many colonies went backwards during this excruciatingly long wait. Some beekeepers told me that hives graded at placement scored better than those graded at bloom (just the opposite of normal)!
I've been carefully observing spring turnover in my "dinks" (weak colonies) in February (Fig. 10). What I find is that the problem is generally not the queen; rather, the colonies are infected with some pathogen- most commonly nosema [10], the paralytic viruses [11], or EFB (or EFB-like brood disease). Those colonies that are able to successfully emerge one solid round of brood are often able to "clear" the infection and completely rebound by April. Those that get hit by frost in February often collapse.
Figure 10. An example of an unsuccessful spring turnover. This colony is in the middle of typical February collapse from nosema or IAPV. You can easily see the outline of the area recently covered with brood, delineated by the crescents of freshly-packed pollen. Colonies undergoing this sort of depopulation tend not to forage for nectar, and do not respond well to supplemental feeding. This colony continued to collapse quickly, and finally died in a cold snap a week later--with only silver-dollar sized patch of dead bees remaining.
Feedback From Brokers
I asked a few of the major pollination brokers for their observations on the colony shortage this season. Their feedback suggested that the causes for the bee shortage were varied and many.
Summary:
Most were able to eventually fill their contracts. Beekeepers often hold colonies in reserve "just in case," or gambling that in "short" years they can rent those last hives at an elevated price. Also, when the offered price went up, hives not originally intended to go to almonds were loaded up at the last minute and shipped to California (I was in Florida at the start of bloom, and had an inspector tell me of certifying colonies for shipment after the bloom had already begun!).
A number of hives received in November were already headed downhill. Some exhibited the symptom of bees not clustering properly (a typical sign preceding sudden colony depopulation/CCD). Some arrived crawling with mites, or with recent mite treatments in place (suggesting that they were treated too late).
Some graders saw piles of dead bees in front of hives--cause unknown. There were reports of some herbicide tank mixes killing bees.
Many of the placed colonies were below standard grade-- growers paid for less than they expected!
Graders told me that there was a huge variation in hive strength from beekeeper to beekeeper. Many hives were strong (12-16 frames of bees) and healthy; other operations graded at zero to three frames of bees (some of the deadouts had spider webs inside, suggesting that they hadn't been occupied by bees for some time).
The unusual winter chill was tough on colonies that had been stimulated into early buildup, and then forced to contract their broodnests. Some colonies kicked out chilled brood and dead bees afterwards.
Many beekeepers watched their colonies go "backward" prior to bloom.
Colonies from the Southern states (especially those delivered in February) were generally in better shape than those from the Midwest.
Midwestern beekeepers blamed drought, mites, poor nutrition.
Several beekeepers said that their best bees came from remote areas, and their worst from ag areas.
A number of beekeepers admitted inadequate mite treatment; mites were a recurrent theme.
There were a number of reports of EFB hitting colonies.
Some had gotten hit last summer with pesticide sprays, and their colonies didn't recover.
"There were good bees and bad bees from every state. They all seemed to have different problems depending on location/state."
Many good beekeepers simply didn't know what happened to their hives; there were lots of lifeless hives delivered. The atmosphere was ripe with speculation as to the actual causes.
"The shortage was also created by beekeepers that chose not to come to California for a variety of reasons. They can make more money with honey, didn't get paid for what they have brought in the past, bees come back home with mites, beetles and whatever else takes a ride on the hives. Beekeepers don't want to risk bee health to chase the dollar." Many out-of-state beekeepers have had bad experiences going to almonds, and simply don't feel that it's worth it. The supply of bees will largely depend upon the price that growers offer for renting them!
The Silent Majority
Buzzkill leaves one with the impression that the entire bee and almond industries are on the verge of collapse. Of course, the news media focus on fear and disaster, so we may consider taking such dire projections with a grain of salt. In the case of Dan Rather, the focus was on the beekeepers with troubles, not upon those who successfully filled their pollination contracts.
So just how severe was the problem? Let's say that there was an overall shortage of 100,000 hives (a figure that I heard floated)--that would represent only about 6% of the total number of hives placed into almond pollination. The other 94% were successfully delivered (although a proportion of those were weak due to the poor season).
Since the debacle, I've heard from plenty of beekeepers whom I'll refer to as the "silent majority," who experienced "normal" colony winter losses in the 5-25% range, and who successfully filled their pollination contracts. Although the hearts of all beekeepers go out to those who suffered severe colony losses, many felt that some of those losses could have been prevented if the afflicted beekeepers had been more proactive than reactive.
And don't forget those upon whom the rest of the industry depends to supply bees for restocking their deadouts! The California package producers, who have been pollinating almonds for decades, are routinely counted on to consistently take strong hives to almonds, and to then shake over a hundred thousand packages of bees for sale afterwards. Few of these major producers experience severe unexplained colony losses.
Beekeeper Management
By no means am I suggesting that those beekeepers who suffered losses engaged in poor beekeeping practices, but I can't help but notice that not all beekeepers were equally affected--a great number provided strong, healthy colonies to almonds. I've spoken to some of them-the common thread is that those who recognized the problems of poor nutrition and mites in August, and took remedial action for the rest of the season, had acceptable winter losses.
Some beekeepers who really put serious effort and money into bee husbandry were even able to sell "shook bees" from their colonies to others in February! For example, watch Keith Jarrett feeding substantial quantities of pollen supplement to very strong colonies in January [12]--Keith consistently brings very strong colonies to almonds every year, and this year was no exception!
Practical application: I'm here to tell you, that one lesson that I've learned during our intense California drought, is that those yards that I fed with protein in late summer before they started going downhill went to almonds much stronger than those that I didn't feed until fall! Proactive is better than reactive--if you wait until colonies are already going downhill, it is much more difficult to turn them around!
I've often been accused of being politically incorrect for speaking frankly. I'd like to make amends at this point by retiring the rude and unsympathetic term "PPB" (Piss Poor Beekeeping). The fact is that the average wintering loss for the past few years has hovered around 30%. So if you experience 30% losses, you can now proudly call yourself an "Average" beekeeper!
But what about those beekeepers who consistently manage to enjoy lower rates of winter loss? I propose that we call them "Lucky" beekeepers, and the best of them, "Consistently Lucky."
Practical application: the harder those beekeepers work, the luckier they get!
But there were clearly "unlucky" beekeepers this year--especially the "big boys" who brought tens of thousands of hives from the drought-ravaged, and corn-converted Midwest to California. California beekeepers are used to summer drought. We have learned to either move our colonies to better (often irrigated) pasture, or to feed expensive pollen supplements. This would be a very expensive proposition to the larger operators, with hives spread all over the place--a cost not covered by current pollination prices.
What Happened To The Bees This Spring?
Part 2: The Contribution From Pesticides
Randy Oliver
ScientificBeekeeping.com
First published in: American Bee Journal, July 2013
It's pretty straightforward to attribute the majority of colony losses this winter to the usual and aforementioned causes, but a number of beekeepers are also pointing the finger at pesticides. There is no doubt that in certain areas pesticides were a serious issue to beekeepers. Colonies set back by pesticide kills may not fully recover over the season, and those going into winter with pesticide residues may go downhill. There is also reason to suspect that pesticides and miticides have something to do with today's high rates of queen failure.
The bees in some drought-stricken areas were forced to forage on irrigated and pesticide-laden crops--the only place in which there was anything to eat. This changes the entire dynamics of pesticide exposure, since residues would no longer be diluted by the pollen and nectar of non crop plants. The lack of good natural forage also suppresses the ability of colonies to deal with the insult of those pesticides. And colonies may be forced, by necessity, to forage upon one treated crop after another, resulting in multiple exposures.
Practical application: under drought conditions, bees may suffer more from pesticides than when times are good.
Due to the current high prices for agricultural commodities, farmers are often applying pesticides indiscriminately as "risk insurance" rather than due to actual need. A chilling recommendation from an extension entomologist reads:
I encourage you to be risk averse and to make an investment that will pay dividends for your valuable crop. Consider applying [flubendiamide, indoxacarb, or spinosad] for corn earworm. If you have stink bugs and are in the [mature plant] stages, you might want to tank mix one of these products with a pyrethroid. A tank mix of a pyrethroid and acephate are an option, but will wipe out all beneficials [13].
The first three insecticides mentioned are considered to be "reduced risk" to bees if residues are allowed to dry for a few hours, but no mention was made to spray at night. Of the five insecticides recommended above for spraying on corn in tassel, at least four are highly toxic to bees if sprayed during the day! No farmer wants to kill bees, but with recommendations like this from state extension agents, well-meaning growers may unwittingly be hurting pollinators.
Bees in agricultural areas are exposed to a vast array of insecticides, miticides, fungicides and surfactants--many of which have clear links to colony health problems. And applications of new mixes of chemicals are up. For example, in addition to the neonicotinoid seed treatments, granular insecticide soil treatments for corn in the Midwest were up by 30% over the previous year [14]. These treatments consist of combinations of organophosphates and pyrethroids.
But I'm not hearing either the bird groups or beekeepers even addressing these treatments! It is scary to read the sales literature for Counter insecticide, the organophosphate terbufos [15]. Growers are encouraged to apply it at planting time, despite the facts that:
"Terbufos is highly toxic to birds, fish, and aquatic invertebrates [and bees]. [It] shows significant acute mortalities of birds, mammals, reptiles, and fish resulting from broadcast application...In the same study, the application of terbufos as a soil-incorporated treatment to corn...resulted in acute mortalities to birds and reptiles" [16].
Terbufos is strongly systemic, meaning that it is absorbed by the plant roots and could be expected to be expressed in the pollen and nectar.
It can synergize with other pesticides since it ties up the critical CP450 enzymes used in detoxification, to the extent that growers are cautioned that it can cause problems to corn from herbicides [17].
During drought, certain insect pests become more problematic, perhaps resulting in increased exposure to insecticides by bees. For example, drought encourages corn leaf aphids. Read this chilling recommendation for aphids on corn during tasseling (when bees are actively foraging):
If less than 50% of pollination has occurred, aphids and honeydew are covering tassels and plants are stressed, an insecticide may be necessary to ensure adequate pollination, but treatments need to be made within 48 hours of tassel emergence. Asana XL, Brigade, Capture, Cobalt, Dimethoate, Lannate, Lorsban, or Malathion may be used for control [18].
Or this:
Prolonged drought always raises the specter of two-spotted spider mite outbreaks in soybeans and corn. As the 2012 drought intensifies in Minnesota, infestations are reaching treatable levels...The only products that are recommended for spider mites in soybean include insecticides containing chlorpyrifos, dimethoate and bifenthrin[18].
The names of the recommended insecticides above strike fear into the hearts of beekeepers!
Practical application: many "consistently lucky" beekeepers go to great effort to allow their colonies to recover after exposure to pesticides--moving them to unsprayed areas or natural forage, or by immediately feeding protein supplement to stimulate increased broodrearing. Unfortunately, such "recovery" areas are getting harder and harder to find.
The Lynch Mob
Despite the fact that a wide range of bee-toxic insecticides are being applied (often during bloom) to corn, soy, sunflowers, alfalfa, cotton, and other major crops, if you Google anything about insecticide use, you'll quickly find that the blogosphere focuses only upon the putative link between a single class of insecticides--the neonicotinoids-and the demise of pollinators [19].
People look at me incredulously when I point out that there is zero firm evidence to date that the neonic seed treatments are a serious problem! But the notion that all honey bee problems are caused by an insidious new insecticide resonates with a distrustful public [20], and has firmly established itself as "common knowledge." But repeating something does not make it true!
"It's easier to fool people than to convince them that they have been fooled"-Mark Twain
Practical application: the question is, "Are the neonic seed treatments being railroaded into a guilty verdict in the media's kangaroo court of public opinion?"
One group recently brought suit against the EPA to ban the use of the seed treatments clothianidin and thiamethoxam [21], neither of which even make California's top 100 list of pesticides applied [22], nor that have ever been demonstrated to harm colonies feeding on the pollen or nectar of seed-treated plants! A number of people have made up their minds that the neonics are the main cause of colony collapse, and it appears that no amount of facts to the contrary will cause them to reconsider!
Debunking The Myths
As anyone who knows me will tell you, I am a stickler for honesty, accuracy, and factuality. I am concerned about the amount of misinformation and speculation going around about the neonics. So let's look at some of the claims vs. the actual facts.
Arguments Against Neonic Seed Treatments Actual Facts
The neonicotinoids have been "linked" to increased colony mortality. In actuality, such a "link" is merely an urban legend, and has never been demonstrated or confirmed in any study.
On the other hand, the residues of other classes of pesticides are more suspect for causing increased brood or adult bee mortality [24].
The timing of CCD coincides with the introduction of the neonic seed treatments in 2004. CCD started in California bees in the winter of 2004/2005, prior to them ever being exposed to seed-treated crops.
But what else could have changed at that time other than the introduction of neonics? In California, Dr. Eric Mussen [25] determined that the increased colony losses were due to poor summer forage and failure of mite control products (just as this last winter).
There is actually a much stronger association between the incidence of the novel gut parasite Nosema ceranae and increased colony mortality [26].
But the main thing that has changed is the dynamics of the varroa/virus complex, which coincidentally occurred at about the same time that the neonics came into use.
European countries banned the neonics, and the bees recovered after those bans. A few countries placed temporary suspensions on certain seed treatments until planting dust issues were resolved [27]--only Germany has one suspension still in place. The foliar applications were not suspended. The suspensions did not resolve bee health problems.
The European Food Safety Authority recently decided that neonics pose a threat to bees. "The Center for Regulatory Effectiveness (CRE) has recently completed a Data Quality Act (DQA) Alert on the ... (EFSA) report on neonicotinoids which found that neonicotinoids pose a risk to bees. The DQA Alert outlines the serious deficiencies of the EFSA report and demonstrates why the EFSA report violates the DQA...In particular, the EFSA report failed to maximize the objectivity of the data by failing to reconcile numerous studies whose conclusions contradicted the findings of the EFSA report" [28].
Several lab studies have found that neonics affect individual bee behavior, longevity, or immunity. True -- although many studies used unrealistically high doses. The question is whether such artificial studies apply to actual colonies in the field. The numerous field studies to date have failed to find any link between seed treatments and later colony health issues.
It is the seed treatments that make corn a problem. As Bret Adee points out in Buzzkill, corn is replacing pastureland (Fig. 4). Corn, as grown today, is a virtual "bee desert" (similar to the way in which suburban lawns are green bee deserts). And it's not only the bees that this is affecting, the populations of birds and other wildlife are plummeting due to loss of favorable habitat (see my blog on birds and neonics [29]).
A recent survey by Dr. Jerry Bromenshenk found that bees actually avoid field corn pollen, and are exposed to very little of the seed treatment residues [30].
Numerous independent studies, and the experiences of stationary beekeepers throughout the Corn Belt, support the conclusion that colonies can thrive when surrounded by corn, provided that there is some alternative forage within flight range.
As the use of neonic seed treatments increases, bee mortality goes up. In actuality, colony mortality rates go up and down year to year, largely dependent upon weather and varroa mite control. If the neonics were to blame for this winter's bee losses, why didn't they cause similar losses last winter, in which the colony mortality rate was the lowest in years?
French beekeepers also started seeing problems with the introduction of the neonics. I've spoken with beekeepers in France whose apiaries are in pesticide-free areas. They tell me that they experience the same sorts of colony mortality problems as do those in areas exposed to neonics.
Bees in the U.S. are commonly exposed to neonicotinoids. In the most recent USDA survey (100 samples across the country), imidacloprid was only detected in 9% of the samples [31] (although I found some of the residue levels alarmingly high). However, the most common seed treatment, clothianidin (or its degradation products), was not detected at all!
The above real-world data suggests that efforts to ban clothianidin as a seed treatment may be misplaced. It appears that imidacloprid, especially as a foliar application, would be of more concern.
Neonics are the most common pesticides that bees are exposed to. In the above survey, other serious insecticides were more commonly prevalent: chlorpyrifos (in 20% of samples), cyhalothrin (in 7%), and endosulfan (in 11%).
Notably, there was also a high prevalence of beekeeper-applied miticides: fluvalinate (in 38%), coumaphos (in 87%), amitraz (in 27%), fenpyroximate (in 11%), and thymol (in 27%).
There was even higher exposure to fungicides and adjuvants.
It is misleading for the pesticide companies to blame the problems on varroa, nosema, or poor nutrition. The above survey (over 1000 samples) found that the average varroa infestation rate in the U.S. in autumn is above the danger level for virus epidemics!
Sixty to 100% of hives are infected with nosema in December.
Summer drought has historically been associated with high winter mortality.
But didn't the planting dust from corn seeding kill colonies in Ontario? Planting dust is separate issue that clearly needs to be remedied. It does on occasion cause bee kills, for which beekeepers are rarely compensated. This situation must change! All parties are actively working on solutions [32].
Bees in certain agricultural areas tend to go downhill later in the season. This has been observed for a long time--long before the neonics. The question is, which chemicals, chemical synergies, or chemical/nutrient interactions are responsible? The Frazier/Mullin team at Penn State has developed a protocol for helping to figure this out. I strongly support its adoption by the EPA for pesticide risk analysis.
Colonies foraging upon nectar or pollen of seed-treated crops get poisoned. Ask yourself this: if neonic residues were actually so harmful to bees, how is it that the Canadian beekeepers, whose bees forage largely on seed-treated canola, feeding solely upon a diet of canola nectar and pollen with well-documented residues of clothianidin, experience very low winter losses, despite the long Canadian winter (so long as they control varroa and nosema)?
And how is it that the vast majority of beekeepers in the U.S. Corn Belt report that their colonies thrive and that they have far fewer pesticide issues these days than in the past?
The neonicotinoids are "systemic," meaning that they are in the plants all the time! True, but this property is not unique to the neonics--a number of other insecticides also go systemic. In any case, with seed treatment, the concentration of the insecticide in the plant is only high when the plant is young--it gets diluted as the plant grows (e.g., clothianidin in canola is at a level high enough to kill aphids for only about the first 30 days of growth).
The only time that residues in the plant matter to pollinators is when the mature plant flowers. The amount of seed treatment is carefully calibrated so that the residue in the pollen and nectar are below the level that causes demonstrable harm to bees.
In the case of foliar, drench, or chemigation applications prior to bloom, there are greater possibilities for bees to be exposed to toxic levels.
There are fewer butterflies and pollinators in the fields these days. Not surprising, since the new push for "clean farming" has removed the host plants upon which the butterfly larvae feed. Pollinators are forced to subsist upon the stretches of weeds growing along roads at the edges of fields. But surprisingly, pollinators may be abundant there, suggesting that even though populations as a whole are reduced by habitat conversion, it is that, rather than the use of seed treatments, that causes the population declines.
The evil pesticide companies want to kill honey bees. Give me a break! Does anyone truly believe that anyone wants to kill honey bees? What pesticide company would want the bad press of being associated with killing bees? The chemists and biologists on their staffs earnestly work to develop insecticides that are bee friendly.
The EPA is being derelict in their duty to protect pollinators. I have spoken at length with EPA staff, and reviewed their risk assessments, as well as those by, DEFRA, EFSA, PMRA, and other regulatory agencies. I find that the risk assessors have not overlooked any evidence, are well-informed on the subject of neonics, and are justified in their assessments that the on-the-ground evidence (to date) indicates that neonic seed treatments pose acceptable risk to pollinators.
We must all remember that the tobacco industry tried to hide the fact that nicotine was addictive [33]. Spare me! Does anyone seriously think that the EPA is unaware that industry executives may stretch the truth? Of course the EPA is skeptical of any reassuring claims by the pesticide industry--that's why they go over all studies with a fine-toothed comb!
This winter's losses spell the end to commercial beekeeping. The fact of the matter is that many observers note that the bee supply for almonds often follows a boom-bust cycle. Although losses were high this year, the trend for the last decade has been for beekeepers keep ramping up the supply of bees for almonds. So long as growers are willing to pay a profitable rental rate for colonies, market forces will encourage the bee industry to meet the demand (for a detailed analysis, see [34]).
The Precautionary Principal
"But," you say, "shouldn't we exercise precaution due to the lab studies that find adverse effects from the neonics?" Look, I make my living as a beekeeper, I'm not out to sell insecticides, and am as concerned as the next person about the environment and the safety of the food I eat. I've researched the neonics exhaustively, and addressed them in several articles [35]. I am acutely aware that there are suggestions that the neonics may be causing insidious effects in the environment, and I've studied the excellent environmental document Late Lessons from Early Warnings [36], which hammers the message that we should use the "precautionary principle" when dealing with chemicals. The problem is, there is nothing without risk--for example, you have a 1 in 83 chance of being killed in an auto accident in your lifetime. But most people still take the risk of getting into cars, since they feel that the benefit outweighs the clearly high risk!
My practical perspective as both a scientist and a beekeeper: if researchers perform lab studies on any insecticide, they will find that there are all kinds of negative effects upon bees--this should be pretty obvious, since insecticides are specifically designed to harm insects! However, the majority of these studies are taken out of the context of full colonies under field conditions, where bees fly free and choose the flowers upon which they forage. The evidence to date supports the contention that the neonics, properly used as seed treatments, are indeed an improvement over other insecticide options.
As Dr. Eric Mussen succinctly notes:
Nobody's really been able to show that [the neonicotinoids] are more problematic than the rest [of the pesticides to which bees are exposed] [37].
Far be it from me to suggest that the neonics (or any other pesticides) are harmless! But consider this--if the neonic seed treatments were indeed as harmful as some make them out to be, you'd think that after a decade of intense study that at least one researcher could have come up with a single solid piece of field evidence against them!
Let's do a thought experiment. Why doesn't someone simply put a bunch of healthy hives into the middle of seed treated crops and see whether they die afterward? Oh, I forgot--this experiment has already been run by thousands of beekeepers year after year in the Corn Belt and the Canadian prairie! And those beekeepers have invited me to look at their colonies, sent me photos of colonies stacked head high with honey supers, and bragged about their high winter survival!
Some will argue 'til they're blue in the face, but the fact remains that virtually every beekeeper that I've spoken with in the Corn Belt and in canola areas feels that the seed treatments are not a problem [38]. In fact, most tell me that this is the best it's ever been as far as bees and pesticides!
Common sense: I just don't get what is so hard to understand about the reality that there are thousands of colonies thriving year after year in areas of intense seed treatment? To any reasonable person it would suggest that the treatments are causing little noticeable harm other than the occasional planting dust kill, which I have repeatedly stated is a problem that needs to be corrected!
See For Yourself
Let's look at actual independent (from the manufacturer) data from corn and canola areas:
Corn
I asked friends in the Corn Belt if they had any data on winter losses. It so happens that the Michiana Beekeepers Association has been collecting exactly that since the spring of 2010 (Fig. 11).
Figure 11. Percentage of winter losses by the "Michiana" hobby beekeepers. The 2013 figure is as of mid March; it may eventually go down a bit due to a prolonged cold spring. Note that the winter survival rate appears to be linked to average winter temperature. Thanks to beekeeper Danny Slabaugh for sharing the data; temp deviations from [[i]].
[i] http://www.ncdc.noaa.gov/temp-and-precip/maps
How could the above be? Eighty percent winter survival despite sitting in the middle of seed-treated corn and soy? So of course I did a fact check to confirm that those beekeepers were indeed sitting in corn/soy areas (Fig. 12).
Figure 12. USDA land cover categories for the region in which the Michiana hobby beekeepers keep bees--corn and soy acreage is color coded yellow and green, respectively. The selected area is the top half of Indiana and bottom of Michigan, with Lake Michigan at the left. Clearly, these apiaries were exposed to seed-treated corn and soy! I created the map at [[i]].
[i] http://nassgeodata.gmu.edu/CropScape/
The above figures suggest that colony winter survival for stationary hobby beekeepers in the above corn/soy region is higher than the national average, despite the fact that about half of them don't even treat for mites! They also suggest that the neonics or other pesticides used in corn/soy in that region do not cause excessive winter loss. Finally, the data indicate that a main factor for winter loss rates is the winter temperature.
Canola
I've heard some beekeepers saying that their bees crashed after working canola, suspecting that the seed treatments were the problem. So as a reality check I called a Dakota beekeeper who has been running bees to canola for over a decade--some 10,000 hives last season. He tells me that colony strength after canola varies from year to year, but that he sees no problem with the seed treatments. He did point out that beekeepers should be aware that colonies can plug the broodnest on intense canola flows.
The biology: The plugging out of the broodnest during an intense bloom means that three weeks afterward, there will be few emerging workers to take the place of the worn-out foragers, and the colony population will temporarily plummet. Even worse, the remaining mites are then concentrated onto fewer bees--which can initiate virus epidemics. These colonies must then attempt to rebuild from scratch, starting in August, meaning that the weakened, mite-infested colonies faced three long months of drought last summer for that rebuilding process.
Every field study that I've seen for canola also supports the conclusion that the seed-treatments are safe for bees. I joined other beekeepers and regulators in observing a large-scale study of seed-treated canola in Canada [41]. Canola (or rapeseed) is likely the best test crop, since bees eagerly (and virtually exclusively) forage upon it for both pollen and nectar, meaning that every bit of their food supply contains contain easily verifiable residues of the insecticides. The preliminary results indicate that the clothianidin seed treatment did not harm the colonies [42].
Another recent independent long-term field study in Poland [43] came to the same conclusion. In it, the researchers followed 50 colonies for more than two years under field conditions as they foraged on five different large fields of oilseed rape treated with various combinations of five different neonicotinoids applied by seed treatment and spraying. Pollen and nectar samples were taken, and demonstrated that the bees were clearly exposed to normal residues of the insecticides (there was also additional exposure to other common agricultural pesticides). The colonies were monitored for health, brood, strength, nosema, viruses, and winter survival, and compared to two control apiaries set in an area free of the crop. The results?
During the time from the placing of the colonies on the rape fields until wintering, the colonies developed properly in all groups... All colonies overwintered properly... In both years, during the period of being placed in the oilseed rape fields as well as after being moved to the stationary apiary, none of the groups showed disturbances in development or functioning.
Following a paper that suggested that the seed treatments would impair bumblebee colonies' ability to rear queens, DEFRA performed a common-sense field study last year [44]. Their findings:
...the study has shown that bumble bee colonies remained viable and productive in the presence of the neonicotinoid pesticides under these field conditions...The study underlines the importance of taking care in extrapolating laboratory toxicology studies to the field, as well as the great need of further studies under natural conditions.
Sunflowers
Some beekeepers report that their colonies later crashed after they chased sunflowers last summer for honey. One must keep in mind that sunflowers are not a natural food for honey bees, and provide only poor-quality, nutritionally-inadequate pollen [45]. But the main problem with putting bees on sunflowers may be related to the fact that sunflowers are a native plant--meaning that there are a number of native insects that evolved to feed upon it:
Maximum seed yields often require the use of insecticides to protect the crop from insect competitors. Unfortunately, many of the major insect pests of sunflower attack the crop when it is flowering. Thus, insecticides used to control the pest also harm pollinating bees [46].
If sunflowers are the only forage available, colonies may eventually go downhill, due to the one-two punch of poor pollen nutrition coupled with insecticide exposure. And which pesticides would those be? One scary list- Asana XL, Baythroid, endosulfan, Furadan , Lorsban , methyl or ethyl parathion, , Proaxis, Scout X-TRA, Sevin, Warrior, Mustang Max, Declare, Cobalt, Yuma, Delta Gold, and Grizzly Z [47]!
Note that none of the above are neonics, other than seed treatments for wireworms. Surprisingly, field evidence indicates that the seed treatments only "stun" the wireworms for a while [48], which certainly raises the question as to how harmful they might be to bees months later when the plants flower! I will return to sunflowers below.
Be Careful What You Ask For!
Allow me to assure you that I am no pitchman for neonics or any other insecticide--the typical farmer practices far too little integrated pest management, and applies far too many pesticides! All insecticides (and several fungicides and adjuvants) cause problems to pollinators--the neonics are no exception. Any systemic insecticide has the potential to harm bees when applied as foliar applications, by chemigation, or to flowering trees, but it there is no compelling evidence that the neonics are any worse than the alternatives in most applications. On the contrary, there is quite a bit of evidence that they may often be "safer" ("reduced risk").
If the neonic seed treatments were banned, it's not as though all agriculture is suddenly going to go pesticide free--only about 1% of U.S. cropland is registered as "organic"! We must consider the likely alternatives. The products that farmers would then use to control insects would need to be sprayed all over the cropland--we'd then be back to the problem that the bulk of sprayed insecticides go into the environment without ever hitting the intended pest!
I hear from knowledgeable beekeepers that worse than in previous years, some of the new formulations of the spray-applied insecticides [49, 50, 51] can really knock the snot out of bees! One large beekeeper found his hives already dead before moving them away from the fields. Again, this was not a neonicotinoid issue.
Practical application: no one is saying that the neonics are "harmless." The question is whether they are better or worse than the alternatives.
The Effect Of Drought
Let's discuss some of the problems (or suspected problems) with the neonics last season. The record warm and dry spring appeared to exacerbate corn planting dust issues (corn seeds are the worst offender due to their non spherical shape). Beekeepers in some areas of the Corn Belt, the East Coast, and in Ontario suffered from confirmed (in at least some of the cases) planting dust kills (although many went on to make good honey crops after their colonies recovered). The final analysis from Ontario is not yet completed, but dry soil conditions and an early clover bloom likely contributed to the problem. Regulators and the seed companies are working on solutions to the problem [52]. Still, IMHO it is unacceptable to ask beekeepers to bear the burden of bee kills without compensation, and no one could blame the affected beekeepers for being pissed!
Drought-stressed plants
There are a number of advantages to the neonic seed treatments. Besides their safety to the farmer and to most wildlife, there is virtually no way for the farmer to misapply them! The timing of application is only at planting time (when bees normally have little interest in the bare fields), and the dose is determined by the seed-treating company. This means that the applicator can't be tempted to apply at the wrong time, or to over apply too strong a dose (however, their excessive near universal use can be expected to accelerate the development of resistant pests).
That said, beekeeper Bret Adee brought an interesting question to my attention: the dose of seed-applied systemic insecticides (whether neonic or other) is based upon the dilution factor as the plant grows, so that the residues in nectar and pollen will be reduced to below the "no observed adverse effects level." But what happens during drought, when the water-stressed plants only grow knee high before desperately flowering? There would be far less plant biomass in which to dilute the insecticide (assuming that drought-stressed plants absorb the same amount from the seed treatment).
Certain plants (including sunflowers and canola) are known to "hyperaccumulate" toxic metals [53], perhaps more so during drought. Could this also be the case with systemic insecticides? Something that's been stuck in the back of my mind is that Bonmantin [54] found that the concentration of imidacloprid first drops in sunflower plant tissue as it grows, and then reconcentrates in the flower heads.
It occurs to me that the translocation of systemic insecticides is generally studied in plants grown under "normal" conditions. I'd very much like to see data for residues in pollen and nectar from seed-treated plants grown under drought. Had we thought of this earlier, we could have collected pollen and nectar samples from drought-stressed plants last summer. I'm currently trying to track down any data or samples from such plants--if any reader has any such sample analyses, please let me know!
Practical application: the above hypothesis is speculative, but we need actual data from drought-stressed plants to see whether such an effect occurs. If so, it would need to be taken into consideration for the registration of seed treatment products!
Once planting was completed and the drought took its toll, the reports that I've heard are that soybean honey saved a lot of bee operations this season, right in the middle of treated corn/soy farmland. In this case, seed treatment with neonicotinoids may have been a blessing to beekeepers:
The benefits of [seed treatment] not only include the early-season disease control but also suppression of soybean aphids for quite a ways into the growing season. With it, we typically make only one foliar insecticide application for aphid control, usually in August, instead of two applications when [treatment] isn't used. In 2012, with the extremely dry conditions in mid-season, there wasn't as much of an aphid problem, and we treated just 300 acres of soybeans...Last year we sprayed closer to 30,000 acres for aphids [55].
On the other hand, some beekeepers on alfalfa or cotton got hit hard by other classes of insecticides. A hit from a pesticide application can lead to poor subsequent colony performance, queen failure, dwindling, or winter collapse. ABJ published an excellent series of articles on pesticides by Drs. Barbara and Eric Erickson in 1983; Editor Joe Graham has graciously granted me permission to post copies of those articles to my website [56]--I strongly suggest any beekeepers interested in pesticide issues read them! In the second article, the authors discuss both the problems with systemic insecticides and of sublethal effects--note that these articles were written long before the introduction of the neonics!
An anti-pesticide group, along with a handful of beekeepers, recently filed suit against the EPA [57], calling for an immediate ban on the two most common neonicotinoid seed treatments, despite the easily-verifiable fact that hundreds of thousands of colonies thrive in the midst of seed-treated corn, soy, and canola! To me, this suit smacks of being some sort of well-orchestrated publicity stunt, and does not serve the interests of either beekeepers or environmentalism. Worse, it now gives the powerful farm lobby cause to label beekeepers as "radical" enemies.
We don't want this battle: do we really want to take on the farm lobby by backing them into a corner? The French beekeepers took a similar case against fipronil all the way to their supreme court and lost [58, 59]-worth reading]. Agriculture is already positioning itself for a fight [60, 61, 62]. Think about it--the EPA lives in fear of a conservative congress slashing their funding. Does anyone really think that they are going to go against the agricultural lobby without unimpeachable evidence? We should also think twice before calling for a ban on the seed treatments--the alternatives are not pretty!
It disturbs me to hear industry executives and lawyers stretching the truth or misrepresenting data. It disturbs me even more to hear my fellow environmentalists and beekeepers doing so! If we wish to maintain credibility, we should hold ourselves to a higher standard. The question we must ask ourselves the way in which we wish to have pesticide regulation decisions made:
1. By the EPA (the Environmental Protection Agency), whose risk assessors carefully study and weigh all available research and evidence in order to make objective and rational decisions, or
2. To have it decided instead by impassioned, fearful, and often misinformed advocacy groups who hire lawyers and pressure politicians who know little about the subject?
We depend upon the EPA to strike a balance between the availability of cheap food and profitability for those who provide it, versus the risks to human and environmental health and safety. It is good to have activists on both sides of the issues (industry and the anti-pesticide groups) to keep the EPA informed. But I don't feel that either of those groups should be telling the EPA which pesticides to register or to ban! Let the regulators do their job!
Rather than wasting EPA's funding to fight frivolous lawsuits, there are more productive actions that we can take:
Help the EPA to do its job by filing "adverse effects incident reports" if you observe a problem due to pesticides [63]. EPA is begging beekeepers to do this! Unless they have documented reports of pesticide problems, their hands are tied as to restricting the uses of those pesticides!
Support the National Pollinator Defense Fund [64]. Our industry is currently represented by a reasoned and knowledgeable group of (mostly) beekeepers. (Challenge to the pesticide companies: why don't you stand behind the safety of your products and donate? The NPDF is about ensuring that your pesticides are properly applied, so there would be no conflict of interest).
If your local state lead agency is not actively investigating bee kills or enforcing pesticide regulations, then use the local media to embarrass them into action!
Keep pressure on the EPA to resolve corn planting dust problems. Here's a wild idea: I'm not sure of the exact figures, but let's say that 90% of the 95 million acres of corn is grown from neonic-treated seed. If the states were to levy a surcharge of 50 cents per acre (neonic seed treatment adds about $12 per acre to seed costs), they could collect over $42 million each year to fund a pool from which to indemnify the occasional beekeeper who suffers a confirmed kill from planting dust!
Tell Congress that we'd like to see wording added to the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) to specifically protect pollinators. Currently, such protection is nebulous (although the EPA is acutely aware of pollinator issues): "The Administrator shall register a pesticide if... when used in accordance with widespread and commonly recognized practice it will not generally cause unreasonable adverse effects on the environment." Unless there is specific wording to protect pollinators, bee kills may not be considered to be "unreasonable"!
We need far more independent field studies to determine which pesticides and application practices are actually causing harm to pollinators. For pesticides in question, keep pressure on the EPA to require additional field trials to demonstrate whether they are indeed safe for pollinators under field conditions. I'd like to see the establishment of monitoring apiaries (and patches of untilled land) in representative agricultural areas nationwide, with the hives in each apiary to be carefully managed by independent parties. Such apiaries and sites could then be closely monitored each summer to see whether honey bees and other pollinators are able to survive local pesticide practices.
Give farmers workable options! Disseminate and promote bee-friendly agricultural practices that don't hurt the farmers' bottom line. For example, by adopting IPM practices, Arizona cotton growers reduced insecticide spraying from 12.5 times a season to only 1.3 times (cutting insecticide use twentyfold), while using more environmentally-friendly insecticides [65]! Another recent study in Iowa found that adding additional clover or alfalfa rotations in corn/soy farmland was equally profitable, improved the soil, used less energy, used far less pesticides, and decreased water pollution [66].
Business and agriculture respond to consumer demand. Consumer demand stopped most dairymen from injecting their cows with the hormone BST. Consumers could do the same by demanding pasture-fed beef and dairy (which would create more pollinator forage)! I'd also like to see the expansion of consumer choices (other than organic certification) that reward farmers who manage their lands to the benefit of wildlife and pollinators. For ideas, see [67. 68. 69].
Bottom Line
In conclusion, it appears that a perfect storm of a preceding exceptionally warm winter, followed by serious drought across the country, the lack of good mite control, a high prevalence of pathogens, and an unexpected California chill in the orchards prior to bloom, resulted in an unusual degree of colony losses. In other words, rather than one specific cause, there were simply not enough of the good things, and too many of the bad things.
I don't see evidence that pesticides were the major factor in the shortage of bees in almonds this winter, although, as usual, a number of individual beekeepers on certain crops certainly took serious hits.
And how about the fear that there won't be enough bees for almond pollination next year? Beekeepers have already told almond growers to expect higher pollination prices next year (especially since California is again going into serious drought, and beekeepers will be forced to invest extra money in feeding their hives). Most every beekeeper I know is madly making increase right now in anticipation of higher pollination prices next season. The fact of the matter is that should conditions allow beekeepers to successfully rebuild their numbers (following the typical swings of our boom/bust cycle), there could possibly even be a glut of bees for almonds next winter!
Feedback And Corrections
A few countries placed temporary suspensions on certain seed treatments until planting dust issues were resolved [27]--only Germany has one suspension still in place. - Actually there are some more: France (Thiamethoxam in oilseed rape, Imidacloprid in corn and sunflower), Italy (all Neonic seed treatment in corn), and Slovenia (Imidacloprid, Thiamethoxam, and Clothianidin seed treatment in all crops)
French beekeepers also started seeing problems with the introduction of the neonics; I've spoken with beekeepers in France whose apiaries are in pesticide-free areas. They tell me that they experience the same sorts of colony mortality problems as do those in areas exposed to neonics - This is, by the way, likewise confirmed by monitoring results from the French authorities.
In the case of foliar, drench, or chemigation applications prior to bloom, there are greater possibilities for bees to be exposed to toxic levels. - This is not the case for foliar application: as Neonics are xylem-systemic, but hardly mobile in the phloem, they can only be distributed in a plant after root uptake, but not be translocated for instance from a leaf to a later developed flower.
Then, on the topic of systemic residues in plants under drought stress: first, I am quite sure that the decrease of concentration in seed-treated plants over time is not only due to dilution, but also to degradation of the compounds - a factor that is not specifically dependent on water availability for the plants (e.g. photodegradation!); second, even if there would be less dilution in plants under drought stress: the concentrations in nectar and pollen of treated crops are normally so low (when we consider average rather than peak concentrations, and when we consider scenarios where colonies have chronically access exclusively to contaminated nectar/pollen over months unlikely in practice), that even an increased concentration due to drought stress-affected plants should not make a significant difference: if we for instance assume an average concentration of let's say 3-4, or even 5 ppb Clothianidin in corn pollen, and likewise assume a dilution reduced to 50% (which is probably exaggerated), then we would still not end up with excessive residues. And finally, we have residue figures from crops grown in different countries, different climatic conditions, and different agronomic practices; though we have not specifically addressed the drought stress scenario, we have seen that residue figures are quite consistent over all scenarios, and there does not appear to be strong evidence that different environmental conditions would substantially (i.e. by orders of magnitude) and systematically alter residue concentrations.
Dr. Christian Maus
Global Pollinator Safety Manager
Bayer CropScience
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A ppt on the impact of CRP lands on wildlife in North Dakota
http://www.redriverbasincommission.org/Conference/Proceedings/26th_Proceedings/Kading_RRBC_09.pdf
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Feedback from a Midwestern apiary inspector:
Just a quick update: This beekeeper who recently told his local newspaper that pesticides were killing his bees, he was making excuses. We examined two of his yards with him yesterday. One yard was showing EFB throughout the whole yard. I think his "mid-summer losses" last year (half of that yard's hives) were EFB kicking in with the mid-summer dearth. In his other yard, most of his dead outs were obvious starve outs. He harvested all of their stores with the first frost, and then didn't feed them. So, in my opinion, and from my observations, pesticides are usually being used responsibly, and aren't killing honey bees. I also think, with the aggressive way bees were on soy fields last summer, the systemic pesticides are not harmful to honeybees. I'm not seeing honey bee problems other than EFB getting the upper hand, due to our cold, late spring. My two cents. Thanks.
References
[1] http://www.frequency.com/video/dan-rather-reports-buzzkill/87705620/-/YouTube
[2] http://www.ars.usda.gov/is/pr/2012/120531.htm and California DPR.
[3] http://www.ncdc.noaa.gov/temp-and-precip/maps.php
[4] Wright, CK & MC Wimberly (2013) Recent land use change in the Western Corn Belt threatens grasslands and wetlands. https://www.motherjones.com/files/pnas201215404_nwow5w1.pdf
[5] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
[6] https://scientificbeekeeping.com/sick-bees-part-2-a-model-of-colony-collapse/
[7] vanEngelsdorp, D, et al (2013) Idiopathic brood disease syndrome and queen events as precursors of colony mortality in migratory beekeeping operations in the eastern United States. Preventive Veterinary Medicine 108(2-3): 225-233. http://www.sciencedirect.com/science/article/pii/S0167587712002656
[8] https://scientificbeekeeping.com/sick-bees-part-18a-colony-collapse-revisited/
[9] http://almondinsights.com/692, http://agfax.com/almonds/2013/reports/03042013-almonds-web.htm
[10] https://scientificbeekeeping.com/sick-bees-part-18a-colony-collaspse-revisited/
[11] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2010-2011-Limited_Survey_Report.pdf
[12] http://www.youtube.com/watch?v=y6B5qm2ut18, http://www.youtube.com/watch?v=PYbLbhZXizY
[13] (Broken Link!) http://www.nccrops.com/2012/07/27/insecticide-recommendations-for-corn-earworm-in-soybeans/
[14] http://www.agriview.com/news/crop/corn-soil-insecticide-use-up-dramatically-to-combat-widespread-rootworm/article_5d09decc-5b40-11e2-b485-001a4bcf887a.html
[15] http://www.amvac-chemical.com/products/documents/Counter20G%20Tech-Sell%20Sheet%20-%202013.pdf
[16] http://pmep.cce.cornell.edu/profiles/insect-mite/propetamphos-zetacyperm/terbufos/insect-prof-terbufos.html
[17] http://www.lewishybrids.com/PDF/3-5-2013Agronomic+ALERT+-+Interaction+between+herbicides+insecticides+corn.pdf
[18] http://pest.ca.uky.edu/EXT/Recs/ENT16-Field%20corn.pdf
[19] (Broken Link!) http://www.soybeans.umn.edu/crop/insects/spider_mites.htm
[20] http://www.nytimes.com/2013/04/07/opinion/sunday/calamity-for-our-most-beneficent-insect.html?nl=todaysheadlines&emc=edit_th_20130407&_r=0
[21] http://www.nytimes.com/2013/04/07/opinion/sunday/calamity-for-our-most-beneficent-insect.html?_r=0
[22] http://www.panna.org/press-release/beekeepers-and-public-interest-groups-sue-epa-over-bee-toxic-pesticides
[23] http://www.cdpr.ca.gov/docs/pur/pur10rep/top_100_ais_lbs10.pdf
[24] http://www.extension.org/pages/60318/pesticides-and-their-involvement-in-colony-collapse-disorder
[25] Mussen, EC (2006) Chaotic almond pollination. http://entomology.ucdavis.edu/faculty/mussen/JanFeb2006.pdf
[26] https://scientificbeekeeping.com/sick-bees-part-18e-colony-collapse-revisited-genetically-modified-plants/
[27] http://www.epa.gov/pesticides/about/intheworks/ccd-european-ban.html
[28] http://www.thecre.com/oira_pd/wp-content/uploads/2013/04/DQA-Alert-EU-Commission-Ban-on-Neonicotinoids-4-10.pdf
[29] https://scientificbeekeeping.com/home/news-and-blogs/
[30] Henderson, CB, JJ Bromenshenk, DL Fischer (2013) Clothianidin exposure levels from bee-collected pollen and nectar in seed-treated corn and canola plantings. Proceedings of the American Bee Research Conference.
[31] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
[32] http://www.ontariograinfarmer.ca/MAGAZINE.aspx?aid=534
[33] http://www.pbs.org/wgbh/pages/frontline/shows/settlement/timelines/april94.html
[34] https://scientificbeekeeping.com/2012-almond-pollination-update/
[35] https://scientificbeekeeping.com/neonicotinoids-trying-to-make-sense-of-the-science/, https://scientificbeekeeping.com/neonicotinoids-trying-to-make-sense-of-the-science-part-2/, https://scientificbeekeeping.com/testing-of-bee-feed-syrups-for-neonicotinoid-residues/
[36] http://www.eea.europa.eu/publications/late-lessons-2
[37] http://www.sciencefriday.com/playlist/#play/segment/9088
[38] https://scientificbeekeeping.com/the-extinction-of-the-honey-bee/
[39] http://www.ncdc.noaa.gov/temp-and-precip/maps
[40] http://nassgeodata.gmu.edu/CropScape/
[41] https://scientificbeekeeping.com/a-new-large-scale-trial-of-clothianidin/
[42] http://www.producer.com/daily/ontario-field-study-finds-no-link-between-seed-treatments-bee-deaths/
[43] Pohorecka, K, et al (2013) Residues of neonicotinoid insecticides in bee collected plant materials from oilseed rape crops and their effect on bee colonies. Journal of Apicultural Science 56(2): 115-134. http://www.degruyter.com/view/j/jas.2012.56.issue-2/v10289-012-0029-3/v10289-012-0029-3.xml?format=INT
[44] http://www.fera.defra.gov.uk/scienceResearch/scienceCapabilities/chemicalsEnvironment/documents/reportPS2371Mar13.pdf
[45] http://repository.up.ac.za/bitstream/handle/2263/20334/Nicolson_Chemical(2012).pdf?sequence=1
[46] (Broken Link!) http://www.ag.ndsu.nodak.edu/aginfo/entomology/entupdates/Sunflower/a1331sunflowerhandbook.pdf
[47] http://www.sunflowernsa.com/growers/approved-chemicals/insecticides-test/
[48] http://www.mydigitalpublication.com/publication/?i=151958&p=41
[49] http://www.sunflowernsa.com/growers/approved-chemicals/insecticides-test/
[50] http://www.farmassist.com/agriedge/images/Resource_PDFs/Soybean/Warrior_Zeon.pdf
[51] http://www2.dupont.com/Production_Agriculture/en_US/assets/downloads/pdfs/K-09315.pdf
[52] http://www.ontariograinfarmer.ca/MAGAZINE.aspx?aid=534
[53] http://en.wikipedia.org/wiki/List_of_hyperaccumulators
[54] Bonmatin, JM, et al (2005) Behaviour of Imidacloprid in Fields. Toxicity for Honey Bees. In Environmental chemistry: green chemistry and pollutants in ecosystems pp. 483-49. http://www.buzzaboutbees.net/support-files/bonmatin2005behaviour-of-imidacloprid-in-fields.pdf
[55] http://cornandsoybeandigest.com/seed/do-soy-seed-treatments-pay?page=2
[56] https://scientificbeekeeping.com/historical-pesticide-overview/
[57] http://www.centerforfoodsafety.org/press-releases/1911/cfs-beekeepers-and-public-interest-groups-sue-epa-over-bee-toxic-pesticides
[58] http://www.theworldlawgroup.com/files/file/docs/Soulier_health_environment_June_2012.pdf
[59] http://www.soulier-avocats.com/upload/documents/Soulier_health_environment_september_2010_F.pdf
[60] http://westernfarmpress.com/government/pesticide-battle-over-honey-bee-health-under-way?page=1
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Category: Practical Beekeeping Management, Topics
Tags: beekeeper management, biotic, diseases, drought, environmental, factors, pesticides, randy oliver, varroa | drought Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/drought/ |
What Happened To The Bees This Spring? (Part 1 & 2)
First published in: American Bee Journal, June 2013
Part 1: Environmental and Biotic Factors
Setting the Stage
The Lead Up
The Drought
Lack of Good Forage
Varroa
Diseases
Other Indicators of Impending Collapse
An Unexpected Chill
Feedback from Brokers
The Silent Majority
Beekeeper Management
Part 2: The Contribution From Pesticides
The Lynch Mob
Debunking The Myths
The Precautionary Principal
See For Yourself
Be Careful What You Ask For!
The Effect Of Drought
Actions To Take
Bottom Line
References
What Happened To The Bees This Spring?
Part 1: Environmental And Biotic Factors
Randy Oliver
ScientificBeekeeping.com
First published in ABJ June 2013
By now, most everyone has heard that honey bee colonies died in massive numbers this winter. Reporter Dan Rather, in his newscast Buzzkill [1], showed unfortunate beekeepers, some of whom had lost half or more of their colonies, predicting gloom and doom for the bee industry. What were the causes of this year's bee shortage? As Rather says, "Everyone has an opinion." The question is whether those opinions are based upon fact! So let's go over the events leading up to the bee supply debacle.
Setting The Stage
Nearly 800,000 acres of almond trees in California came into bloom this winter--the trees typically start flowering about Valentine's Day, and the bloom lasts for only about two weeks. Almonds require cross fertilization between adjacent rows of varieties (Fig. 1), and honey bees are trucked in from all over the country to do the job (roughly a million and a half colonies). Many large commercial beekeepers move their hives into California in November to overwinter in holding yards; others build them up on winter pollen flows in Florida or Texas, or hold them in temperature-controlled potato cellars until shortly before bloom. The hives are generally placed into the orchards about a week before the first flowers appear. There is virtually no forage in the orchards prior to, or after bloom in many areas.
Figure 1. An almond orchard in late February, showing the flowering of rows of different cultivars required for cross pollination. The bare "late" varieties have not yet bloomed; the green "early" pollenizers have finished bloom. Grading of colonies is normally done during the bloom of the main crop (usually Nonpareil).
The Lead Up
Two seasons ago there was also a shortage of bees in almonds, following the coldest January (2011) in 17 years (cold being a major stressor of wintering bee colonies). Beekeepers then replaced their deadouts with package bees and splits, thus starting a new generation of colonies, which tend to have lower varroa mite levels than established colonies. These colonies entered autumn 2011 in pretty good shape, and then enjoyed the fourth warmest January (2012) on record! As a result, there was the lowest rate of winter mortality in years, and plenty of bees for almonds in 2012 (Fig. 2).
Figure 2. Percent winter losses since the beginning of the national survey--the data is not yet in for 2012/13. Note that there has been a general downward trend, suggesting that whatever caused the high losses in 2007/8 has not been such a problem in recent years. Note also the cyclical nature of colony winter losses, with high losses in 2004/5, 2007/8, 2009/10, and 2012/13 (some data not shown) Data from [[i]].
[i] http://www.ars.usda.gov/is/pr/2012/120531.htm and California DPR.
I was curious as to whether the colony loss rate was linked to the use of neonicotinoid insecticides. There is no recent USDA data, so I went through the California Pesticide Use Reports (data available through 2010). I plotted the amount of imidacloprid applied to crops in California in the preceding year in red (the seed treatment clothianidin didn't even make the top 100 list of pesticides applied). Although there appears to be a possible correlation from 2006 through 2009, the trends were reversed for 2010. I will be curious to add the 2011 data when it becomes available.
In March of 2012 I received a phone call from a California queen producer who had a prescient insight as to a potential brewing disaster. He was receiving calls for queen bees from Northern beekeepers whose bees had already grown to swarming condition due to the unseasonably warm spring weather (Fig. 3).
Figure 3. Last year's warm spring in much of the country lead to early broodrearing, and as a result, early buildup of varroa levels. Note the record warm spring in the Midwest.
The queen producer noted that such early brood rearing also meant early mite buildup, and predicted that since most Midwestern beekeepers treat for mites by the calendar, that they would unknowingly allow mites to build to excessive levels before treatment. This was strike one against the bees.
The Drought
Then it didn't rain-by midsummer, it was clear that the continental U.S. was in serious drought, including California, whose beekeepers supply nearly half the bees for almond pollination. The only ways that we kept our colonies strong was to either feed expensive pollen supplement and sugar syrup, or to move them to elusive better pasture out of state. By late summer, 60% of the U.S. was in drought, meaning that unless your bees were next to soybeans or irrigated crops, there was little forage for them. This lack of good nutrition was strike two against the bees (Fig. 4).
Figure 4. The severe drought in the Midwest really put the hurt to bee pasture in those states in which the majority of commercial hives spend the summer. Source [[i]].
[i] http://www.ncdc.noaa.gov/temp-and-precip/maps.php
Drought not only dries up nectar and pollen sources, but also forces bees to fly further and more frequently for water. Plus it concentrates ag chemicals and pesticides in the few sources of surface water available to bees. The bees started to show the hurt.
Beekeepers tried to move their hives to areas of better forage, sometimes overstocking an area with too many hives, which led to excessive competition for resources, and the spreading of parasites. Others desperately chased less desirable crops such as sunflowers. Colonies in holding yards in California found little to eat, due to our record dry weather. Some beekeepers with winter eucalyptus locations found them crowded with other hives.
Lack Of Good Forage
In Buzzkill, Bret Adee brought up the fact that bee pasture in the Midwest is disappearing under the plow, largely due to our environmentally-irresponsible taxpayer-subsidized policies that encourage farmers to plant every square foot of land into corn (Fig. 5). Bee brokers told me that colonies coming to almonds from the Midwest were in generally poorer shape this year than those coming from the southern states.
Practical application: some Midwestern beekeepers split their operations, hauling some to the South to rebuild over winter, and the rest directly to California-there was a night and day difference as to how the colonies looked in February!
Figure 5. Grasslands and wetlands in the Corn Belt are rapidly being converted to monocultural, heavily herbicided corn/soy, which eliminates virtually all bee and wildlife forage. A new study found that between 2006 and 2011 there was a net loss of 1.3 million acres of grassland. This affects not only bees--the authors [[i]] state that "As a consequence, populations of grassland nesting birds are declining faster than any other group of birds in North America."
[i] Wright, CK & MC Wimberly (2013) Recent land use change in the Western Corn Belt threatens grasslands and wetlands. https://www.motherjones.com/files/pnas201215404_nwow5w1.pdf
To put this loss of bee pasture into perspective, I asked some Dakota beekeepers for estimates of how many acres of CRP grassland are needed to sustain a colony of bees. In recent years, the overall hive density in North Dakota has been more than 10 hives per square mile (less than 64 acres per hive, including wastelands).
Practical application: the best guess by those beekeepers was that each colony of bees requires about 5-15 acres of productive land for forage (late summer forage being the critical factor). If we use the figure of 10 acres per colony, then the conversion of 1.3 million acres of grassland to herbicided cropland suggests that forage for 130,000 colonies of bees has been eliminated in the past five years in the Corn Belt alone! This figure represents nearly 9% of all colonies needed for almond pollination.
Varroa
An excellent window into the causes of colony health problems is the USDA National Honey Bee Pests and Diseases Survey Report [5] (the latest data have not yet been released). It is worrisome that varroa levels appear to be steadily climbing year after year.
And if the drought and forage problems weren't enough, the favored miticide of commercial beekeepers became unavailable for a time last summer, and mite levels built to killing levels in a number of operations. By late July, some of us were already predicting a disaster for the upcoming almond pollination season. Although many beekeepers finally got mite levels down with late-season treatments, the damage had already been done, and there was no turning the colonies around. Strike three for the bees!
In November semi loads of hives started moving into California, or had been placed in potato cellars. Some of the colonies that arrived from the Midwest were in poor shape, or crawling with mites. Oddly, few beekeepers at the time owned up to having problems, despite the reports that I kept hearing of mite and forage issues! I'm not sure whether this was due to denial, wishful thinking, simple lack of lifting the lids, or something else.
Diseases
Nosema infection also runs rampant across the country--70% of colonies were infected in June of last year. The stressful factors leading up to almond bloom apparently put a lot of hives close to the "tip point" at which pathogens can overwhelm the colony immune system and start it going backwards, or initiate the slide into sudden depopulation (detailed at [6]). Few seem to be mentioning signs of CCD-it is unfortunate that the media keep using that term as a catch-all for all hive problems!
One should keep in mind that the winter collapse issue appears to be cyclical, similar to flu or other pathogen epidemics. I have strong reason to suspect that the constantly-evolving viruses are involved in these colony collapse epidemics.
There has also been a strong resurgence of European Foulbrood and other unidentified brood diseases [7] (Figs. 6, 7, and 8). Unlike EFB of old, the new forms don't go away with a nectar flow.
Figure 6. "Shot brood" due to EFB. Note the fat queen near the center. Despite her vigorous egglaying, this colony is unable to pull ahead due to excessive brood mortality. Lots of beekeepers reported EFB symptoms this winter.
Figure 7. You really have to look hard in some colonies with spotty brood to see the cause! Two larvae in this photo show signs of EFB infection.
Figure 8. Dying brood from one of my sick colonies this spring with EFB-like symptoms. Note the "shot" pattern, the twisted larvae, and the dried larval remains. There is also some AFB-like coloration, but lack of roping or AFB odor (this odor is distinct and sour), nor a positive Holst milk test. In this colony, even pupae were dying. I observe these symptoms independent of whether the hives went to almond pollination or not. Colonies with this (or similar) infection cannot grow. Treatment with oxytetracycline generally clears it up.
One thing that I noticed in Buzzkill was the uneaten pollen supplement patties in many of the crashed hives. I've mentioned before [8] that I've found a colony's failure to consume pollen supplement to be a reliable predictor that that colony will later collapse.
Another strong predictor of winter collapse is weak strength in fall (upcoming article), again strongly suggesting that those colonies already have some sort of health issue going into winter. I heard reports from all over the country that bees went into winter in poor condition.
An Unexpected Chill
The final blow to hives in California was a blast of icy weather (Fig. 9). This unexpected chilling compounded all the existing problems! I've previously pointed out that colony collapse often follows unseasonable chills, since it shifts the tip point for virus and nosema epidemics. Clusters that had expanded for broodrearing contracted, resulting in chilled brood and dead young bees on the ground. My own colonies simply shut down broodrearing completely, losing about two weeks of buildup.
Figure 9. Chilling events (blue arrows) in Modesto, California this winter (the dark blue lines represent normal highs and lows). The unusual chilling in late December and early January (hitting the '20's in a number of areas) came at the time when colonies normally begin to build up for almonds. This severe (for California) cold set the already-stressed colonies back hard, and may have allowed nosema and viruses to gain the upper hand. Graph from wunderground.com.
At the national convention in January, the first reports of beekeepers with collapsing operations were heard. But still, the industry was in denial, with an apparent glut of promised bees as late as the end of the month (two weeks before start of bloom)! But when the rubber finally hit the road in mid February, that illusory supply quickly evaporated, with desperate growers and brokers scrambling to obtain bees--some offering obscenely high prices for substandard colonies.
And then, due to the cool spring, the trees held off on blooming for an extra 10-14 days [9]-colonies placed in anticipation of normal start of bloom just sat there starving and shivering on the cold orchard floors.
Practical application: the biology here is that this is the time of the "spring turnover" in bee populations in California, during which the old overwintered adult bees must rear their replacements for the spring buildup of population. The conditions in the almond orchards prior to bloom are miserable for smaller colonies--it is warm enough to encourage them to break winter cluster and expand the broodnest, but overnight frosts on the Valley floor can cause serious chill stress. Furthermore, it is often warm enough to fly at midday, but there is virtually nothing to forage upon until the trees start blooming! Such fruitless foraging further wears out the workers, and allows sick bees to drift to adjacent hives. Worse yet, the desperate foragers rob out any dead or dying colonies in adjacent orchards, rapidly and effectively transmitting mites, nosema, viruses, and anything else harmful in the deadouts.
Many colonies went backwards during this excruciatingly long wait. Some beekeepers told me that hives graded at placement scored better than those graded at bloom (just the opposite of normal)!
I've been carefully observing spring turnover in my "dinks" (weak colonies) in February (Fig. 10). What I find is that the problem is generally not the queen; rather, the colonies are infected with some pathogen- most commonly nosema [10], the paralytic viruses [11], or EFB (or EFB-like brood disease). Those colonies that are able to successfully emerge one solid round of brood are often able to "clear" the infection and completely rebound by April. Those that get hit by frost in February often collapse.
Figure 10. An example of an unsuccessful spring turnover. This colony is in the middle of typical February collapse from nosema or IAPV. You can easily see the outline of the area recently covered with brood, delineated by the crescents of freshly-packed pollen. Colonies undergoing this sort of depopulation tend not to forage for nectar, and do not respond well to supplemental feeding. This colony continued to collapse quickly, and finally died in a cold snap a week later--with only silver-dollar sized patch of dead bees remaining.
Feedback From Brokers
I asked a few of the major pollination brokers for their observations on the colony shortage this season. Their feedback suggested that the causes for the bee shortage were varied and many.
Summary:
Most were able to eventually fill their contracts. Beekeepers often hold colonies in reserve "just in case," or gambling that in "short" years they can rent those last hives at an elevated price. Also, when the offered price went up, hives not originally intended to go to almonds were loaded up at the last minute and shipped to California (I was in Florida at the start of bloom, and had an inspector tell me of certifying colonies for shipment after the bloom had already begun!).
A number of hives received in November were already headed downhill. Some exhibited the symptom of bees not clustering properly (a typical sign preceding sudden colony depopulation/CCD). Some arrived crawling with mites, or with recent mite treatments in place (suggesting that they were treated too late).
Some graders saw piles of dead bees in front of hives--cause unknown. There were reports of some herbicide tank mixes killing bees.
Many of the placed colonies were below standard grade-- growers paid for less than they expected!
Graders told me that there was a huge variation in hive strength from beekeeper to beekeeper. Many hives were strong (12-16 frames of bees) and healthy; other operations graded at zero to three frames of bees (some of the deadouts had spider webs inside, suggesting that they hadn't been occupied by bees for some time).
The unusual winter chill was tough on colonies that had been stimulated into early buildup, and then forced to contract their broodnests. Some colonies kicked out chilled brood and dead bees afterwards.
Many beekeepers watched their colonies go "backward" prior to bloom.
Colonies from the Southern states (especially those delivered in February) were generally in better shape than those from the Midwest.
Midwestern beekeepers blamed drought, mites, poor nutrition.
Several beekeepers said that their best bees came from remote areas, and their worst from ag areas.
A number of beekeepers admitted inadequate mite treatment; mites were a recurrent theme.
There were a number of reports of EFB hitting colonies.
Some had gotten hit last summer with pesticide sprays, and their colonies didn't recover.
"There were good bees and bad bees from every state. They all seemed to have different problems depending on location/state."
Many good beekeepers simply didn't know what happened to their hives; there were lots of lifeless hives delivered. The atmosphere was ripe with speculation as to the actual causes.
"The shortage was also created by beekeepers that chose not to come to California for a variety of reasons. They can make more money with honey, didn't get paid for what they have brought in the past, bees come back home with mites, beetles and whatever else takes a ride on the hives. Beekeepers don't want to risk bee health to chase the dollar." Many out-of-state beekeepers have had bad experiences going to almonds, and simply don't feel that it's worth it. The supply of bees will largely depend upon the price that growers offer for renting them!
The Silent Majority
Buzzkill leaves one with the impression that the entire bee and almond industries are on the verge of collapse. Of course, the news media focus on fear and disaster, so we may consider taking such dire projections with a grain of salt. In the case of Dan Rather, the focus was on the beekeepers with troubles, not upon those who successfully filled their pollination contracts.
So just how severe was the problem? Let's say that there was an overall shortage of 100,000 hives (a figure that I heard floated)--that would represent only about 6% of the total number of hives placed into almond pollination. The other 94% were successfully delivered (although a proportion of those were weak due to the poor season).
Since the debacle, I've heard from plenty of beekeepers whom I'll refer to as the "silent majority," who experienced "normal" colony winter losses in the 5-25% range, and who successfully filled their pollination contracts. Although the hearts of all beekeepers go out to those who suffered severe colony losses, many felt that some of those losses could have been prevented if the afflicted beekeepers had been more proactive than reactive.
And don't forget those upon whom the rest of the industry depends to supply bees for restocking their deadouts! The California package producers, who have been pollinating almonds for decades, are routinely counted on to consistently take strong hives to almonds, and to then shake over a hundred thousand packages of bees for sale afterwards. Few of these major producers experience severe unexplained colony losses.
Beekeeper Management
By no means am I suggesting that those beekeepers who suffered losses engaged in poor beekeeping practices, but I can't help but notice that not all beekeepers were equally affected--a great number provided strong, healthy colonies to almonds. I've spoken to some of them-the common thread is that those who recognized the problems of poor nutrition and mites in August, and took remedial action for the rest of the season, had acceptable winter losses.
Some beekeepers who really put serious effort and money into bee husbandry were even able to sell "shook bees" from their colonies to others in February! For example, watch Keith Jarrett feeding substantial quantities of pollen supplement to very strong colonies in January [12]--Keith consistently brings very strong colonies to almonds every year, and this year was no exception!
Practical application: I'm here to tell you, that one lesson that I've learned during our intense California drought, is that those yards that I fed with protein in late summer before they started going downhill went to almonds much stronger than those that I didn't feed until fall! Proactive is better than reactive--if you wait until colonies are already going downhill, it is much more difficult to turn them around!
I've often been accused of being politically incorrect for speaking frankly. I'd like to make amends at this point by retiring the rude and unsympathetic term "PPB" (Piss Poor Beekeeping). The fact is that the average wintering loss for the past few years has hovered around 30%. So if you experience 30% losses, you can now proudly call yourself an "Average" beekeeper!
But what about those beekeepers who consistently manage to enjoy lower rates of winter loss? I propose that we call them "Lucky" beekeepers, and the best of them, "Consistently Lucky."
Practical application: the harder those beekeepers work, the luckier they get!
But there were clearly "unlucky" beekeepers this year--especially the "big boys" who brought tens of thousands of hives from the drought-ravaged, and corn-converted Midwest to California. California beekeepers are used to summer drought. We have learned to either move our colonies to better (often irrigated) pasture, or to feed expensive pollen supplements. This would be a very expensive proposition to the larger operators, with hives spread all over the place--a cost not covered by current pollination prices.
What Happened To The Bees This Spring?
Part 2: The Contribution From Pesticides
Randy Oliver
ScientificBeekeeping.com
First published in: American Bee Journal, July 2013
It's pretty straightforward to attribute the majority of colony losses this winter to the usual and aforementioned causes, but a number of beekeepers are also pointing the finger at pesticides. There is no doubt that in certain areas pesticides were a serious issue to beekeepers. Colonies set back by pesticide kills may not fully recover over the season, and those going into winter with pesticide residues may go downhill. There is also reason to suspect that pesticides and miticides have something to do with today's high rates of queen failure.
The bees in some drought-stricken areas were forced to forage on irrigated and pesticide-laden crops--the only place in which there was anything to eat. This changes the entire dynamics of pesticide exposure, since residues would no longer be diluted by the pollen and nectar of non crop plants. The lack of good natural forage also suppresses the ability of colonies to deal with the insult of those pesticides. And colonies may be forced, by necessity, to forage upon one treated crop after another, resulting in multiple exposures.
Practical application: under drought conditions, bees may suffer more from pesticides than when times are good.
Due to the current high prices for agricultural commodities, farmers are often applying pesticides indiscriminately as "risk insurance" rather than due to actual need. A chilling recommendation from an extension entomologist reads:
I encourage you to be risk averse and to make an investment that will pay dividends for your valuable crop. Consider applying [flubendiamide, indoxacarb, or spinosad] for corn earworm. If you have stink bugs and are in the [mature plant] stages, you might want to tank mix one of these products with a pyrethroid. A tank mix of a pyrethroid and acephate are an option, but will wipe out all beneficials [13].
The first three insecticides mentioned are considered to be "reduced risk" to bees if residues are allowed to dry for a few hours, but no mention was made to spray at night. Of the five insecticides recommended above for spraying on corn in tassel, at least four are highly toxic to bees if sprayed during the day! No farmer wants to kill bees, but with recommendations like this from state extension agents, well-meaning growers may unwittingly be hurting pollinators.
Bees in agricultural areas are exposed to a vast array of insecticides, miticides, fungicides and surfactants--many of which have clear links to colony health problems. And applications of new mixes of chemicals are up. For example, in addition to the neonicotinoid seed treatments, granular insecticide soil treatments for corn in the Midwest were up by 30% over the previous year [14]. These treatments consist of combinations of organophosphates and pyrethroids.
But I'm not hearing either the bird groups or beekeepers even addressing these treatments! It is scary to read the sales literature for Counter insecticide, the organophosphate terbufos [15]. Growers are encouraged to apply it at planting time, despite the facts that:
"Terbufos is highly toxic to birds, fish, and aquatic invertebrates [and bees]. [It] shows significant acute mortalities of birds, mammals, reptiles, and fish resulting from broadcast application...In the same study, the application of terbufos as a soil-incorporated treatment to corn...resulted in acute mortalities to birds and reptiles" [16].
Terbufos is strongly systemic, meaning that it is absorbed by the plant roots and could be expected to be expressed in the pollen and nectar.
It can synergize with other pesticides since it ties up the critical CP450 enzymes used in detoxification, to the extent that growers are cautioned that it can cause problems to corn from herbicides [17].
During drought, certain insect pests become more problematic, perhaps resulting in increased exposure to insecticides by bees. For example, drought encourages corn leaf aphids. Read this chilling recommendation for aphids on corn during tasseling (when bees are actively foraging):
If less than 50% of pollination has occurred, aphids and honeydew are covering tassels and plants are stressed, an insecticide may be necessary to ensure adequate pollination, but treatments need to be made within 48 hours of tassel emergence. Asana XL, Brigade, Capture, Cobalt, Dimethoate, Lannate, Lorsban, or Malathion may be used for control [18].
Or this:
Prolonged drought always raises the specter of two-spotted spider mite outbreaks in soybeans and corn. As the 2012 drought intensifies in Minnesota, infestations are reaching treatable levels...The only products that are recommended for spider mites in soybean include insecticides containing chlorpyrifos, dimethoate and bifenthrin[18].
The names of the recommended insecticides above strike fear into the hearts of beekeepers!
Practical application: many "consistently lucky" beekeepers go to great effort to allow their colonies to recover after exposure to pesticides--moving them to unsprayed areas or natural forage, or by immediately feeding protein supplement to stimulate increased broodrearing. Unfortunately, such "recovery" areas are getting harder and harder to find.
The Lynch Mob
Despite the fact that a wide range of bee-toxic insecticides are being applied (often during bloom) to corn, soy, sunflowers, alfalfa, cotton, and other major crops, if you Google anything about insecticide use, you'll quickly find that the blogosphere focuses only upon the putative link between a single class of insecticides--the neonicotinoids-and the demise of pollinators [19].
People look at me incredulously when I point out that there is zero firm evidence to date that the neonic seed treatments are a serious problem! But the notion that all honey bee problems are caused by an insidious new insecticide resonates with a distrustful public [20], and has firmly established itself as "common knowledge." But repeating something does not make it true!
"It's easier to fool people than to convince them that they have been fooled"-Mark Twain
Practical application: the question is, "Are the neonic seed treatments being railroaded into a guilty verdict in the media's kangaroo court of public opinion?"
One group recently brought suit against the EPA to ban the use of the seed treatments clothianidin and thiamethoxam [21], neither of which even make California's top 100 list of pesticides applied [22], nor that have ever been demonstrated to harm colonies feeding on the pollen or nectar of seed-treated plants! A number of people have made up their minds that the neonics are the main cause of colony collapse, and it appears that no amount of facts to the contrary will cause them to reconsider!
Debunking The Myths
As anyone who knows me will tell you, I am a stickler for honesty, accuracy, and factuality. I am concerned about the amount of misinformation and speculation going around about the neonics. So let's look at some of the claims vs. the actual facts.
Arguments Against Neonic Seed Treatments Actual Facts
The neonicotinoids have been "linked" to increased colony mortality. In actuality, such a "link" is merely an urban legend, and has never been demonstrated or confirmed in any study.
On the other hand, the residues of other classes of pesticides are more suspect for causing increased brood or adult bee mortality [24].
The timing of CCD coincides with the introduction of the neonic seed treatments in 2004. CCD started in California bees in the winter of 2004/2005, prior to them ever being exposed to seed-treated crops.
But what else could have changed at that time other than the introduction of neonics? In California, Dr. Eric Mussen [25] determined that the increased colony losses were due to poor summer forage and failure of mite control products (just as this last winter).
There is actually a much stronger association between the incidence of the novel gut parasite Nosema ceranae and increased colony mortality [26].
But the main thing that has changed is the dynamics of the varroa/virus complex, which coincidentally occurred at about the same time that the neonics came into use.
European countries banned the neonics, and the bees recovered after those bans. A few countries placed temporary suspensions on certain seed treatments until planting dust issues were resolved [27]--only Germany has one suspension still in place. The foliar applications were not suspended. The suspensions did not resolve bee health problems.
The European Food Safety Authority recently decided that neonics pose a threat to bees. "The Center for Regulatory Effectiveness (CRE) has recently completed a Data Quality Act (DQA) Alert on the ... (EFSA) report on neonicotinoids which found that neonicotinoids pose a risk to bees. The DQA Alert outlines the serious deficiencies of the EFSA report and demonstrates why the EFSA report violates the DQA...In particular, the EFSA report failed to maximize the objectivity of the data by failing to reconcile numerous studies whose conclusions contradicted the findings of the EFSA report" [28].
Several lab studies have found that neonics affect individual bee behavior, longevity, or immunity. True -- although many studies used unrealistically high doses. The question is whether such artificial studies apply to actual colonies in the field. The numerous field studies to date have failed to find any link between seed treatments and later colony health issues.
It is the seed treatments that make corn a problem. As Bret Adee points out in Buzzkill, corn is replacing pastureland (Fig. 4). Corn, as grown today, is a virtual "bee desert" (similar to the way in which suburban lawns are green bee deserts). And it's not only the bees that this is affecting, the populations of birds and other wildlife are plummeting due to loss of favorable habitat (see my blog on birds and neonics [29]).
A recent survey by Dr. Jerry Bromenshenk found that bees actually avoid field corn pollen, and are exposed to very little of the seed treatment residues [30].
Numerous independent studies, and the experiences of stationary beekeepers throughout the Corn Belt, support the conclusion that colonies can thrive when surrounded by corn, provided that there is some alternative forage within flight range.
As the use of neonic seed treatments increases, bee mortality goes up. In actuality, colony mortality rates go up and down year to year, largely dependent upon weather and varroa mite control. If the neonics were to blame for this winter's bee losses, why didn't they cause similar losses last winter, in which the colony mortality rate was the lowest in years?
French beekeepers also started seeing problems with the introduction of the neonics. I've spoken with beekeepers in France whose apiaries are in pesticide-free areas. They tell me that they experience the same sorts of colony mortality problems as do those in areas exposed to neonics.
Bees in the U.S. are commonly exposed to neonicotinoids. In the most recent USDA survey (100 samples across the country), imidacloprid was only detected in 9% of the samples [31] (although I found some of the residue levels alarmingly high). However, the most common seed treatment, clothianidin (or its degradation products), was not detected at all!
The above real-world data suggests that efforts to ban clothianidin as a seed treatment may be misplaced. It appears that imidacloprid, especially as a foliar application, would be of more concern.
Neonics are the most common pesticides that bees are exposed to. In the above survey, other serious insecticides were more commonly prevalent: chlorpyrifos (in 20% of samples), cyhalothrin (in 7%), and endosulfan (in 11%).
Notably, there was also a high prevalence of beekeeper-applied miticides: fluvalinate (in 38%), coumaphos (in 87%), amitraz (in 27%), fenpyroximate (in 11%), and thymol (in 27%).
There was even higher exposure to fungicides and adjuvants.
It is misleading for the pesticide companies to blame the problems on varroa, nosema, or poor nutrition. The above survey (over 1000 samples) found that the average varroa infestation rate in the U.S. in autumn is above the danger level for virus epidemics!
Sixty to 100% of hives are infected with nosema in December.
Summer drought has historically been associated with high winter mortality.
But didn't the planting dust from corn seeding kill colonies in Ontario? Planting dust is separate issue that clearly needs to be remedied. It does on occasion cause bee kills, for which beekeepers are rarely compensated. This situation must change! All parties are actively working on solutions [32].
Bees in certain agricultural areas tend to go downhill later in the season. This has been observed for a long time--long before the neonics. The question is, which chemicals, chemical synergies, or chemical/nutrient interactions are responsible? The Frazier/Mullin team at Penn State has developed a protocol for helping to figure this out. I strongly support its adoption by the EPA for pesticide risk analysis.
Colonies foraging upon nectar or pollen of seed-treated crops get poisoned. Ask yourself this: if neonic residues were actually so harmful to bees, how is it that the Canadian beekeepers, whose bees forage largely on seed-treated canola, feeding solely upon a diet of canola nectar and pollen with well-documented residues of clothianidin, experience very low winter losses, despite the long Canadian winter (so long as they control varroa and nosema)?
And how is it that the vast majority of beekeepers in the U.S. Corn Belt report that their colonies thrive and that they have far fewer pesticide issues these days than in the past?
The neonicotinoids are "systemic," meaning that they are in the plants all the time! True, but this property is not unique to the neonics--a number of other insecticides also go systemic. In any case, with seed treatment, the concentration of the insecticide in the plant is only high when the plant is young--it gets diluted as the plant grows (e.g., clothianidin in canola is at a level high enough to kill aphids for only about the first 30 days of growth).
The only time that residues in the plant matter to pollinators is when the mature plant flowers. The amount of seed treatment is carefully calibrated so that the residue in the pollen and nectar are below the level that causes demonstrable harm to bees.
In the case of foliar, drench, or chemigation applications prior to bloom, there are greater possibilities for bees to be exposed to toxic levels.
There are fewer butterflies and pollinators in the fields these days. Not surprising, since the new push for "clean farming" has removed the host plants upon which the butterfly larvae feed. Pollinators are forced to subsist upon the stretches of weeds growing along roads at the edges of fields. But surprisingly, pollinators may be abundant there, suggesting that even though populations as a whole are reduced by habitat conversion, it is that, rather than the use of seed treatments, that causes the population declines.
The evil pesticide companies want to kill honey bees. Give me a break! Does anyone truly believe that anyone wants to kill honey bees? What pesticide company would want the bad press of being associated with killing bees? The chemists and biologists on their staffs earnestly work to develop insecticides that are bee friendly.
The EPA is being derelict in their duty to protect pollinators. I have spoken at length with EPA staff, and reviewed their risk assessments, as well as those by, DEFRA, EFSA, PMRA, and other regulatory agencies. I find that the risk assessors have not overlooked any evidence, are well-informed on the subject of neonics, and are justified in their assessments that the on-the-ground evidence (to date) indicates that neonic seed treatments pose acceptable risk to pollinators.
We must all remember that the tobacco industry tried to hide the fact that nicotine was addictive [33]. Spare me! Does anyone seriously think that the EPA is unaware that industry executives may stretch the truth? Of course the EPA is skeptical of any reassuring claims by the pesticide industry--that's why they go over all studies with a fine-toothed comb!
This winter's losses spell the end to commercial beekeeping. The fact of the matter is that many observers note that the bee supply for almonds often follows a boom-bust cycle. Although losses were high this year, the trend for the last decade has been for beekeepers keep ramping up the supply of bees for almonds. So long as growers are willing to pay a profitable rental rate for colonies, market forces will encourage the bee industry to meet the demand (for a detailed analysis, see [34]).
The Precautionary Principal
"But," you say, "shouldn't we exercise precaution due to the lab studies that find adverse effects from the neonics?" Look, I make my living as a beekeeper, I'm not out to sell insecticides, and am as concerned as the next person about the environment and the safety of the food I eat. I've researched the neonics exhaustively, and addressed them in several articles [35]. I am acutely aware that there are suggestions that the neonics may be causing insidious effects in the environment, and I've studied the excellent environmental document Late Lessons from Early Warnings [36], which hammers the message that we should use the "precautionary principle" when dealing with chemicals. The problem is, there is nothing without risk--for example, you have a 1 in 83 chance of being killed in an auto accident in your lifetime. But most people still take the risk of getting into cars, since they feel that the benefit outweighs the clearly high risk!
My practical perspective as both a scientist and a beekeeper: if researchers perform lab studies on any insecticide, they will find that there are all kinds of negative effects upon bees--this should be pretty obvious, since insecticides are specifically designed to harm insects! However, the majority of these studies are taken out of the context of full colonies under field conditions, where bees fly free and choose the flowers upon which they forage. The evidence to date supports the contention that the neonics, properly used as seed treatments, are indeed an improvement over other insecticide options.
As Dr. Eric Mussen succinctly notes:
Nobody's really been able to show that [the neonicotinoids] are more problematic than the rest [of the pesticides to which bees are exposed] [37].
Far be it from me to suggest that the neonics (or any other pesticides) are harmless! But consider this--if the neonic seed treatments were indeed as harmful as some make them out to be, you'd think that after a decade of intense study that at least one researcher could have come up with a single solid piece of field evidence against them!
Let's do a thought experiment. Why doesn't someone simply put a bunch of healthy hives into the middle of seed treated crops and see whether they die afterward? Oh, I forgot--this experiment has already been run by thousands of beekeepers year after year in the Corn Belt and the Canadian prairie! And those beekeepers have invited me to look at their colonies, sent me photos of colonies stacked head high with honey supers, and bragged about their high winter survival!
Some will argue 'til they're blue in the face, but the fact remains that virtually every beekeeper that I've spoken with in the Corn Belt and in canola areas feels that the seed treatments are not a problem [38]. In fact, most tell me that this is the best it's ever been as far as bees and pesticides!
Common sense: I just don't get what is so hard to understand about the reality that there are thousands of colonies thriving year after year in areas of intense seed treatment? To any reasonable person it would suggest that the treatments are causing little noticeable harm other than the occasional planting dust kill, which I have repeatedly stated is a problem that needs to be corrected!
See For Yourself
Let's look at actual independent (from the manufacturer) data from corn and canola areas:
Corn
I asked friends in the Corn Belt if they had any data on winter losses. It so happens that the Michiana Beekeepers Association has been collecting exactly that since the spring of 2010 (Fig. 11).
Figure 11. Percentage of winter losses by the "Michiana" hobby beekeepers. The 2013 figure is as of mid March; it may eventually go down a bit due to a prolonged cold spring. Note that the winter survival rate appears to be linked to average winter temperature. Thanks to beekeeper Danny Slabaugh for sharing the data; temp deviations from [[i]].
[i] http://www.ncdc.noaa.gov/temp-and-precip/maps
How could the above be? Eighty percent winter survival despite sitting in the middle of seed-treated corn and soy? So of course I did a fact check to confirm that those beekeepers were indeed sitting in corn/soy areas (Fig. 12).
Figure 12. USDA land cover categories for the region in which the Michiana hobby beekeepers keep bees--corn and soy acreage is color coded yellow and green, respectively. The selected area is the top half of Indiana and bottom of Michigan, with Lake Michigan at the left. Clearly, these apiaries were exposed to seed-treated corn and soy! I created the map at [[i]].
[i] http://nassgeodata.gmu.edu/CropScape/
The above figures suggest that colony winter survival for stationary hobby beekeepers in the above corn/soy region is higher than the national average, despite the fact that about half of them don't even treat for mites! They also suggest that the neonics or other pesticides used in corn/soy in that region do not cause excessive winter loss. Finally, the data indicate that a main factor for winter loss rates is the winter temperature.
Canola
I've heard some beekeepers saying that their bees crashed after working canola, suspecting that the seed treatments were the problem. So as a reality check I called a Dakota beekeeper who has been running bees to canola for over a decade--some 10,000 hives last season. He tells me that colony strength after canola varies from year to year, but that he sees no problem with the seed treatments. He did point out that beekeepers should be aware that colonies can plug the broodnest on intense canola flows.
The biology: The plugging out of the broodnest during an intense bloom means that three weeks afterward, there will be few emerging workers to take the place of the worn-out foragers, and the colony population will temporarily plummet. Even worse, the remaining mites are then concentrated onto fewer bees--which can initiate virus epidemics. These colonies must then attempt to rebuild from scratch, starting in August, meaning that the weakened, mite-infested colonies faced three long months of drought last summer for that rebuilding process.
Every field study that I've seen for canola also supports the conclusion that the seed-treatments are safe for bees. I joined other beekeepers and regulators in observing a large-scale study of seed-treated canola in Canada [41]. Canola (or rapeseed) is likely the best test crop, since bees eagerly (and virtually exclusively) forage upon it for both pollen and nectar, meaning that every bit of their food supply contains contain easily verifiable residues of the insecticides. The preliminary results indicate that the clothianidin seed treatment did not harm the colonies [42].
Another recent independent long-term field study in Poland [43] came to the same conclusion. In it, the researchers followed 50 colonies for more than two years under field conditions as they foraged on five different large fields of oilseed rape treated with various combinations of five different neonicotinoids applied by seed treatment and spraying. Pollen and nectar samples were taken, and demonstrated that the bees were clearly exposed to normal residues of the insecticides (there was also additional exposure to other common agricultural pesticides). The colonies were monitored for health, brood, strength, nosema, viruses, and winter survival, and compared to two control apiaries set in an area free of the crop. The results?
During the time from the placing of the colonies on the rape fields until wintering, the colonies developed properly in all groups... All colonies overwintered properly... In both years, during the period of being placed in the oilseed rape fields as well as after being moved to the stationary apiary, none of the groups showed disturbances in development or functioning.
Following a paper that suggested that the seed treatments would impair bumblebee colonies' ability to rear queens, DEFRA performed a common-sense field study last year [44]. Their findings:
...the study has shown that bumble bee colonies remained viable and productive in the presence of the neonicotinoid pesticides under these field conditions...The study underlines the importance of taking care in extrapolating laboratory toxicology studies to the field, as well as the great need of further studies under natural conditions.
Sunflowers
Some beekeepers report that their colonies later crashed after they chased sunflowers last summer for honey. One must keep in mind that sunflowers are not a natural food for honey bees, and provide only poor-quality, nutritionally-inadequate pollen [45]. But the main problem with putting bees on sunflowers may be related to the fact that sunflowers are a native plant--meaning that there are a number of native insects that evolved to feed upon it:
Maximum seed yields often require the use of insecticides to protect the crop from insect competitors. Unfortunately, many of the major insect pests of sunflower attack the crop when it is flowering. Thus, insecticides used to control the pest also harm pollinating bees [46].
If sunflowers are the only forage available, colonies may eventually go downhill, due to the one-two punch of poor pollen nutrition coupled with insecticide exposure. And which pesticides would those be? One scary list- Asana XL, Baythroid, endosulfan, Furadan , Lorsban , methyl or ethyl parathion, , Proaxis, Scout X-TRA, Sevin, Warrior, Mustang Max, Declare, Cobalt, Yuma, Delta Gold, and Grizzly Z [47]!
Note that none of the above are neonics, other than seed treatments for wireworms. Surprisingly, field evidence indicates that the seed treatments only "stun" the wireworms for a while [48], which certainly raises the question as to how harmful they might be to bees months later when the plants flower! I will return to sunflowers below.
Be Careful What You Ask For!
Allow me to assure you that I am no pitchman for neonics or any other insecticide--the typical farmer practices far too little integrated pest management, and applies far too many pesticides! All insecticides (and several fungicides and adjuvants) cause problems to pollinators--the neonics are no exception. Any systemic insecticide has the potential to harm bees when applied as foliar applications, by chemigation, or to flowering trees, but it there is no compelling evidence that the neonics are any worse than the alternatives in most applications. On the contrary, there is quite a bit of evidence that they may often be "safer" ("reduced risk").
If the neonic seed treatments were banned, it's not as though all agriculture is suddenly going to go pesticide free--only about 1% of U.S. cropland is registered as "organic"! We must consider the likely alternatives. The products that farmers would then use to control insects would need to be sprayed all over the cropland--we'd then be back to the problem that the bulk of sprayed insecticides go into the environment without ever hitting the intended pest!
I hear from knowledgeable beekeepers that worse than in previous years, some of the new formulations of the spray-applied insecticides [49, 50, 51] can really knock the snot out of bees! One large beekeeper found his hives already dead before moving them away from the fields. Again, this was not a neonicotinoid issue.
Practical application: no one is saying that the neonics are "harmless." The question is whether they are better or worse than the alternatives.
The Effect Of Drought
Let's discuss some of the problems (or suspected problems) with the neonics last season. The record warm and dry spring appeared to exacerbate corn planting dust issues (corn seeds are the worst offender due to their non spherical shape). Beekeepers in some areas of the Corn Belt, the East Coast, and in Ontario suffered from confirmed (in at least some of the cases) planting dust kills (although many went on to make good honey crops after their colonies recovered). The final analysis from Ontario is not yet completed, but dry soil conditions and an early clover bloom likely contributed to the problem. Regulators and the seed companies are working on solutions to the problem [52]. Still, IMHO it is unacceptable to ask beekeepers to bear the burden of bee kills without compensation, and no one could blame the affected beekeepers for being pissed!
Drought-stressed plants
There are a number of advantages to the neonic seed treatments. Besides their safety to the farmer and to most wildlife, there is virtually no way for the farmer to misapply them! The timing of application is only at planting time (when bees normally have little interest in the bare fields), and the dose is determined by the seed-treating company. This means that the applicator can't be tempted to apply at the wrong time, or to over apply too strong a dose (however, their excessive near universal use can be expected to accelerate the development of resistant pests).
That said, beekeeper Bret Adee brought an interesting question to my attention: the dose of seed-applied systemic insecticides (whether neonic or other) is based upon the dilution factor as the plant grows, so that the residues in nectar and pollen will be reduced to below the "no observed adverse effects level." But what happens during drought, when the water-stressed plants only grow knee high before desperately flowering? There would be far less plant biomass in which to dilute the insecticide (assuming that drought-stressed plants absorb the same amount from the seed treatment).
Certain plants (including sunflowers and canola) are known to "hyperaccumulate" toxic metals [53], perhaps more so during drought. Could this also be the case with systemic insecticides? Something that's been stuck in the back of my mind is that Bonmantin [54] found that the concentration of imidacloprid first drops in sunflower plant tissue as it grows, and then reconcentrates in the flower heads.
It occurs to me that the translocation of systemic insecticides is generally studied in plants grown under "normal" conditions. I'd very much like to see data for residues in pollen and nectar from seed-treated plants grown under drought. Had we thought of this earlier, we could have collected pollen and nectar samples from drought-stressed plants last summer. I'm currently trying to track down any data or samples from such plants--if any reader has any such sample analyses, please let me know!
Practical application: the above hypothesis is speculative, but we need actual data from drought-stressed plants to see whether such an effect occurs. If so, it would need to be taken into consideration for the registration of seed treatment products!
Once planting was completed and the drought took its toll, the reports that I've heard are that soybean honey saved a lot of bee operations this season, right in the middle of treated corn/soy farmland. In this case, seed treatment with neonicotinoids may have been a blessing to beekeepers:
The benefits of [seed treatment] not only include the early-season disease control but also suppression of soybean aphids for quite a ways into the growing season. With it, we typically make only one foliar insecticide application for aphid control, usually in August, instead of two applications when [treatment] isn't used. In 2012, with the extremely dry conditions in mid-season, there wasn't as much of an aphid problem, and we treated just 300 acres of soybeans...Last year we sprayed closer to 30,000 acres for aphids [55].
On the other hand, some beekeepers on alfalfa or cotton got hit hard by other classes of insecticides. A hit from a pesticide application can lead to poor subsequent colony performance, queen failure, dwindling, or winter collapse. ABJ published an excellent series of articles on pesticides by Drs. Barbara and Eric Erickson in 1983; Editor Joe Graham has graciously granted me permission to post copies of those articles to my website [56]--I strongly suggest any beekeepers interested in pesticide issues read them! In the second article, the authors discuss both the problems with systemic insecticides and of sublethal effects--note that these articles were written long before the introduction of the neonics!
An anti-pesticide group, along with a handful of beekeepers, recently filed suit against the EPA [57], calling for an immediate ban on the two most common neonicotinoid seed treatments, despite the easily-verifiable fact that hundreds of thousands of colonies thrive in the midst of seed-treated corn, soy, and canola! To me, this suit smacks of being some sort of well-orchestrated publicity stunt, and does not serve the interests of either beekeepers or environmentalism. Worse, it now gives the powerful farm lobby cause to label beekeepers as "radical" enemies.
We don't want this battle: do we really want to take on the farm lobby by backing them into a corner? The French beekeepers took a similar case against fipronil all the way to their supreme court and lost [58, 59]-worth reading]. Agriculture is already positioning itself for a fight [60, 61, 62]. Think about it--the EPA lives in fear of a conservative congress slashing their funding. Does anyone really think that they are going to go against the agricultural lobby without unimpeachable evidence? We should also think twice before calling for a ban on the seed treatments--the alternatives are not pretty!
It disturbs me to hear industry executives and lawyers stretching the truth or misrepresenting data. It disturbs me even more to hear my fellow environmentalists and beekeepers doing so! If we wish to maintain credibility, we should hold ourselves to a higher standard. The question we must ask ourselves the way in which we wish to have pesticide regulation decisions made:
1. By the EPA (the Environmental Protection Agency), whose risk assessors carefully study and weigh all available research and evidence in order to make objective and rational decisions, or
2. To have it decided instead by impassioned, fearful, and often misinformed advocacy groups who hire lawyers and pressure politicians who know little about the subject?
We depend upon the EPA to strike a balance between the availability of cheap food and profitability for those who provide it, versus the risks to human and environmental health and safety. It is good to have activists on both sides of the issues (industry and the anti-pesticide groups) to keep the EPA informed. But I don't feel that either of those groups should be telling the EPA which pesticides to register or to ban! Let the regulators do their job!
Rather than wasting EPA's funding to fight frivolous lawsuits, there are more productive actions that we can take:
Help the EPA to do its job by filing "adverse effects incident reports" if you observe a problem due to pesticides [63]. EPA is begging beekeepers to do this! Unless they have documented reports of pesticide problems, their hands are tied as to restricting the uses of those pesticides!
Support the National Pollinator Defense Fund [64]. Our industry is currently represented by a reasoned and knowledgeable group of (mostly) beekeepers. (Challenge to the pesticide companies: why don't you stand behind the safety of your products and donate? The NPDF is about ensuring that your pesticides are properly applied, so there would be no conflict of interest).
If your local state lead agency is not actively investigating bee kills or enforcing pesticide regulations, then use the local media to embarrass them into action!
Keep pressure on the EPA to resolve corn planting dust problems. Here's a wild idea: I'm not sure of the exact figures, but let's say that 90% of the 95 million acres of corn is grown from neonic-treated seed. If the states were to levy a surcharge of 50 cents per acre (neonic seed treatment adds about $12 per acre to seed costs), they could collect over $42 million each year to fund a pool from which to indemnify the occasional beekeeper who suffers a confirmed kill from planting dust!
Tell Congress that we'd like to see wording added to the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) to specifically protect pollinators. Currently, such protection is nebulous (although the EPA is acutely aware of pollinator issues): "The Administrator shall register a pesticide if... when used in accordance with widespread and commonly recognized practice it will not generally cause unreasonable adverse effects on the environment." Unless there is specific wording to protect pollinators, bee kills may not be considered to be "unreasonable"!
We need far more independent field studies to determine which pesticides and application practices are actually causing harm to pollinators. For pesticides in question, keep pressure on the EPA to require additional field trials to demonstrate whether they are indeed safe for pollinators under field conditions. I'd like to see the establishment of monitoring apiaries (and patches of untilled land) in representative agricultural areas nationwide, with the hives in each apiary to be carefully managed by independent parties. Such apiaries and sites could then be closely monitored each summer to see whether honey bees and other pollinators are able to survive local pesticide practices.
Give farmers workable options! Disseminate and promote bee-friendly agricultural practices that don't hurt the farmers' bottom line. For example, by adopting IPM practices, Arizona cotton growers reduced insecticide spraying from 12.5 times a season to only 1.3 times (cutting insecticide use twentyfold), while using more environmentally-friendly insecticides [65]! Another recent study in Iowa found that adding additional clover or alfalfa rotations in corn/soy farmland was equally profitable, improved the soil, used less energy, used far less pesticides, and decreased water pollution [66].
Business and agriculture respond to consumer demand. Consumer demand stopped most dairymen from injecting their cows with the hormone BST. Consumers could do the same by demanding pasture-fed beef and dairy (which would create more pollinator forage)! I'd also like to see the expansion of consumer choices (other than organic certification) that reward farmers who manage their lands to the benefit of wildlife and pollinators. For ideas, see [67. 68. 69].
Bottom Line
In conclusion, it appears that a perfect storm of a preceding exceptionally warm winter, followed by serious drought across the country, the lack of good mite control, a high prevalence of pathogens, and an unexpected California chill in the orchards prior to bloom, resulted in an unusual degree of colony losses. In other words, rather than one specific cause, there were simply not enough of the good things, and too many of the bad things.
I don't see evidence that pesticides were the major factor in the shortage of bees in almonds this winter, although, as usual, a number of individual beekeepers on certain crops certainly took serious hits.
And how about the fear that there won't be enough bees for almond pollination next year? Beekeepers have already told almond growers to expect higher pollination prices next year (especially since California is again going into serious drought, and beekeepers will be forced to invest extra money in feeding their hives). Most every beekeeper I know is madly making increase right now in anticipation of higher pollination prices next season. The fact of the matter is that should conditions allow beekeepers to successfully rebuild their numbers (following the typical swings of our boom/bust cycle), there could possibly even be a glut of bees for almonds next winter!
Feedback And Corrections
A few countries placed temporary suspensions on certain seed treatments until planting dust issues were resolved [27]--only Germany has one suspension still in place. - Actually there are some more: France (Thiamethoxam in oilseed rape, Imidacloprid in corn and sunflower), Italy (all Neonic seed treatment in corn), and Slovenia (Imidacloprid, Thiamethoxam, and Clothianidin seed treatment in all crops)
French beekeepers also started seeing problems with the introduction of the neonics; I've spoken with beekeepers in France whose apiaries are in pesticide-free areas. They tell me that they experience the same sorts of colony mortality problems as do those in areas exposed to neonics - This is, by the way, likewise confirmed by monitoring results from the French authorities.
In the case of foliar, drench, or chemigation applications prior to bloom, there are greater possibilities for bees to be exposed to toxic levels. - This is not the case for foliar application: as Neonics are xylem-systemic, but hardly mobile in the phloem, they can only be distributed in a plant after root uptake, but not be translocated for instance from a leaf to a later developed flower.
Then, on the topic of systemic residues in plants under drought stress: first, I am quite sure that the decrease of concentration in seed-treated plants over time is not only due to dilution, but also to degradation of the compounds - a factor that is not specifically dependent on water availability for the plants (e.g. photodegradation!); second, even if there would be less dilution in plants under drought stress: the concentrations in nectar and pollen of treated crops are normally so low (when we consider average rather than peak concentrations, and when we consider scenarios where colonies have chronically access exclusively to contaminated nectar/pollen over months unlikely in practice), that even an increased concentration due to drought stress-affected plants should not make a significant difference: if we for instance assume an average concentration of let's say 3-4, or even 5 ppb Clothianidin in corn pollen, and likewise assume a dilution reduced to 50% (which is probably exaggerated), then we would still not end up with excessive residues. And finally, we have residue figures from crops grown in different countries, different climatic conditions, and different agronomic practices; though we have not specifically addressed the drought stress scenario, we have seen that residue figures are quite consistent over all scenarios, and there does not appear to be strong evidence that different environmental conditions would substantially (i.e. by orders of magnitude) and systematically alter residue concentrations.
Dr. Christian Maus
Global Pollinator Safety Manager
Bayer CropScience
/
A ppt on the impact of CRP lands on wildlife in North Dakota
http://www.redriverbasincommission.org/Conference/Proceedings/26th_Proceedings/Kading_RRBC_09.pdf
/
Feedback from a Midwestern apiary inspector:
Just a quick update: This beekeeper who recently told his local newspaper that pesticides were killing his bees, he was making excuses. We examined two of his yards with him yesterday. One yard was showing EFB throughout the whole yard. I think his "mid-summer losses" last year (half of that yard's hives) were EFB kicking in with the mid-summer dearth. In his other yard, most of his dead outs were obvious starve outs. He harvested all of their stores with the first frost, and then didn't feed them. So, in my opinion, and from my observations, pesticides are usually being used responsibly, and aren't killing honey bees. I also think, with the aggressive way bees were on soy fields last summer, the systemic pesticides are not harmful to honeybees. I'm not seeing honey bee problems other than EFB getting the upper hand, due to our cold, late spring. My two cents. Thanks.
References
[1] http://www.frequency.com/video/dan-rather-reports-buzzkill/87705620/-/YouTube
[2] http://www.ars.usda.gov/is/pr/2012/120531.htm and California DPR.
[3] http://www.ncdc.noaa.gov/temp-and-precip/maps.php
[4] Wright, CK & MC Wimberly (2013) Recent land use change in the Western Corn Belt threatens grasslands and wetlands. https://www.motherjones.com/files/pnas201215404_nwow5w1.pdf
[5] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
[6] https://scientificbeekeeping.com/sick-bees-part-2-a-model-of-colony-collapse/
[7] vanEngelsdorp, D, et al (2013) Idiopathic brood disease syndrome and queen events as precursors of colony mortality in migratory beekeeping operations in the eastern United States. Preventive Veterinary Medicine 108(2-3): 225-233. http://www.sciencedirect.com/science/article/pii/S0167587712002656
[8] https://scientificbeekeeping.com/sick-bees-part-18a-colony-collapse-revisited/
[9] http://almondinsights.com/692, http://agfax.com/almonds/2013/reports/03042013-almonds-web.htm
[10] https://scientificbeekeeping.com/sick-bees-part-18a-colony-collaspse-revisited/
[11] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2010-2011-Limited_Survey_Report.pdf
[12] http://www.youtube.com/watch?v=y6B5qm2ut18, http://www.youtube.com/watch?v=PYbLbhZXizY
[13] (Broken Link!) http://www.nccrops.com/2012/07/27/insecticide-recommendations-for-corn-earworm-in-soybeans/
[14] http://www.agriview.com/news/crop/corn-soil-insecticide-use-up-dramatically-to-combat-widespread-rootworm/article_5d09decc-5b40-11e2-b485-001a4bcf887a.html
[15] http://www.amvac-chemical.com/products/documents/Counter20G%20Tech-Sell%20Sheet%20-%202013.pdf
[16] http://pmep.cce.cornell.edu/profiles/insect-mite/propetamphos-zetacyperm/terbufos/insect-prof-terbufos.html
[17] http://www.lewishybrids.com/PDF/3-5-2013Agronomic+ALERT+-+Interaction+between+herbicides+insecticides+corn.pdf
[18] http://pest.ca.uky.edu/EXT/Recs/ENT16-Field%20corn.pdf
[19] (Broken Link!) http://www.soybeans.umn.edu/crop/insects/spider_mites.htm
[20] http://www.nytimes.com/2013/04/07/opinion/sunday/calamity-for-our-most-beneficent-insect.html?nl=todaysheadlines&emc=edit_th_20130407&_r=0
[21] http://www.nytimes.com/2013/04/07/opinion/sunday/calamity-for-our-most-beneficent-insect.html?_r=0
[22] http://www.panna.org/press-release/beekeepers-and-public-interest-groups-sue-epa-over-bee-toxic-pesticides
[23] http://www.cdpr.ca.gov/docs/pur/pur10rep/top_100_ais_lbs10.pdf
[24] http://www.extension.org/pages/60318/pesticides-and-their-involvement-in-colony-collapse-disorder
[25] Mussen, EC (2006) Chaotic almond pollination. http://entomology.ucdavis.edu/faculty/mussen/JanFeb2006.pdf
[26] https://scientificbeekeeping.com/sick-bees-part-18e-colony-collapse-revisited-genetically-modified-plants/
[27] http://www.epa.gov/pesticides/about/intheworks/ccd-european-ban.html
[28] http://www.thecre.com/oira_pd/wp-content/uploads/2013/04/DQA-Alert-EU-Commission-Ban-on-Neonicotinoids-4-10.pdf
[29] https://scientificbeekeeping.com/home/news-and-blogs/
[30] Henderson, CB, JJ Bromenshenk, DL Fischer (2013) Clothianidin exposure levels from bee-collected pollen and nectar in seed-treated corn and canola plantings. Proceedings of the American Bee Research Conference.
[31] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
[32] http://www.ontariograinfarmer.ca/MAGAZINE.aspx?aid=534
[33] http://www.pbs.org/wgbh/pages/frontline/shows/settlement/timelines/april94.html
[34] https://scientificbeekeeping.com/2012-almond-pollination-update/
[35] https://scientificbeekeeping.com/neonicotinoids-trying-to-make-sense-of-the-science/, https://scientificbeekeeping.com/neonicotinoids-trying-to-make-sense-of-the-science-part-2/, https://scientificbeekeeping.com/testing-of-bee-feed-syrups-for-neonicotinoid-residues/
[36] http://www.eea.europa.eu/publications/late-lessons-2
[37] http://www.sciencefriday.com/playlist/#play/segment/9088
[38] https://scientificbeekeeping.com/the-extinction-of-the-honey-bee/
[39] http://www.ncdc.noaa.gov/temp-and-precip/maps
[40] http://nassgeodata.gmu.edu/CropScape/
[41] https://scientificbeekeeping.com/a-new-large-scale-trial-of-clothianidin/
[42] http://www.producer.com/daily/ontario-field-study-finds-no-link-between-seed-treatments-bee-deaths/
[43] Pohorecka, K, et al (2013) Residues of neonicotinoid insecticides in bee collected plant materials from oilseed rape crops and their effect on bee colonies. Journal of Apicultural Science 56(2): 115-134. http://www.degruyter.com/view/j/jas.2012.56.issue-2/v10289-012-0029-3/v10289-012-0029-3.xml?format=INT
[44] http://www.fera.defra.gov.uk/scienceResearch/scienceCapabilities/chemicalsEnvironment/documents/reportPS2371Mar13.pdf
[45] http://repository.up.ac.za/bitstream/handle/2263/20334/Nicolson_Chemical(2012).pdf?sequence=1
[46] (Broken Link!) http://www.ag.ndsu.nodak.edu/aginfo/entomology/entupdates/Sunflower/a1331sunflowerhandbook.pdf
[47] http://www.sunflowernsa.com/growers/approved-chemicals/insecticides-test/
[48] http://www.mydigitalpublication.com/publication/?i=151958&p=41
[49] http://www.sunflowernsa.com/growers/approved-chemicals/insecticides-test/
[50] http://www.farmassist.com/agriedge/images/Resource_PDFs/Soybean/Warrior_Zeon.pdf
[51] http://www2.dupont.com/Production_Agriculture/en_US/assets/downloads/pdfs/K-09315.pdf
[52] http://www.ontariograinfarmer.ca/MAGAZINE.aspx?aid=534
[53] http://en.wikipedia.org/wiki/List_of_hyperaccumulators
[54] Bonmatin, JM, et al (2005) Behaviour of Imidacloprid in Fields. Toxicity for Honey Bees. In Environmental chemistry: green chemistry and pollutants in ecosystems pp. 483-49. http://www.buzzaboutbees.net/support-files/bonmatin2005behaviour-of-imidacloprid-in-fields.pdf
[55] http://cornandsoybeandigest.com/seed/do-soy-seed-treatments-pay?page=2
[56] https://scientificbeekeeping.com/historical-pesticide-overview/
[57] http://www.centerforfoodsafety.org/press-releases/1911/cfs-beekeepers-and-public-interest-groups-sue-epa-over-bee-toxic-pesticides
[58] http://www.theworldlawgroup.com/files/file/docs/Soulier_health_environment_June_2012.pdf
[59] http://www.soulier-avocats.com/upload/documents/Soulier_health_environment_september_2010_F.pdf
[60] http://westernfarmpress.com/government/pesticide-battle-over-honey-bee-health-under-way?page=1
[61] http://westernfarmpress.com/management/total-ag-pesticide-elimination-sought-radicals
[62] http://www.neonicreport.com/home/project-compass/
[63] https://scientificbeekeeping.com/pesticide-incident-reporting/
[64] http://pollinatordefense.org/site/
[65] http://cals.arizona.edu/apmc/docs/IPM_Delivers.pdf
[66] Davis, AS, et al (2012) Increasing cropping system diversity balances productivity, profitability and environmental health. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0047149
[67] http://www.pcl.org/pcl_files/5_Wildlife_Habitat_Farmland.pdf
[68] http://pfspbees.org/
[69] http://www.nwf.org/CertifiedWildlifeHabitat/UserAccount/SignIn
Category: Practical Beekeeping Management, Topics
Tags: beekeeper management, biotic, diseases, drought, environmental, factors, pesticides, randy oliver, varroa | diseases Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/diseases/ |
What Happened To The Bees This Spring? (Part 1 & 2)
First published in: American Bee Journal, June 2013
Part 1: Environmental and Biotic Factors
Setting the Stage
The Lead Up
The Drought
Lack of Good Forage
Varroa
Diseases
Other Indicators of Impending Collapse
An Unexpected Chill
Feedback from Brokers
The Silent Majority
Beekeeper Management
Part 2: The Contribution From Pesticides
The Lynch Mob
Debunking The Myths
The Precautionary Principal
See For Yourself
Be Careful What You Ask For!
The Effect Of Drought
Actions To Take
Bottom Line
References
What Happened To The Bees This Spring?
Part 1: Environmental And Biotic Factors
Randy Oliver
ScientificBeekeeping.com
First published in ABJ June 2013
By now, most everyone has heard that honey bee colonies died in massive numbers this winter. Reporter Dan Rather, in his newscast Buzzkill [1], showed unfortunate beekeepers, some of whom had lost half or more of their colonies, predicting gloom and doom for the bee industry. What were the causes of this year's bee shortage? As Rather says, "Everyone has an opinion." The question is whether those opinions are based upon fact! So let's go over the events leading up to the bee supply debacle.
Setting The Stage
Nearly 800,000 acres of almond trees in California came into bloom this winter--the trees typically start flowering about Valentine's Day, and the bloom lasts for only about two weeks. Almonds require cross fertilization between adjacent rows of varieties (Fig. 1), and honey bees are trucked in from all over the country to do the job (roughly a million and a half colonies). Many large commercial beekeepers move their hives into California in November to overwinter in holding yards; others build them up on winter pollen flows in Florida or Texas, or hold them in temperature-controlled potato cellars until shortly before bloom. The hives are generally placed into the orchards about a week before the first flowers appear. There is virtually no forage in the orchards prior to, or after bloom in many areas.
Figure 1. An almond orchard in late February, showing the flowering of rows of different cultivars required for cross pollination. The bare "late" varieties have not yet bloomed; the green "early" pollenizers have finished bloom. Grading of colonies is normally done during the bloom of the main crop (usually Nonpareil).
The Lead Up
Two seasons ago there was also a shortage of bees in almonds, following the coldest January (2011) in 17 years (cold being a major stressor of wintering bee colonies). Beekeepers then replaced their deadouts with package bees and splits, thus starting a new generation of colonies, which tend to have lower varroa mite levels than established colonies. These colonies entered autumn 2011 in pretty good shape, and then enjoyed the fourth warmest January (2012) on record! As a result, there was the lowest rate of winter mortality in years, and plenty of bees for almonds in 2012 (Fig. 2).
Figure 2. Percent winter losses since the beginning of the national survey--the data is not yet in for 2012/13. Note that there has been a general downward trend, suggesting that whatever caused the high losses in 2007/8 has not been such a problem in recent years. Note also the cyclical nature of colony winter losses, with high losses in 2004/5, 2007/8, 2009/10, and 2012/13 (some data not shown) Data from [[i]].
[i] http://www.ars.usda.gov/is/pr/2012/120531.htm and California DPR.
I was curious as to whether the colony loss rate was linked to the use of neonicotinoid insecticides. There is no recent USDA data, so I went through the California Pesticide Use Reports (data available through 2010). I plotted the amount of imidacloprid applied to crops in California in the preceding year in red (the seed treatment clothianidin didn't even make the top 100 list of pesticides applied). Although there appears to be a possible correlation from 2006 through 2009, the trends were reversed for 2010. I will be curious to add the 2011 data when it becomes available.
In March of 2012 I received a phone call from a California queen producer who had a prescient insight as to a potential brewing disaster. He was receiving calls for queen bees from Northern beekeepers whose bees had already grown to swarming condition due to the unseasonably warm spring weather (Fig. 3).
Figure 3. Last year's warm spring in much of the country lead to early broodrearing, and as a result, early buildup of varroa levels. Note the record warm spring in the Midwest.
The queen producer noted that such early brood rearing also meant early mite buildup, and predicted that since most Midwestern beekeepers treat for mites by the calendar, that they would unknowingly allow mites to build to excessive levels before treatment. This was strike one against the bees.
The Drought
Then it didn't rain-by midsummer, it was clear that the continental U.S. was in serious drought, including California, whose beekeepers supply nearly half the bees for almond pollination. The only ways that we kept our colonies strong was to either feed expensive pollen supplement and sugar syrup, or to move them to elusive better pasture out of state. By late summer, 60% of the U.S. was in drought, meaning that unless your bees were next to soybeans or irrigated crops, there was little forage for them. This lack of good nutrition was strike two against the bees (Fig. 4).
Figure 4. The severe drought in the Midwest really put the hurt to bee pasture in those states in which the majority of commercial hives spend the summer. Source [[i]].
[i] http://www.ncdc.noaa.gov/temp-and-precip/maps.php
Drought not only dries up nectar and pollen sources, but also forces bees to fly further and more frequently for water. Plus it concentrates ag chemicals and pesticides in the few sources of surface water available to bees. The bees started to show the hurt.
Beekeepers tried to move their hives to areas of better forage, sometimes overstocking an area with too many hives, which led to excessive competition for resources, and the spreading of parasites. Others desperately chased less desirable crops such as sunflowers. Colonies in holding yards in California found little to eat, due to our record dry weather. Some beekeepers with winter eucalyptus locations found them crowded with other hives.
Lack Of Good Forage
In Buzzkill, Bret Adee brought up the fact that bee pasture in the Midwest is disappearing under the plow, largely due to our environmentally-irresponsible taxpayer-subsidized policies that encourage farmers to plant every square foot of land into corn (Fig. 5). Bee brokers told me that colonies coming to almonds from the Midwest were in generally poorer shape this year than those coming from the southern states.
Practical application: some Midwestern beekeepers split their operations, hauling some to the South to rebuild over winter, and the rest directly to California-there was a night and day difference as to how the colonies looked in February!
Figure 5. Grasslands and wetlands in the Corn Belt are rapidly being converted to monocultural, heavily herbicided corn/soy, which eliminates virtually all bee and wildlife forage. A new study found that between 2006 and 2011 there was a net loss of 1.3 million acres of grassland. This affects not only bees--the authors [[i]] state that "As a consequence, populations of grassland nesting birds are declining faster than any other group of birds in North America."
[i] Wright, CK & MC Wimberly (2013) Recent land use change in the Western Corn Belt threatens grasslands and wetlands. https://www.motherjones.com/files/pnas201215404_nwow5w1.pdf
To put this loss of bee pasture into perspective, I asked some Dakota beekeepers for estimates of how many acres of CRP grassland are needed to sustain a colony of bees. In recent years, the overall hive density in North Dakota has been more than 10 hives per square mile (less than 64 acres per hive, including wastelands).
Practical application: the best guess by those beekeepers was that each colony of bees requires about 5-15 acres of productive land for forage (late summer forage being the critical factor). If we use the figure of 10 acres per colony, then the conversion of 1.3 million acres of grassland to herbicided cropland suggests that forage for 130,000 colonies of bees has been eliminated in the past five years in the Corn Belt alone! This figure represents nearly 9% of all colonies needed for almond pollination.
Varroa
An excellent window into the causes of colony health problems is the USDA National Honey Bee Pests and Diseases Survey Report [5] (the latest data have not yet been released). It is worrisome that varroa levels appear to be steadily climbing year after year.
And if the drought and forage problems weren't enough, the favored miticide of commercial beekeepers became unavailable for a time last summer, and mite levels built to killing levels in a number of operations. By late July, some of us were already predicting a disaster for the upcoming almond pollination season. Although many beekeepers finally got mite levels down with late-season treatments, the damage had already been done, and there was no turning the colonies around. Strike three for the bees!
In November semi loads of hives started moving into California, or had been placed in potato cellars. Some of the colonies that arrived from the Midwest were in poor shape, or crawling with mites. Oddly, few beekeepers at the time owned up to having problems, despite the reports that I kept hearing of mite and forage issues! I'm not sure whether this was due to denial, wishful thinking, simple lack of lifting the lids, or something else.
Diseases
Nosema infection also runs rampant across the country--70% of colonies were infected in June of last year. The stressful factors leading up to almond bloom apparently put a lot of hives close to the "tip point" at which pathogens can overwhelm the colony immune system and start it going backwards, or initiate the slide into sudden depopulation (detailed at [6]). Few seem to be mentioning signs of CCD-it is unfortunate that the media keep using that term as a catch-all for all hive problems!
One should keep in mind that the winter collapse issue appears to be cyclical, similar to flu or other pathogen epidemics. I have strong reason to suspect that the constantly-evolving viruses are involved in these colony collapse epidemics.
There has also been a strong resurgence of European Foulbrood and other unidentified brood diseases [7] (Figs. 6, 7, and 8). Unlike EFB of old, the new forms don't go away with a nectar flow.
Figure 6. "Shot brood" due to EFB. Note the fat queen near the center. Despite her vigorous egglaying, this colony is unable to pull ahead due to excessive brood mortality. Lots of beekeepers reported EFB symptoms this winter.
Figure 7. You really have to look hard in some colonies with spotty brood to see the cause! Two larvae in this photo show signs of EFB infection.
Figure 8. Dying brood from one of my sick colonies this spring with EFB-like symptoms. Note the "shot" pattern, the twisted larvae, and the dried larval remains. There is also some AFB-like coloration, but lack of roping or AFB odor (this odor is distinct and sour), nor a positive Holst milk test. In this colony, even pupae were dying. I observe these symptoms independent of whether the hives went to almond pollination or not. Colonies with this (or similar) infection cannot grow. Treatment with oxytetracycline generally clears it up.
One thing that I noticed in Buzzkill was the uneaten pollen supplement patties in many of the crashed hives. I've mentioned before [8] that I've found a colony's failure to consume pollen supplement to be a reliable predictor that that colony will later collapse.
Another strong predictor of winter collapse is weak strength in fall (upcoming article), again strongly suggesting that those colonies already have some sort of health issue going into winter. I heard reports from all over the country that bees went into winter in poor condition.
An Unexpected Chill
The final blow to hives in California was a blast of icy weather (Fig. 9). This unexpected chilling compounded all the existing problems! I've previously pointed out that colony collapse often follows unseasonable chills, since it shifts the tip point for virus and nosema epidemics. Clusters that had expanded for broodrearing contracted, resulting in chilled brood and dead young bees on the ground. My own colonies simply shut down broodrearing completely, losing about two weeks of buildup.
Figure 9. Chilling events (blue arrows) in Modesto, California this winter (the dark blue lines represent normal highs and lows). The unusual chilling in late December and early January (hitting the '20's in a number of areas) came at the time when colonies normally begin to build up for almonds. This severe (for California) cold set the already-stressed colonies back hard, and may have allowed nosema and viruses to gain the upper hand. Graph from wunderground.com.
At the national convention in January, the first reports of beekeepers with collapsing operations were heard. But still, the industry was in denial, with an apparent glut of promised bees as late as the end of the month (two weeks before start of bloom)! But when the rubber finally hit the road in mid February, that illusory supply quickly evaporated, with desperate growers and brokers scrambling to obtain bees--some offering obscenely high prices for substandard colonies.
And then, due to the cool spring, the trees held off on blooming for an extra 10-14 days [9]-colonies placed in anticipation of normal start of bloom just sat there starving and shivering on the cold orchard floors.
Practical application: the biology here is that this is the time of the "spring turnover" in bee populations in California, during which the old overwintered adult bees must rear their replacements for the spring buildup of population. The conditions in the almond orchards prior to bloom are miserable for smaller colonies--it is warm enough to encourage them to break winter cluster and expand the broodnest, but overnight frosts on the Valley floor can cause serious chill stress. Furthermore, it is often warm enough to fly at midday, but there is virtually nothing to forage upon until the trees start blooming! Such fruitless foraging further wears out the workers, and allows sick bees to drift to adjacent hives. Worse yet, the desperate foragers rob out any dead or dying colonies in adjacent orchards, rapidly and effectively transmitting mites, nosema, viruses, and anything else harmful in the deadouts.
Many colonies went backwards during this excruciatingly long wait. Some beekeepers told me that hives graded at placement scored better than those graded at bloom (just the opposite of normal)!
I've been carefully observing spring turnover in my "dinks" (weak colonies) in February (Fig. 10). What I find is that the problem is generally not the queen; rather, the colonies are infected with some pathogen- most commonly nosema [10], the paralytic viruses [11], or EFB (or EFB-like brood disease). Those colonies that are able to successfully emerge one solid round of brood are often able to "clear" the infection and completely rebound by April. Those that get hit by frost in February often collapse.
Figure 10. An example of an unsuccessful spring turnover. This colony is in the middle of typical February collapse from nosema or IAPV. You can easily see the outline of the area recently covered with brood, delineated by the crescents of freshly-packed pollen. Colonies undergoing this sort of depopulation tend not to forage for nectar, and do not respond well to supplemental feeding. This colony continued to collapse quickly, and finally died in a cold snap a week later--with only silver-dollar sized patch of dead bees remaining.
Feedback From Brokers
I asked a few of the major pollination brokers for their observations on the colony shortage this season. Their feedback suggested that the causes for the bee shortage were varied and many.
Summary:
Most were able to eventually fill their contracts. Beekeepers often hold colonies in reserve "just in case," or gambling that in "short" years they can rent those last hives at an elevated price. Also, when the offered price went up, hives not originally intended to go to almonds were loaded up at the last minute and shipped to California (I was in Florida at the start of bloom, and had an inspector tell me of certifying colonies for shipment after the bloom had already begun!).
A number of hives received in November were already headed downhill. Some exhibited the symptom of bees not clustering properly (a typical sign preceding sudden colony depopulation/CCD). Some arrived crawling with mites, or with recent mite treatments in place (suggesting that they were treated too late).
Some graders saw piles of dead bees in front of hives--cause unknown. There were reports of some herbicide tank mixes killing bees.
Many of the placed colonies were below standard grade-- growers paid for less than they expected!
Graders told me that there was a huge variation in hive strength from beekeeper to beekeeper. Many hives were strong (12-16 frames of bees) and healthy; other operations graded at zero to three frames of bees (some of the deadouts had spider webs inside, suggesting that they hadn't been occupied by bees for some time).
The unusual winter chill was tough on colonies that had been stimulated into early buildup, and then forced to contract their broodnests. Some colonies kicked out chilled brood and dead bees afterwards.
Many beekeepers watched their colonies go "backward" prior to bloom.
Colonies from the Southern states (especially those delivered in February) were generally in better shape than those from the Midwest.
Midwestern beekeepers blamed drought, mites, poor nutrition.
Several beekeepers said that their best bees came from remote areas, and their worst from ag areas.
A number of beekeepers admitted inadequate mite treatment; mites were a recurrent theme.
There were a number of reports of EFB hitting colonies.
Some had gotten hit last summer with pesticide sprays, and their colonies didn't recover.
"There were good bees and bad bees from every state. They all seemed to have different problems depending on location/state."
Many good beekeepers simply didn't know what happened to their hives; there were lots of lifeless hives delivered. The atmosphere was ripe with speculation as to the actual causes.
"The shortage was also created by beekeepers that chose not to come to California for a variety of reasons. They can make more money with honey, didn't get paid for what they have brought in the past, bees come back home with mites, beetles and whatever else takes a ride on the hives. Beekeepers don't want to risk bee health to chase the dollar." Many out-of-state beekeepers have had bad experiences going to almonds, and simply don't feel that it's worth it. The supply of bees will largely depend upon the price that growers offer for renting them!
The Silent Majority
Buzzkill leaves one with the impression that the entire bee and almond industries are on the verge of collapse. Of course, the news media focus on fear and disaster, so we may consider taking such dire projections with a grain of salt. In the case of Dan Rather, the focus was on the beekeepers with troubles, not upon those who successfully filled their pollination contracts.
So just how severe was the problem? Let's say that there was an overall shortage of 100,000 hives (a figure that I heard floated)--that would represent only about 6% of the total number of hives placed into almond pollination. The other 94% were successfully delivered (although a proportion of those were weak due to the poor season).
Since the debacle, I've heard from plenty of beekeepers whom I'll refer to as the "silent majority," who experienced "normal" colony winter losses in the 5-25% range, and who successfully filled their pollination contracts. Although the hearts of all beekeepers go out to those who suffered severe colony losses, many felt that some of those losses could have been prevented if the afflicted beekeepers had been more proactive than reactive.
And don't forget those upon whom the rest of the industry depends to supply bees for restocking their deadouts! The California package producers, who have been pollinating almonds for decades, are routinely counted on to consistently take strong hives to almonds, and to then shake over a hundred thousand packages of bees for sale afterwards. Few of these major producers experience severe unexplained colony losses.
Beekeeper Management
By no means am I suggesting that those beekeepers who suffered losses engaged in poor beekeeping practices, but I can't help but notice that not all beekeepers were equally affected--a great number provided strong, healthy colonies to almonds. I've spoken to some of them-the common thread is that those who recognized the problems of poor nutrition and mites in August, and took remedial action for the rest of the season, had acceptable winter losses.
Some beekeepers who really put serious effort and money into bee husbandry were even able to sell "shook bees" from their colonies to others in February! For example, watch Keith Jarrett feeding substantial quantities of pollen supplement to very strong colonies in January [12]--Keith consistently brings very strong colonies to almonds every year, and this year was no exception!
Practical application: I'm here to tell you, that one lesson that I've learned during our intense California drought, is that those yards that I fed with protein in late summer before they started going downhill went to almonds much stronger than those that I didn't feed until fall! Proactive is better than reactive--if you wait until colonies are already going downhill, it is much more difficult to turn them around!
I've often been accused of being politically incorrect for speaking frankly. I'd like to make amends at this point by retiring the rude and unsympathetic term "PPB" (Piss Poor Beekeeping). The fact is that the average wintering loss for the past few years has hovered around 30%. So if you experience 30% losses, you can now proudly call yourself an "Average" beekeeper!
But what about those beekeepers who consistently manage to enjoy lower rates of winter loss? I propose that we call them "Lucky" beekeepers, and the best of them, "Consistently Lucky."
Practical application: the harder those beekeepers work, the luckier they get!
But there were clearly "unlucky" beekeepers this year--especially the "big boys" who brought tens of thousands of hives from the drought-ravaged, and corn-converted Midwest to California. California beekeepers are used to summer drought. We have learned to either move our colonies to better (often irrigated) pasture, or to feed expensive pollen supplements. This would be a very expensive proposition to the larger operators, with hives spread all over the place--a cost not covered by current pollination prices.
What Happened To The Bees This Spring?
Part 2: The Contribution From Pesticides
Randy Oliver
ScientificBeekeeping.com
First published in: American Bee Journal, July 2013
It's pretty straightforward to attribute the majority of colony losses this winter to the usual and aforementioned causes, but a number of beekeepers are also pointing the finger at pesticides. There is no doubt that in certain areas pesticides were a serious issue to beekeepers. Colonies set back by pesticide kills may not fully recover over the season, and those going into winter with pesticide residues may go downhill. There is also reason to suspect that pesticides and miticides have something to do with today's high rates of queen failure.
The bees in some drought-stricken areas were forced to forage on irrigated and pesticide-laden crops--the only place in which there was anything to eat. This changes the entire dynamics of pesticide exposure, since residues would no longer be diluted by the pollen and nectar of non crop plants. The lack of good natural forage also suppresses the ability of colonies to deal with the insult of those pesticides. And colonies may be forced, by necessity, to forage upon one treated crop after another, resulting in multiple exposures.
Practical application: under drought conditions, bees may suffer more from pesticides than when times are good.
Due to the current high prices for agricultural commodities, farmers are often applying pesticides indiscriminately as "risk insurance" rather than due to actual need. A chilling recommendation from an extension entomologist reads:
I encourage you to be risk averse and to make an investment that will pay dividends for your valuable crop. Consider applying [flubendiamide, indoxacarb, or spinosad] for corn earworm. If you have stink bugs and are in the [mature plant] stages, you might want to tank mix one of these products with a pyrethroid. A tank mix of a pyrethroid and acephate are an option, but will wipe out all beneficials [13].
The first three insecticides mentioned are considered to be "reduced risk" to bees if residues are allowed to dry for a few hours, but no mention was made to spray at night. Of the five insecticides recommended above for spraying on corn in tassel, at least four are highly toxic to bees if sprayed during the day! No farmer wants to kill bees, but with recommendations like this from state extension agents, well-meaning growers may unwittingly be hurting pollinators.
Bees in agricultural areas are exposed to a vast array of insecticides, miticides, fungicides and surfactants--many of which have clear links to colony health problems. And applications of new mixes of chemicals are up. For example, in addition to the neonicotinoid seed treatments, granular insecticide soil treatments for corn in the Midwest were up by 30% over the previous year [14]. These treatments consist of combinations of organophosphates and pyrethroids.
But I'm not hearing either the bird groups or beekeepers even addressing these treatments! It is scary to read the sales literature for Counter insecticide, the organophosphate terbufos [15]. Growers are encouraged to apply it at planting time, despite the facts that:
"Terbufos is highly toxic to birds, fish, and aquatic invertebrates [and bees]. [It] shows significant acute mortalities of birds, mammals, reptiles, and fish resulting from broadcast application...In the same study, the application of terbufos as a soil-incorporated treatment to corn...resulted in acute mortalities to birds and reptiles" [16].
Terbufos is strongly systemic, meaning that it is absorbed by the plant roots and could be expected to be expressed in the pollen and nectar.
It can synergize with other pesticides since it ties up the critical CP450 enzymes used in detoxification, to the extent that growers are cautioned that it can cause problems to corn from herbicides [17].
During drought, certain insect pests become more problematic, perhaps resulting in increased exposure to insecticides by bees. For example, drought encourages corn leaf aphids. Read this chilling recommendation for aphids on corn during tasseling (when bees are actively foraging):
If less than 50% of pollination has occurred, aphids and honeydew are covering tassels and plants are stressed, an insecticide may be necessary to ensure adequate pollination, but treatments need to be made within 48 hours of tassel emergence. Asana XL, Brigade, Capture, Cobalt, Dimethoate, Lannate, Lorsban, or Malathion may be used for control [18].
Or this:
Prolonged drought always raises the specter of two-spotted spider mite outbreaks in soybeans and corn. As the 2012 drought intensifies in Minnesota, infestations are reaching treatable levels...The only products that are recommended for spider mites in soybean include insecticides containing chlorpyrifos, dimethoate and bifenthrin[18].
The names of the recommended insecticides above strike fear into the hearts of beekeepers!
Practical application: many "consistently lucky" beekeepers go to great effort to allow their colonies to recover after exposure to pesticides--moving them to unsprayed areas or natural forage, or by immediately feeding protein supplement to stimulate increased broodrearing. Unfortunately, such "recovery" areas are getting harder and harder to find.
The Lynch Mob
Despite the fact that a wide range of bee-toxic insecticides are being applied (often during bloom) to corn, soy, sunflowers, alfalfa, cotton, and other major crops, if you Google anything about insecticide use, you'll quickly find that the blogosphere focuses only upon the putative link between a single class of insecticides--the neonicotinoids-and the demise of pollinators [19].
People look at me incredulously when I point out that there is zero firm evidence to date that the neonic seed treatments are a serious problem! But the notion that all honey bee problems are caused by an insidious new insecticide resonates with a distrustful public [20], and has firmly established itself as "common knowledge." But repeating something does not make it true!
"It's easier to fool people than to convince them that they have been fooled"-Mark Twain
Practical application: the question is, "Are the neonic seed treatments being railroaded into a guilty verdict in the media's kangaroo court of public opinion?"
One group recently brought suit against the EPA to ban the use of the seed treatments clothianidin and thiamethoxam [21], neither of which even make California's top 100 list of pesticides applied [22], nor that have ever been demonstrated to harm colonies feeding on the pollen or nectar of seed-treated plants! A number of people have made up their minds that the neonics are the main cause of colony collapse, and it appears that no amount of facts to the contrary will cause them to reconsider!
Debunking The Myths
As anyone who knows me will tell you, I am a stickler for honesty, accuracy, and factuality. I am concerned about the amount of misinformation and speculation going around about the neonics. So let's look at some of the claims vs. the actual facts.
Arguments Against Neonic Seed Treatments Actual Facts
The neonicotinoids have been "linked" to increased colony mortality. In actuality, such a "link" is merely an urban legend, and has never been demonstrated or confirmed in any study.
On the other hand, the residues of other classes of pesticides are more suspect for causing increased brood or adult bee mortality [24].
The timing of CCD coincides with the introduction of the neonic seed treatments in 2004. CCD started in California bees in the winter of 2004/2005, prior to them ever being exposed to seed-treated crops.
But what else could have changed at that time other than the introduction of neonics? In California, Dr. Eric Mussen [25] determined that the increased colony losses were due to poor summer forage and failure of mite control products (just as this last winter).
There is actually a much stronger association between the incidence of the novel gut parasite Nosema ceranae and increased colony mortality [26].
But the main thing that has changed is the dynamics of the varroa/virus complex, which coincidentally occurred at about the same time that the neonics came into use.
European countries banned the neonics, and the bees recovered after those bans. A few countries placed temporary suspensions on certain seed treatments until planting dust issues were resolved [27]--only Germany has one suspension still in place. The foliar applications were not suspended. The suspensions did not resolve bee health problems.
The European Food Safety Authority recently decided that neonics pose a threat to bees. "The Center for Regulatory Effectiveness (CRE) has recently completed a Data Quality Act (DQA) Alert on the ... (EFSA) report on neonicotinoids which found that neonicotinoids pose a risk to bees. The DQA Alert outlines the serious deficiencies of the EFSA report and demonstrates why the EFSA report violates the DQA...In particular, the EFSA report failed to maximize the objectivity of the data by failing to reconcile numerous studies whose conclusions contradicted the findings of the EFSA report" [28].
Several lab studies have found that neonics affect individual bee behavior, longevity, or immunity. True -- although many studies used unrealistically high doses. The question is whether such artificial studies apply to actual colonies in the field. The numerous field studies to date have failed to find any link between seed treatments and later colony health issues.
It is the seed treatments that make corn a problem. As Bret Adee points out in Buzzkill, corn is replacing pastureland (Fig. 4). Corn, as grown today, is a virtual "bee desert" (similar to the way in which suburban lawns are green bee deserts). And it's not only the bees that this is affecting, the populations of birds and other wildlife are plummeting due to loss of favorable habitat (see my blog on birds and neonics [29]).
A recent survey by Dr. Jerry Bromenshenk found that bees actually avoid field corn pollen, and are exposed to very little of the seed treatment residues [30].
Numerous independent studies, and the experiences of stationary beekeepers throughout the Corn Belt, support the conclusion that colonies can thrive when surrounded by corn, provided that there is some alternative forage within flight range.
As the use of neonic seed treatments increases, bee mortality goes up. In actuality, colony mortality rates go up and down year to year, largely dependent upon weather and varroa mite control. If the neonics were to blame for this winter's bee losses, why didn't they cause similar losses last winter, in which the colony mortality rate was the lowest in years?
French beekeepers also started seeing problems with the introduction of the neonics. I've spoken with beekeepers in France whose apiaries are in pesticide-free areas. They tell me that they experience the same sorts of colony mortality problems as do those in areas exposed to neonics.
Bees in the U.S. are commonly exposed to neonicotinoids. In the most recent USDA survey (100 samples across the country), imidacloprid was only detected in 9% of the samples [31] (although I found some of the residue levels alarmingly high). However, the most common seed treatment, clothianidin (or its degradation products), was not detected at all!
The above real-world data suggests that efforts to ban clothianidin as a seed treatment may be misplaced. It appears that imidacloprid, especially as a foliar application, would be of more concern.
Neonics are the most common pesticides that bees are exposed to. In the above survey, other serious insecticides were more commonly prevalent: chlorpyrifos (in 20% of samples), cyhalothrin (in 7%), and endosulfan (in 11%).
Notably, there was also a high prevalence of beekeeper-applied miticides: fluvalinate (in 38%), coumaphos (in 87%), amitraz (in 27%), fenpyroximate (in 11%), and thymol (in 27%).
There was even higher exposure to fungicides and adjuvants.
It is misleading for the pesticide companies to blame the problems on varroa, nosema, or poor nutrition. The above survey (over 1000 samples) found that the average varroa infestation rate in the U.S. in autumn is above the danger level for virus epidemics!
Sixty to 100% of hives are infected with nosema in December.
Summer drought has historically been associated with high winter mortality.
But didn't the planting dust from corn seeding kill colonies in Ontario? Planting dust is separate issue that clearly needs to be remedied. It does on occasion cause bee kills, for which beekeepers are rarely compensated. This situation must change! All parties are actively working on solutions [32].
Bees in certain agricultural areas tend to go downhill later in the season. This has been observed for a long time--long before the neonics. The question is, which chemicals, chemical synergies, or chemical/nutrient interactions are responsible? The Frazier/Mullin team at Penn State has developed a protocol for helping to figure this out. I strongly support its adoption by the EPA for pesticide risk analysis.
Colonies foraging upon nectar or pollen of seed-treated crops get poisoned. Ask yourself this: if neonic residues were actually so harmful to bees, how is it that the Canadian beekeepers, whose bees forage largely on seed-treated canola, feeding solely upon a diet of canola nectar and pollen with well-documented residues of clothianidin, experience very low winter losses, despite the long Canadian winter (so long as they control varroa and nosema)?
And how is it that the vast majority of beekeepers in the U.S. Corn Belt report that their colonies thrive and that they have far fewer pesticide issues these days than in the past?
The neonicotinoids are "systemic," meaning that they are in the plants all the time! True, but this property is not unique to the neonics--a number of other insecticides also go systemic. In any case, with seed treatment, the concentration of the insecticide in the plant is only high when the plant is young--it gets diluted as the plant grows (e.g., clothianidin in canola is at a level high enough to kill aphids for only about the first 30 days of growth).
The only time that residues in the plant matter to pollinators is when the mature plant flowers. The amount of seed treatment is carefully calibrated so that the residue in the pollen and nectar are below the level that causes demonstrable harm to bees.
In the case of foliar, drench, or chemigation applications prior to bloom, there are greater possibilities for bees to be exposed to toxic levels.
There are fewer butterflies and pollinators in the fields these days. Not surprising, since the new push for "clean farming" has removed the host plants upon which the butterfly larvae feed. Pollinators are forced to subsist upon the stretches of weeds growing along roads at the edges of fields. But surprisingly, pollinators may be abundant there, suggesting that even though populations as a whole are reduced by habitat conversion, it is that, rather than the use of seed treatments, that causes the population declines.
The evil pesticide companies want to kill honey bees. Give me a break! Does anyone truly believe that anyone wants to kill honey bees? What pesticide company would want the bad press of being associated with killing bees? The chemists and biologists on their staffs earnestly work to develop insecticides that are bee friendly.
The EPA is being derelict in their duty to protect pollinators. I have spoken at length with EPA staff, and reviewed their risk assessments, as well as those by, DEFRA, EFSA, PMRA, and other regulatory agencies. I find that the risk assessors have not overlooked any evidence, are well-informed on the subject of neonics, and are justified in their assessments that the on-the-ground evidence (to date) indicates that neonic seed treatments pose acceptable risk to pollinators.
We must all remember that the tobacco industry tried to hide the fact that nicotine was addictive [33]. Spare me! Does anyone seriously think that the EPA is unaware that industry executives may stretch the truth? Of course the EPA is skeptical of any reassuring claims by the pesticide industry--that's why they go over all studies with a fine-toothed comb!
This winter's losses spell the end to commercial beekeeping. The fact of the matter is that many observers note that the bee supply for almonds often follows a boom-bust cycle. Although losses were high this year, the trend for the last decade has been for beekeepers keep ramping up the supply of bees for almonds. So long as growers are willing to pay a profitable rental rate for colonies, market forces will encourage the bee industry to meet the demand (for a detailed analysis, see [34]).
The Precautionary Principal
"But," you say, "shouldn't we exercise precaution due to the lab studies that find adverse effects from the neonics?" Look, I make my living as a beekeeper, I'm not out to sell insecticides, and am as concerned as the next person about the environment and the safety of the food I eat. I've researched the neonics exhaustively, and addressed them in several articles [35]. I am acutely aware that there are suggestions that the neonics may be causing insidious effects in the environment, and I've studied the excellent environmental document Late Lessons from Early Warnings [36], which hammers the message that we should use the "precautionary principle" when dealing with chemicals. The problem is, there is nothing without risk--for example, you have a 1 in 83 chance of being killed in an auto accident in your lifetime. But most people still take the risk of getting into cars, since they feel that the benefit outweighs the clearly high risk!
My practical perspective as both a scientist and a beekeeper: if researchers perform lab studies on any insecticide, they will find that there are all kinds of negative effects upon bees--this should be pretty obvious, since insecticides are specifically designed to harm insects! However, the majority of these studies are taken out of the context of full colonies under field conditions, where bees fly free and choose the flowers upon which they forage. The evidence to date supports the contention that the neonics, properly used as seed treatments, are indeed an improvement over other insecticide options.
As Dr. Eric Mussen succinctly notes:
Nobody's really been able to show that [the neonicotinoids] are more problematic than the rest [of the pesticides to which bees are exposed] [37].
Far be it from me to suggest that the neonics (or any other pesticides) are harmless! But consider this--if the neonic seed treatments were indeed as harmful as some make them out to be, you'd think that after a decade of intense study that at least one researcher could have come up with a single solid piece of field evidence against them!
Let's do a thought experiment. Why doesn't someone simply put a bunch of healthy hives into the middle of seed treated crops and see whether they die afterward? Oh, I forgot--this experiment has already been run by thousands of beekeepers year after year in the Corn Belt and the Canadian prairie! And those beekeepers have invited me to look at their colonies, sent me photos of colonies stacked head high with honey supers, and bragged about their high winter survival!
Some will argue 'til they're blue in the face, but the fact remains that virtually every beekeeper that I've spoken with in the Corn Belt and in canola areas feels that the seed treatments are not a problem [38]. In fact, most tell me that this is the best it's ever been as far as bees and pesticides!
Common sense: I just don't get what is so hard to understand about the reality that there are thousands of colonies thriving year after year in areas of intense seed treatment? To any reasonable person it would suggest that the treatments are causing little noticeable harm other than the occasional planting dust kill, which I have repeatedly stated is a problem that needs to be corrected!
See For Yourself
Let's look at actual independent (from the manufacturer) data from corn and canola areas:
Corn
I asked friends in the Corn Belt if they had any data on winter losses. It so happens that the Michiana Beekeepers Association has been collecting exactly that since the spring of 2010 (Fig. 11).
Figure 11. Percentage of winter losses by the "Michiana" hobby beekeepers. The 2013 figure is as of mid March; it may eventually go down a bit due to a prolonged cold spring. Note that the winter survival rate appears to be linked to average winter temperature. Thanks to beekeeper Danny Slabaugh for sharing the data; temp deviations from [[i]].
[i] http://www.ncdc.noaa.gov/temp-and-precip/maps
How could the above be? Eighty percent winter survival despite sitting in the middle of seed-treated corn and soy? So of course I did a fact check to confirm that those beekeepers were indeed sitting in corn/soy areas (Fig. 12).
Figure 12. USDA land cover categories for the region in which the Michiana hobby beekeepers keep bees--corn and soy acreage is color coded yellow and green, respectively. The selected area is the top half of Indiana and bottom of Michigan, with Lake Michigan at the left. Clearly, these apiaries were exposed to seed-treated corn and soy! I created the map at [[i]].
[i] http://nassgeodata.gmu.edu/CropScape/
The above figures suggest that colony winter survival for stationary hobby beekeepers in the above corn/soy region is higher than the national average, despite the fact that about half of them don't even treat for mites! They also suggest that the neonics or other pesticides used in corn/soy in that region do not cause excessive winter loss. Finally, the data indicate that a main factor for winter loss rates is the winter temperature.
Canola
I've heard some beekeepers saying that their bees crashed after working canola, suspecting that the seed treatments were the problem. So as a reality check I called a Dakota beekeeper who has been running bees to canola for over a decade--some 10,000 hives last season. He tells me that colony strength after canola varies from year to year, but that he sees no problem with the seed treatments. He did point out that beekeepers should be aware that colonies can plug the broodnest on intense canola flows.
The biology: The plugging out of the broodnest during an intense bloom means that three weeks afterward, there will be few emerging workers to take the place of the worn-out foragers, and the colony population will temporarily plummet. Even worse, the remaining mites are then concentrated onto fewer bees--which can initiate virus epidemics. These colonies must then attempt to rebuild from scratch, starting in August, meaning that the weakened, mite-infested colonies faced three long months of drought last summer for that rebuilding process.
Every field study that I've seen for canola also supports the conclusion that the seed-treatments are safe for bees. I joined other beekeepers and regulators in observing a large-scale study of seed-treated canola in Canada [41]. Canola (or rapeseed) is likely the best test crop, since bees eagerly (and virtually exclusively) forage upon it for both pollen and nectar, meaning that every bit of their food supply contains contain easily verifiable residues of the insecticides. The preliminary results indicate that the clothianidin seed treatment did not harm the colonies [42].
Another recent independent long-term field study in Poland [43] came to the same conclusion. In it, the researchers followed 50 colonies for more than two years under field conditions as they foraged on five different large fields of oilseed rape treated with various combinations of five different neonicotinoids applied by seed treatment and spraying. Pollen and nectar samples were taken, and demonstrated that the bees were clearly exposed to normal residues of the insecticides (there was also additional exposure to other common agricultural pesticides). The colonies were monitored for health, brood, strength, nosema, viruses, and winter survival, and compared to two control apiaries set in an area free of the crop. The results?
During the time from the placing of the colonies on the rape fields until wintering, the colonies developed properly in all groups... All colonies overwintered properly... In both years, during the period of being placed in the oilseed rape fields as well as after being moved to the stationary apiary, none of the groups showed disturbances in development or functioning.
Following a paper that suggested that the seed treatments would impair bumblebee colonies' ability to rear queens, DEFRA performed a common-sense field study last year [44]. Their findings:
...the study has shown that bumble bee colonies remained viable and productive in the presence of the neonicotinoid pesticides under these field conditions...The study underlines the importance of taking care in extrapolating laboratory toxicology studies to the field, as well as the great need of further studies under natural conditions.
Sunflowers
Some beekeepers report that their colonies later crashed after they chased sunflowers last summer for honey. One must keep in mind that sunflowers are not a natural food for honey bees, and provide only poor-quality, nutritionally-inadequate pollen [45]. But the main problem with putting bees on sunflowers may be related to the fact that sunflowers are a native plant--meaning that there are a number of native insects that evolved to feed upon it:
Maximum seed yields often require the use of insecticides to protect the crop from insect competitors. Unfortunately, many of the major insect pests of sunflower attack the crop when it is flowering. Thus, insecticides used to control the pest also harm pollinating bees [46].
If sunflowers are the only forage available, colonies may eventually go downhill, due to the one-two punch of poor pollen nutrition coupled with insecticide exposure. And which pesticides would those be? One scary list- Asana XL, Baythroid, endosulfan, Furadan , Lorsban , methyl or ethyl parathion, , Proaxis, Scout X-TRA, Sevin, Warrior, Mustang Max, Declare, Cobalt, Yuma, Delta Gold, and Grizzly Z [47]!
Note that none of the above are neonics, other than seed treatments for wireworms. Surprisingly, field evidence indicates that the seed treatments only "stun" the wireworms for a while [48], which certainly raises the question as to how harmful they might be to bees months later when the plants flower! I will return to sunflowers below.
Be Careful What You Ask For!
Allow me to assure you that I am no pitchman for neonics or any other insecticide--the typical farmer practices far too little integrated pest management, and applies far too many pesticides! All insecticides (and several fungicides and adjuvants) cause problems to pollinators--the neonics are no exception. Any systemic insecticide has the potential to harm bees when applied as foliar applications, by chemigation, or to flowering trees, but it there is no compelling evidence that the neonics are any worse than the alternatives in most applications. On the contrary, there is quite a bit of evidence that they may often be "safer" ("reduced risk").
If the neonic seed treatments were banned, it's not as though all agriculture is suddenly going to go pesticide free--only about 1% of U.S. cropland is registered as "organic"! We must consider the likely alternatives. The products that farmers would then use to control insects would need to be sprayed all over the cropland--we'd then be back to the problem that the bulk of sprayed insecticides go into the environment without ever hitting the intended pest!
I hear from knowledgeable beekeepers that worse than in previous years, some of the new formulations of the spray-applied insecticides [49, 50, 51] can really knock the snot out of bees! One large beekeeper found his hives already dead before moving them away from the fields. Again, this was not a neonicotinoid issue.
Practical application: no one is saying that the neonics are "harmless." The question is whether they are better or worse than the alternatives.
The Effect Of Drought
Let's discuss some of the problems (or suspected problems) with the neonics last season. The record warm and dry spring appeared to exacerbate corn planting dust issues (corn seeds are the worst offender due to their non spherical shape). Beekeepers in some areas of the Corn Belt, the East Coast, and in Ontario suffered from confirmed (in at least some of the cases) planting dust kills (although many went on to make good honey crops after their colonies recovered). The final analysis from Ontario is not yet completed, but dry soil conditions and an early clover bloom likely contributed to the problem. Regulators and the seed companies are working on solutions to the problem [52]. Still, IMHO it is unacceptable to ask beekeepers to bear the burden of bee kills without compensation, and no one could blame the affected beekeepers for being pissed!
Drought-stressed plants
There are a number of advantages to the neonic seed treatments. Besides their safety to the farmer and to most wildlife, there is virtually no way for the farmer to misapply them! The timing of application is only at planting time (when bees normally have little interest in the bare fields), and the dose is determined by the seed-treating company. This means that the applicator can't be tempted to apply at the wrong time, or to over apply too strong a dose (however, their excessive near universal use can be expected to accelerate the development of resistant pests).
That said, beekeeper Bret Adee brought an interesting question to my attention: the dose of seed-applied systemic insecticides (whether neonic or other) is based upon the dilution factor as the plant grows, so that the residues in nectar and pollen will be reduced to below the "no observed adverse effects level." But what happens during drought, when the water-stressed plants only grow knee high before desperately flowering? There would be far less plant biomass in which to dilute the insecticide (assuming that drought-stressed plants absorb the same amount from the seed treatment).
Certain plants (including sunflowers and canola) are known to "hyperaccumulate" toxic metals [53], perhaps more so during drought. Could this also be the case with systemic insecticides? Something that's been stuck in the back of my mind is that Bonmantin [54] found that the concentration of imidacloprid first drops in sunflower plant tissue as it grows, and then reconcentrates in the flower heads.
It occurs to me that the translocation of systemic insecticides is generally studied in plants grown under "normal" conditions. I'd very much like to see data for residues in pollen and nectar from seed-treated plants grown under drought. Had we thought of this earlier, we could have collected pollen and nectar samples from drought-stressed plants last summer. I'm currently trying to track down any data or samples from such plants--if any reader has any such sample analyses, please let me know!
Practical application: the above hypothesis is speculative, but we need actual data from drought-stressed plants to see whether such an effect occurs. If so, it would need to be taken into consideration for the registration of seed treatment products!
Once planting was completed and the drought took its toll, the reports that I've heard are that soybean honey saved a lot of bee operations this season, right in the middle of treated corn/soy farmland. In this case, seed treatment with neonicotinoids may have been a blessing to beekeepers:
The benefits of [seed treatment] not only include the early-season disease control but also suppression of soybean aphids for quite a ways into the growing season. With it, we typically make only one foliar insecticide application for aphid control, usually in August, instead of two applications when [treatment] isn't used. In 2012, with the extremely dry conditions in mid-season, there wasn't as much of an aphid problem, and we treated just 300 acres of soybeans...Last year we sprayed closer to 30,000 acres for aphids [55].
On the other hand, some beekeepers on alfalfa or cotton got hit hard by other classes of insecticides. A hit from a pesticide application can lead to poor subsequent colony performance, queen failure, dwindling, or winter collapse. ABJ published an excellent series of articles on pesticides by Drs. Barbara and Eric Erickson in 1983; Editor Joe Graham has graciously granted me permission to post copies of those articles to my website [56]--I strongly suggest any beekeepers interested in pesticide issues read them! In the second article, the authors discuss both the problems with systemic insecticides and of sublethal effects--note that these articles were written long before the introduction of the neonics!
An anti-pesticide group, along with a handful of beekeepers, recently filed suit against the EPA [57], calling for an immediate ban on the two most common neonicotinoid seed treatments, despite the easily-verifiable fact that hundreds of thousands of colonies thrive in the midst of seed-treated corn, soy, and canola! To me, this suit smacks of being some sort of well-orchestrated publicity stunt, and does not serve the interests of either beekeepers or environmentalism. Worse, it now gives the powerful farm lobby cause to label beekeepers as "radical" enemies.
We don't want this battle: do we really want to take on the farm lobby by backing them into a corner? The French beekeepers took a similar case against fipronil all the way to their supreme court and lost [58, 59]-worth reading]. Agriculture is already positioning itself for a fight [60, 61, 62]. Think about it--the EPA lives in fear of a conservative congress slashing their funding. Does anyone really think that they are going to go against the agricultural lobby without unimpeachable evidence? We should also think twice before calling for a ban on the seed treatments--the alternatives are not pretty!
It disturbs me to hear industry executives and lawyers stretching the truth or misrepresenting data. It disturbs me even more to hear my fellow environmentalists and beekeepers doing so! If we wish to maintain credibility, we should hold ourselves to a higher standard. The question we must ask ourselves the way in which we wish to have pesticide regulation decisions made:
1. By the EPA (the Environmental Protection Agency), whose risk assessors carefully study and weigh all available research and evidence in order to make objective and rational decisions, or
2. To have it decided instead by impassioned, fearful, and often misinformed advocacy groups who hire lawyers and pressure politicians who know little about the subject?
We depend upon the EPA to strike a balance between the availability of cheap food and profitability for those who provide it, versus the risks to human and environmental health and safety. It is good to have activists on both sides of the issues (industry and the anti-pesticide groups) to keep the EPA informed. But I don't feel that either of those groups should be telling the EPA which pesticides to register or to ban! Let the regulators do their job!
Rather than wasting EPA's funding to fight frivolous lawsuits, there are more productive actions that we can take:
Help the EPA to do its job by filing "adverse effects incident reports" if you observe a problem due to pesticides [63]. EPA is begging beekeepers to do this! Unless they have documented reports of pesticide problems, their hands are tied as to restricting the uses of those pesticides!
Support the National Pollinator Defense Fund [64]. Our industry is currently represented by a reasoned and knowledgeable group of (mostly) beekeepers. (Challenge to the pesticide companies: why don't you stand behind the safety of your products and donate? The NPDF is about ensuring that your pesticides are properly applied, so there would be no conflict of interest).
If your local state lead agency is not actively investigating bee kills or enforcing pesticide regulations, then use the local media to embarrass them into action!
Keep pressure on the EPA to resolve corn planting dust problems. Here's a wild idea: I'm not sure of the exact figures, but let's say that 90% of the 95 million acres of corn is grown from neonic-treated seed. If the states were to levy a surcharge of 50 cents per acre (neonic seed treatment adds about $12 per acre to seed costs), they could collect over $42 million each year to fund a pool from which to indemnify the occasional beekeeper who suffers a confirmed kill from planting dust!
Tell Congress that we'd like to see wording added to the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) to specifically protect pollinators. Currently, such protection is nebulous (although the EPA is acutely aware of pollinator issues): "The Administrator shall register a pesticide if... when used in accordance with widespread and commonly recognized practice it will not generally cause unreasonable adverse effects on the environment." Unless there is specific wording to protect pollinators, bee kills may not be considered to be "unreasonable"!
We need far more independent field studies to determine which pesticides and application practices are actually causing harm to pollinators. For pesticides in question, keep pressure on the EPA to require additional field trials to demonstrate whether they are indeed safe for pollinators under field conditions. I'd like to see the establishment of monitoring apiaries (and patches of untilled land) in representative agricultural areas nationwide, with the hives in each apiary to be carefully managed by independent parties. Such apiaries and sites could then be closely monitored each summer to see whether honey bees and other pollinators are able to survive local pesticide practices.
Give farmers workable options! Disseminate and promote bee-friendly agricultural practices that don't hurt the farmers' bottom line. For example, by adopting IPM practices, Arizona cotton growers reduced insecticide spraying from 12.5 times a season to only 1.3 times (cutting insecticide use twentyfold), while using more environmentally-friendly insecticides [65]! Another recent study in Iowa found that adding additional clover or alfalfa rotations in corn/soy farmland was equally profitable, improved the soil, used less energy, used far less pesticides, and decreased water pollution [66].
Business and agriculture respond to consumer demand. Consumer demand stopped most dairymen from injecting their cows with the hormone BST. Consumers could do the same by demanding pasture-fed beef and dairy (which would create more pollinator forage)! I'd also like to see the expansion of consumer choices (other than organic certification) that reward farmers who manage their lands to the benefit of wildlife and pollinators. For ideas, see [67. 68. 69].
Bottom Line
In conclusion, it appears that a perfect storm of a preceding exceptionally warm winter, followed by serious drought across the country, the lack of good mite control, a high prevalence of pathogens, and an unexpected California chill in the orchards prior to bloom, resulted in an unusual degree of colony losses. In other words, rather than one specific cause, there were simply not enough of the good things, and too many of the bad things.
I don't see evidence that pesticides were the major factor in the shortage of bees in almonds this winter, although, as usual, a number of individual beekeepers on certain crops certainly took serious hits.
And how about the fear that there won't be enough bees for almond pollination next year? Beekeepers have already told almond growers to expect higher pollination prices next year (especially since California is again going into serious drought, and beekeepers will be forced to invest extra money in feeding their hives). Most every beekeeper I know is madly making increase right now in anticipation of higher pollination prices next season. The fact of the matter is that should conditions allow beekeepers to successfully rebuild their numbers (following the typical swings of our boom/bust cycle), there could possibly even be a glut of bees for almonds next winter!
Feedback And Corrections
A few countries placed temporary suspensions on certain seed treatments until planting dust issues were resolved [27]--only Germany has one suspension still in place. - Actually there are some more: France (Thiamethoxam in oilseed rape, Imidacloprid in corn and sunflower), Italy (all Neonic seed treatment in corn), and Slovenia (Imidacloprid, Thiamethoxam, and Clothianidin seed treatment in all crops)
French beekeepers also started seeing problems with the introduction of the neonics; I've spoken with beekeepers in France whose apiaries are in pesticide-free areas. They tell me that they experience the same sorts of colony mortality problems as do those in areas exposed to neonics - This is, by the way, likewise confirmed by monitoring results from the French authorities.
In the case of foliar, drench, or chemigation applications prior to bloom, there are greater possibilities for bees to be exposed to toxic levels. - This is not the case for foliar application: as Neonics are xylem-systemic, but hardly mobile in the phloem, they can only be distributed in a plant after root uptake, but not be translocated for instance from a leaf to a later developed flower.
Then, on the topic of systemic residues in plants under drought stress: first, I am quite sure that the decrease of concentration in seed-treated plants over time is not only due to dilution, but also to degradation of the compounds - a factor that is not specifically dependent on water availability for the plants (e.g. photodegradation!); second, even if there would be less dilution in plants under drought stress: the concentrations in nectar and pollen of treated crops are normally so low (when we consider average rather than peak concentrations, and when we consider scenarios where colonies have chronically access exclusively to contaminated nectar/pollen over months unlikely in practice), that even an increased concentration due to drought stress-affected plants should not make a significant difference: if we for instance assume an average concentration of let's say 3-4, or even 5 ppb Clothianidin in corn pollen, and likewise assume a dilution reduced to 50% (which is probably exaggerated), then we would still not end up with excessive residues. And finally, we have residue figures from crops grown in different countries, different climatic conditions, and different agronomic practices; though we have not specifically addressed the drought stress scenario, we have seen that residue figures are quite consistent over all scenarios, and there does not appear to be strong evidence that different environmental conditions would substantially (i.e. by orders of magnitude) and systematically alter residue concentrations.
Dr. Christian Maus
Global Pollinator Safety Manager
Bayer CropScience
/
A ppt on the impact of CRP lands on wildlife in North Dakota
http://www.redriverbasincommission.org/Conference/Proceedings/26th_Proceedings/Kading_RRBC_09.pdf
/
Feedback from a Midwestern apiary inspector:
Just a quick update: This beekeeper who recently told his local newspaper that pesticides were killing his bees, he was making excuses. We examined two of his yards with him yesterday. One yard was showing EFB throughout the whole yard. I think his "mid-summer losses" last year (half of that yard's hives) were EFB kicking in with the mid-summer dearth. In his other yard, most of his dead outs were obvious starve outs. He harvested all of their stores with the first frost, and then didn't feed them. So, in my opinion, and from my observations, pesticides are usually being used responsibly, and aren't killing honey bees. I also think, with the aggressive way bees were on soy fields last summer, the systemic pesticides are not harmful to honeybees. I'm not seeing honey bee problems other than EFB getting the upper hand, due to our cold, late spring. My two cents. Thanks.
References
[1] http://www.frequency.com/video/dan-rather-reports-buzzkill/87705620/-/YouTube
[2] http://www.ars.usda.gov/is/pr/2012/120531.htm and California DPR.
[3] http://www.ncdc.noaa.gov/temp-and-precip/maps.php
[4] Wright, CK & MC Wimberly (2013) Recent land use change in the Western Corn Belt threatens grasslands and wetlands. https://www.motherjones.com/files/pnas201215404_nwow5w1.pdf
[5] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
[6] https://scientificbeekeeping.com/sick-bees-part-2-a-model-of-colony-collapse/
[7] vanEngelsdorp, D, et al (2013) Idiopathic brood disease syndrome and queen events as precursors of colony mortality in migratory beekeeping operations in the eastern United States. Preventive Veterinary Medicine 108(2-3): 225-233. http://www.sciencedirect.com/science/article/pii/S0167587712002656
[8] https://scientificbeekeeping.com/sick-bees-part-18a-colony-collapse-revisited/
[9] http://almondinsights.com/692, http://agfax.com/almonds/2013/reports/03042013-almonds-web.htm
[10] https://scientificbeekeeping.com/sick-bees-part-18a-colony-collaspse-revisited/
[11] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2010-2011-Limited_Survey_Report.pdf
[12] http://www.youtube.com/watch?v=y6B5qm2ut18, http://www.youtube.com/watch?v=PYbLbhZXizY
[13] (Broken Link!) http://www.nccrops.com/2012/07/27/insecticide-recommendations-for-corn-earworm-in-soybeans/
[14] http://www.agriview.com/news/crop/corn-soil-insecticide-use-up-dramatically-to-combat-widespread-rootworm/article_5d09decc-5b40-11e2-b485-001a4bcf887a.html
[15] http://www.amvac-chemical.com/products/documents/Counter20G%20Tech-Sell%20Sheet%20-%202013.pdf
[16] http://pmep.cce.cornell.edu/profiles/insect-mite/propetamphos-zetacyperm/terbufos/insect-prof-terbufos.html
[17] http://www.lewishybrids.com/PDF/3-5-2013Agronomic+ALERT+-+Interaction+between+herbicides+insecticides+corn.pdf
[18] http://pest.ca.uky.edu/EXT/Recs/ENT16-Field%20corn.pdf
[19] (Broken Link!) http://www.soybeans.umn.edu/crop/insects/spider_mites.htm
[20] http://www.nytimes.com/2013/04/07/opinion/sunday/calamity-for-our-most-beneficent-insect.html?nl=todaysheadlines&emc=edit_th_20130407&_r=0
[21] http://www.nytimes.com/2013/04/07/opinion/sunday/calamity-for-our-most-beneficent-insect.html?_r=0
[22] http://www.panna.org/press-release/beekeepers-and-public-interest-groups-sue-epa-over-bee-toxic-pesticides
[23] http://www.cdpr.ca.gov/docs/pur/pur10rep/top_100_ais_lbs10.pdf
[24] http://www.extension.org/pages/60318/pesticides-and-their-involvement-in-colony-collapse-disorder
[25] Mussen, EC (2006) Chaotic almond pollination. http://entomology.ucdavis.edu/faculty/mussen/JanFeb2006.pdf
[26] https://scientificbeekeeping.com/sick-bees-part-18e-colony-collapse-revisited-genetically-modified-plants/
[27] http://www.epa.gov/pesticides/about/intheworks/ccd-european-ban.html
[28] http://www.thecre.com/oira_pd/wp-content/uploads/2013/04/DQA-Alert-EU-Commission-Ban-on-Neonicotinoids-4-10.pdf
[29] https://scientificbeekeeping.com/home/news-and-blogs/
[30] Henderson, CB, JJ Bromenshenk, DL Fischer (2013) Clothianidin exposure levels from bee-collected pollen and nectar in seed-treated corn and canola plantings. Proceedings of the American Bee Research Conference.
[31] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
[32] http://www.ontariograinfarmer.ca/MAGAZINE.aspx?aid=534
[33] http://www.pbs.org/wgbh/pages/frontline/shows/settlement/timelines/april94.html
[34] https://scientificbeekeeping.com/2012-almond-pollination-update/
[35] https://scientificbeekeeping.com/neonicotinoids-trying-to-make-sense-of-the-science/, https://scientificbeekeeping.com/neonicotinoids-trying-to-make-sense-of-the-science-part-2/, https://scientificbeekeeping.com/testing-of-bee-feed-syrups-for-neonicotinoid-residues/
[36] http://www.eea.europa.eu/publications/late-lessons-2
[37] http://www.sciencefriday.com/playlist/#play/segment/9088
[38] https://scientificbeekeeping.com/the-extinction-of-the-honey-bee/
[39] http://www.ncdc.noaa.gov/temp-and-precip/maps
[40] http://nassgeodata.gmu.edu/CropScape/
[41] https://scientificbeekeeping.com/a-new-large-scale-trial-of-clothianidin/
[42] http://www.producer.com/daily/ontario-field-study-finds-no-link-between-seed-treatments-bee-deaths/
[43] Pohorecka, K, et al (2013) Residues of neonicotinoid insecticides in bee collected plant materials from oilseed rape crops and their effect on bee colonies. Journal of Apicultural Science 56(2): 115-134. http://www.degruyter.com/view/j/jas.2012.56.issue-2/v10289-012-0029-3/v10289-012-0029-3.xml?format=INT
[44] http://www.fera.defra.gov.uk/scienceResearch/scienceCapabilities/chemicalsEnvironment/documents/reportPS2371Mar13.pdf
[45] http://repository.up.ac.za/bitstream/handle/2263/20334/Nicolson_Chemical(2012).pdf?sequence=1
[46] (Broken Link!) http://www.ag.ndsu.nodak.edu/aginfo/entomology/entupdates/Sunflower/a1331sunflowerhandbook.pdf
[47] http://www.sunflowernsa.com/growers/approved-chemicals/insecticides-test/
[48] http://www.mydigitalpublication.com/publication/?i=151958&p=41
[49] http://www.sunflowernsa.com/growers/approved-chemicals/insecticides-test/
[50] http://www.farmassist.com/agriedge/images/Resource_PDFs/Soybean/Warrior_Zeon.pdf
[51] http://www2.dupont.com/Production_Agriculture/en_US/assets/downloads/pdfs/K-09315.pdf
[52] http://www.ontariograinfarmer.ca/MAGAZINE.aspx?aid=534
[53] http://en.wikipedia.org/wiki/List_of_hyperaccumulators
[54] Bonmatin, JM, et al (2005) Behaviour of Imidacloprid in Fields. Toxicity for Honey Bees. In Environmental chemistry: green chemistry and pollutants in ecosystems pp. 483-49. http://www.buzzaboutbees.net/support-files/bonmatin2005behaviour-of-imidacloprid-in-fields.pdf
[55] http://cornandsoybeandigest.com/seed/do-soy-seed-treatments-pay?page=2
[56] https://scientificbeekeeping.com/historical-pesticide-overview/
[57] http://www.centerforfoodsafety.org/press-releases/1911/cfs-beekeepers-and-public-interest-groups-sue-epa-over-bee-toxic-pesticides
[58] http://www.theworldlawgroup.com/files/file/docs/Soulier_health_environment_June_2012.pdf
[59] http://www.soulier-avocats.com/upload/documents/Soulier_health_environment_september_2010_F.pdf
[60] http://westernfarmpress.com/government/pesticide-battle-over-honey-bee-health-under-way?page=1
[61] http://westernfarmpress.com/management/total-ag-pesticide-elimination-sought-radicals
[62] http://www.neonicreport.com/home/project-compass/
[63] https://scientificbeekeeping.com/pesticide-incident-reporting/
[64] http://pollinatordefense.org/site/
[65] http://cals.arizona.edu/apmc/docs/IPM_Delivers.pdf
[66] Davis, AS, et al (2012) Increasing cropping system diversity balances productivity, profitability and environmental health. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0047149
[67] http://www.pcl.org/pcl_files/5_Wildlife_Habitat_Farmland.pdf
[68] http://pfspbees.org/
[69] http://www.nwf.org/CertifiedWildlifeHabitat/UserAccount/SignIn
Category: Practical Beekeeping Management, Topics
Tags: beekeeper management, biotic, diseases, drought, environmental, factors, pesticides, randy oliver, varroa | randy oliver Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/randy-oliver/ |
What Happened To The Bees This Spring? (Part 1 & 2)
First published in: American Bee Journal, June 2013
Part 1: Environmental and Biotic Factors
Setting the Stage
The Lead Up
The Drought
Lack of Good Forage
Varroa
Diseases
Other Indicators of Impending Collapse
An Unexpected Chill
Feedback from Brokers
The Silent Majority
Beekeeper Management
Part 2: The Contribution From Pesticides
The Lynch Mob
Debunking The Myths
The Precautionary Principal
See For Yourself
Be Careful What You Ask For!
The Effect Of Drought
Actions To Take
Bottom Line
References
What Happened To The Bees This Spring?
Part 1: Environmental And Biotic Factors
Randy Oliver
ScientificBeekeeping.com
First published in ABJ June 2013
By now, most everyone has heard that honey bee colonies died in massive numbers this winter. Reporter Dan Rather, in his newscast Buzzkill [1], showed unfortunate beekeepers, some of whom had lost half or more of their colonies, predicting gloom and doom for the bee industry. What were the causes of this year's bee shortage? As Rather says, "Everyone has an opinion." The question is whether those opinions are based upon fact! So let's go over the events leading up to the bee supply debacle.
Setting The Stage
Nearly 800,000 acres of almond trees in California came into bloom this winter--the trees typically start flowering about Valentine's Day, and the bloom lasts for only about two weeks. Almonds require cross fertilization between adjacent rows of varieties (Fig. 1), and honey bees are trucked in from all over the country to do the job (roughly a million and a half colonies). Many large commercial beekeepers move their hives into California in November to overwinter in holding yards; others build them up on winter pollen flows in Florida or Texas, or hold them in temperature-controlled potato cellars until shortly before bloom. The hives are generally placed into the orchards about a week before the first flowers appear. There is virtually no forage in the orchards prior to, or after bloom in many areas.
Figure 1. An almond orchard in late February, showing the flowering of rows of different cultivars required for cross pollination. The bare "late" varieties have not yet bloomed; the green "early" pollenizers have finished bloom. Grading of colonies is normally done during the bloom of the main crop (usually Nonpareil).
The Lead Up
Two seasons ago there was also a shortage of bees in almonds, following the coldest January (2011) in 17 years (cold being a major stressor of wintering bee colonies). Beekeepers then replaced their deadouts with package bees and splits, thus starting a new generation of colonies, which tend to have lower varroa mite levels than established colonies. These colonies entered autumn 2011 in pretty good shape, and then enjoyed the fourth warmest January (2012) on record! As a result, there was the lowest rate of winter mortality in years, and plenty of bees for almonds in 2012 (Fig. 2).
Figure 2. Percent winter losses since the beginning of the national survey--the data is not yet in for 2012/13. Note that there has been a general downward trend, suggesting that whatever caused the high losses in 2007/8 has not been such a problem in recent years. Note also the cyclical nature of colony winter losses, with high losses in 2004/5, 2007/8, 2009/10, and 2012/13 (some data not shown) Data from [[i]].
[i] http://www.ars.usda.gov/is/pr/2012/120531.htm and California DPR.
I was curious as to whether the colony loss rate was linked to the use of neonicotinoid insecticides. There is no recent USDA data, so I went through the California Pesticide Use Reports (data available through 2010). I plotted the amount of imidacloprid applied to crops in California in the preceding year in red (the seed treatment clothianidin didn't even make the top 100 list of pesticides applied). Although there appears to be a possible correlation from 2006 through 2009, the trends were reversed for 2010. I will be curious to add the 2011 data when it becomes available.
In March of 2012 I received a phone call from a California queen producer who had a prescient insight as to a potential brewing disaster. He was receiving calls for queen bees from Northern beekeepers whose bees had already grown to swarming condition due to the unseasonably warm spring weather (Fig. 3).
Figure 3. Last year's warm spring in much of the country lead to early broodrearing, and as a result, early buildup of varroa levels. Note the record warm spring in the Midwest.
The queen producer noted that such early brood rearing also meant early mite buildup, and predicted that since most Midwestern beekeepers treat for mites by the calendar, that they would unknowingly allow mites to build to excessive levels before treatment. This was strike one against the bees.
The Drought
Then it didn't rain-by midsummer, it was clear that the continental U.S. was in serious drought, including California, whose beekeepers supply nearly half the bees for almond pollination. The only ways that we kept our colonies strong was to either feed expensive pollen supplement and sugar syrup, or to move them to elusive better pasture out of state. By late summer, 60% of the U.S. was in drought, meaning that unless your bees were next to soybeans or irrigated crops, there was little forage for them. This lack of good nutrition was strike two against the bees (Fig. 4).
Figure 4. The severe drought in the Midwest really put the hurt to bee pasture in those states in which the majority of commercial hives spend the summer. Source [[i]].
[i] http://www.ncdc.noaa.gov/temp-and-precip/maps.php
Drought not only dries up nectar and pollen sources, but also forces bees to fly further and more frequently for water. Plus it concentrates ag chemicals and pesticides in the few sources of surface water available to bees. The bees started to show the hurt.
Beekeepers tried to move their hives to areas of better forage, sometimes overstocking an area with too many hives, which led to excessive competition for resources, and the spreading of parasites. Others desperately chased less desirable crops such as sunflowers. Colonies in holding yards in California found little to eat, due to our record dry weather. Some beekeepers with winter eucalyptus locations found them crowded with other hives.
Lack Of Good Forage
In Buzzkill, Bret Adee brought up the fact that bee pasture in the Midwest is disappearing under the plow, largely due to our environmentally-irresponsible taxpayer-subsidized policies that encourage farmers to plant every square foot of land into corn (Fig. 5). Bee brokers told me that colonies coming to almonds from the Midwest were in generally poorer shape this year than those coming from the southern states.
Practical application: some Midwestern beekeepers split their operations, hauling some to the South to rebuild over winter, and the rest directly to California-there was a night and day difference as to how the colonies looked in February!
Figure 5. Grasslands and wetlands in the Corn Belt are rapidly being converted to monocultural, heavily herbicided corn/soy, which eliminates virtually all bee and wildlife forage. A new study found that between 2006 and 2011 there was a net loss of 1.3 million acres of grassland. This affects not only bees--the authors [[i]] state that "As a consequence, populations of grassland nesting birds are declining faster than any other group of birds in North America."
[i] Wright, CK & MC Wimberly (2013) Recent land use change in the Western Corn Belt threatens grasslands and wetlands. https://www.motherjones.com/files/pnas201215404_nwow5w1.pdf
To put this loss of bee pasture into perspective, I asked some Dakota beekeepers for estimates of how many acres of CRP grassland are needed to sustain a colony of bees. In recent years, the overall hive density in North Dakota has been more than 10 hives per square mile (less than 64 acres per hive, including wastelands).
Practical application: the best guess by those beekeepers was that each colony of bees requires about 5-15 acres of productive land for forage (late summer forage being the critical factor). If we use the figure of 10 acres per colony, then the conversion of 1.3 million acres of grassland to herbicided cropland suggests that forage for 130,000 colonies of bees has been eliminated in the past five years in the Corn Belt alone! This figure represents nearly 9% of all colonies needed for almond pollination.
Varroa
An excellent window into the causes of colony health problems is the USDA National Honey Bee Pests and Diseases Survey Report [5] (the latest data have not yet been released). It is worrisome that varroa levels appear to be steadily climbing year after year.
And if the drought and forage problems weren't enough, the favored miticide of commercial beekeepers became unavailable for a time last summer, and mite levels built to killing levels in a number of operations. By late July, some of us were already predicting a disaster for the upcoming almond pollination season. Although many beekeepers finally got mite levels down with late-season treatments, the damage had already been done, and there was no turning the colonies around. Strike three for the bees!
In November semi loads of hives started moving into California, or had been placed in potato cellars. Some of the colonies that arrived from the Midwest were in poor shape, or crawling with mites. Oddly, few beekeepers at the time owned up to having problems, despite the reports that I kept hearing of mite and forage issues! I'm not sure whether this was due to denial, wishful thinking, simple lack of lifting the lids, or something else.
Diseases
Nosema infection also runs rampant across the country--70% of colonies were infected in June of last year. The stressful factors leading up to almond bloom apparently put a lot of hives close to the "tip point" at which pathogens can overwhelm the colony immune system and start it going backwards, or initiate the slide into sudden depopulation (detailed at [6]). Few seem to be mentioning signs of CCD-it is unfortunate that the media keep using that term as a catch-all for all hive problems!
One should keep in mind that the winter collapse issue appears to be cyclical, similar to flu or other pathogen epidemics. I have strong reason to suspect that the constantly-evolving viruses are involved in these colony collapse epidemics.
There has also been a strong resurgence of European Foulbrood and other unidentified brood diseases [7] (Figs. 6, 7, and 8). Unlike EFB of old, the new forms don't go away with a nectar flow.
Figure 6. "Shot brood" due to EFB. Note the fat queen near the center. Despite her vigorous egglaying, this colony is unable to pull ahead due to excessive brood mortality. Lots of beekeepers reported EFB symptoms this winter.
Figure 7. You really have to look hard in some colonies with spotty brood to see the cause! Two larvae in this photo show signs of EFB infection.
Figure 8. Dying brood from one of my sick colonies this spring with EFB-like symptoms. Note the "shot" pattern, the twisted larvae, and the dried larval remains. There is also some AFB-like coloration, but lack of roping or AFB odor (this odor is distinct and sour), nor a positive Holst milk test. In this colony, even pupae were dying. I observe these symptoms independent of whether the hives went to almond pollination or not. Colonies with this (or similar) infection cannot grow. Treatment with oxytetracycline generally clears it up.
One thing that I noticed in Buzzkill was the uneaten pollen supplement patties in many of the crashed hives. I've mentioned before [8] that I've found a colony's failure to consume pollen supplement to be a reliable predictor that that colony will later collapse.
Another strong predictor of winter collapse is weak strength in fall (upcoming article), again strongly suggesting that those colonies already have some sort of health issue going into winter. I heard reports from all over the country that bees went into winter in poor condition.
An Unexpected Chill
The final blow to hives in California was a blast of icy weather (Fig. 9). This unexpected chilling compounded all the existing problems! I've previously pointed out that colony collapse often follows unseasonable chills, since it shifts the tip point for virus and nosema epidemics. Clusters that had expanded for broodrearing contracted, resulting in chilled brood and dead young bees on the ground. My own colonies simply shut down broodrearing completely, losing about two weeks of buildup.
Figure 9. Chilling events (blue arrows) in Modesto, California this winter (the dark blue lines represent normal highs and lows). The unusual chilling in late December and early January (hitting the '20's in a number of areas) came at the time when colonies normally begin to build up for almonds. This severe (for California) cold set the already-stressed colonies back hard, and may have allowed nosema and viruses to gain the upper hand. Graph from wunderground.com.
At the national convention in January, the first reports of beekeepers with collapsing operations were heard. But still, the industry was in denial, with an apparent glut of promised bees as late as the end of the month (two weeks before start of bloom)! But when the rubber finally hit the road in mid February, that illusory supply quickly evaporated, with desperate growers and brokers scrambling to obtain bees--some offering obscenely high prices for substandard colonies.
And then, due to the cool spring, the trees held off on blooming for an extra 10-14 days [9]-colonies placed in anticipation of normal start of bloom just sat there starving and shivering on the cold orchard floors.
Practical application: the biology here is that this is the time of the "spring turnover" in bee populations in California, during which the old overwintered adult bees must rear their replacements for the spring buildup of population. The conditions in the almond orchards prior to bloom are miserable for smaller colonies--it is warm enough to encourage them to break winter cluster and expand the broodnest, but overnight frosts on the Valley floor can cause serious chill stress. Furthermore, it is often warm enough to fly at midday, but there is virtually nothing to forage upon until the trees start blooming! Such fruitless foraging further wears out the workers, and allows sick bees to drift to adjacent hives. Worse yet, the desperate foragers rob out any dead or dying colonies in adjacent orchards, rapidly and effectively transmitting mites, nosema, viruses, and anything else harmful in the deadouts.
Many colonies went backwards during this excruciatingly long wait. Some beekeepers told me that hives graded at placement scored better than those graded at bloom (just the opposite of normal)!
I've been carefully observing spring turnover in my "dinks" (weak colonies) in February (Fig. 10). What I find is that the problem is generally not the queen; rather, the colonies are infected with some pathogen- most commonly nosema [10], the paralytic viruses [11], or EFB (or EFB-like brood disease). Those colonies that are able to successfully emerge one solid round of brood are often able to "clear" the infection and completely rebound by April. Those that get hit by frost in February often collapse.
Figure 10. An example of an unsuccessful spring turnover. This colony is in the middle of typical February collapse from nosema or IAPV. You can easily see the outline of the area recently covered with brood, delineated by the crescents of freshly-packed pollen. Colonies undergoing this sort of depopulation tend not to forage for nectar, and do not respond well to supplemental feeding. This colony continued to collapse quickly, and finally died in a cold snap a week later--with only silver-dollar sized patch of dead bees remaining.
Feedback From Brokers
I asked a few of the major pollination brokers for their observations on the colony shortage this season. Their feedback suggested that the causes for the bee shortage were varied and many.
Summary:
Most were able to eventually fill their contracts. Beekeepers often hold colonies in reserve "just in case," or gambling that in "short" years they can rent those last hives at an elevated price. Also, when the offered price went up, hives not originally intended to go to almonds were loaded up at the last minute and shipped to California (I was in Florida at the start of bloom, and had an inspector tell me of certifying colonies for shipment after the bloom had already begun!).
A number of hives received in November were already headed downhill. Some exhibited the symptom of bees not clustering properly (a typical sign preceding sudden colony depopulation/CCD). Some arrived crawling with mites, or with recent mite treatments in place (suggesting that they were treated too late).
Some graders saw piles of dead bees in front of hives--cause unknown. There were reports of some herbicide tank mixes killing bees.
Many of the placed colonies were below standard grade-- growers paid for less than they expected!
Graders told me that there was a huge variation in hive strength from beekeeper to beekeeper. Many hives were strong (12-16 frames of bees) and healthy; other operations graded at zero to three frames of bees (some of the deadouts had spider webs inside, suggesting that they hadn't been occupied by bees for some time).
The unusual winter chill was tough on colonies that had been stimulated into early buildup, and then forced to contract their broodnests. Some colonies kicked out chilled brood and dead bees afterwards.
Many beekeepers watched their colonies go "backward" prior to bloom.
Colonies from the Southern states (especially those delivered in February) were generally in better shape than those from the Midwest.
Midwestern beekeepers blamed drought, mites, poor nutrition.
Several beekeepers said that their best bees came from remote areas, and their worst from ag areas.
A number of beekeepers admitted inadequate mite treatment; mites were a recurrent theme.
There were a number of reports of EFB hitting colonies.
Some had gotten hit last summer with pesticide sprays, and their colonies didn't recover.
"There were good bees and bad bees from every state. They all seemed to have different problems depending on location/state."
Many good beekeepers simply didn't know what happened to their hives; there were lots of lifeless hives delivered. The atmosphere was ripe with speculation as to the actual causes.
"The shortage was also created by beekeepers that chose not to come to California for a variety of reasons. They can make more money with honey, didn't get paid for what they have brought in the past, bees come back home with mites, beetles and whatever else takes a ride on the hives. Beekeepers don't want to risk bee health to chase the dollar." Many out-of-state beekeepers have had bad experiences going to almonds, and simply don't feel that it's worth it. The supply of bees will largely depend upon the price that growers offer for renting them!
The Silent Majority
Buzzkill leaves one with the impression that the entire bee and almond industries are on the verge of collapse. Of course, the news media focus on fear and disaster, so we may consider taking such dire projections with a grain of salt. In the case of Dan Rather, the focus was on the beekeepers with troubles, not upon those who successfully filled their pollination contracts.
So just how severe was the problem? Let's say that there was an overall shortage of 100,000 hives (a figure that I heard floated)--that would represent only about 6% of the total number of hives placed into almond pollination. The other 94% were successfully delivered (although a proportion of those were weak due to the poor season).
Since the debacle, I've heard from plenty of beekeepers whom I'll refer to as the "silent majority," who experienced "normal" colony winter losses in the 5-25% range, and who successfully filled their pollination contracts. Although the hearts of all beekeepers go out to those who suffered severe colony losses, many felt that some of those losses could have been prevented if the afflicted beekeepers had been more proactive than reactive.
And don't forget those upon whom the rest of the industry depends to supply bees for restocking their deadouts! The California package producers, who have been pollinating almonds for decades, are routinely counted on to consistently take strong hives to almonds, and to then shake over a hundred thousand packages of bees for sale afterwards. Few of these major producers experience severe unexplained colony losses.
Beekeeper Management
By no means am I suggesting that those beekeepers who suffered losses engaged in poor beekeeping practices, but I can't help but notice that not all beekeepers were equally affected--a great number provided strong, healthy colonies to almonds. I've spoken to some of them-the common thread is that those who recognized the problems of poor nutrition and mites in August, and took remedial action for the rest of the season, had acceptable winter losses.
Some beekeepers who really put serious effort and money into bee husbandry were even able to sell "shook bees" from their colonies to others in February! For example, watch Keith Jarrett feeding substantial quantities of pollen supplement to very strong colonies in January [12]--Keith consistently brings very strong colonies to almonds every year, and this year was no exception!
Practical application: I'm here to tell you, that one lesson that I've learned during our intense California drought, is that those yards that I fed with protein in late summer before they started going downhill went to almonds much stronger than those that I didn't feed until fall! Proactive is better than reactive--if you wait until colonies are already going downhill, it is much more difficult to turn them around!
I've often been accused of being politically incorrect for speaking frankly. I'd like to make amends at this point by retiring the rude and unsympathetic term "PPB" (Piss Poor Beekeeping). The fact is that the average wintering loss for the past few years has hovered around 30%. So if you experience 30% losses, you can now proudly call yourself an "Average" beekeeper!
But what about those beekeepers who consistently manage to enjoy lower rates of winter loss? I propose that we call them "Lucky" beekeepers, and the best of them, "Consistently Lucky."
Practical application: the harder those beekeepers work, the luckier they get!
But there were clearly "unlucky" beekeepers this year--especially the "big boys" who brought tens of thousands of hives from the drought-ravaged, and corn-converted Midwest to California. California beekeepers are used to summer drought. We have learned to either move our colonies to better (often irrigated) pasture, or to feed expensive pollen supplements. This would be a very expensive proposition to the larger operators, with hives spread all over the place--a cost not covered by current pollination prices.
What Happened To The Bees This Spring?
Part 2: The Contribution From Pesticides
Randy Oliver
ScientificBeekeeping.com
First published in: American Bee Journal, July 2013
It's pretty straightforward to attribute the majority of colony losses this winter to the usual and aforementioned causes, but a number of beekeepers are also pointing the finger at pesticides. There is no doubt that in certain areas pesticides were a serious issue to beekeepers. Colonies set back by pesticide kills may not fully recover over the season, and those going into winter with pesticide residues may go downhill. There is also reason to suspect that pesticides and miticides have something to do with today's high rates of queen failure.
The bees in some drought-stricken areas were forced to forage on irrigated and pesticide-laden crops--the only place in which there was anything to eat. This changes the entire dynamics of pesticide exposure, since residues would no longer be diluted by the pollen and nectar of non crop plants. The lack of good natural forage also suppresses the ability of colonies to deal with the insult of those pesticides. And colonies may be forced, by necessity, to forage upon one treated crop after another, resulting in multiple exposures.
Practical application: under drought conditions, bees may suffer more from pesticides than when times are good.
Due to the current high prices for agricultural commodities, farmers are often applying pesticides indiscriminately as "risk insurance" rather than due to actual need. A chilling recommendation from an extension entomologist reads:
I encourage you to be risk averse and to make an investment that will pay dividends for your valuable crop. Consider applying [flubendiamide, indoxacarb, or spinosad] for corn earworm. If you have stink bugs and are in the [mature plant] stages, you might want to tank mix one of these products with a pyrethroid. A tank mix of a pyrethroid and acephate are an option, but will wipe out all beneficials [13].
The first three insecticides mentioned are considered to be "reduced risk" to bees if residues are allowed to dry for a few hours, but no mention was made to spray at night. Of the five insecticides recommended above for spraying on corn in tassel, at least four are highly toxic to bees if sprayed during the day! No farmer wants to kill bees, but with recommendations like this from state extension agents, well-meaning growers may unwittingly be hurting pollinators.
Bees in agricultural areas are exposed to a vast array of insecticides, miticides, fungicides and surfactants--many of which have clear links to colony health problems. And applications of new mixes of chemicals are up. For example, in addition to the neonicotinoid seed treatments, granular insecticide soil treatments for corn in the Midwest were up by 30% over the previous year [14]. These treatments consist of combinations of organophosphates and pyrethroids.
But I'm not hearing either the bird groups or beekeepers even addressing these treatments! It is scary to read the sales literature for Counter insecticide, the organophosphate terbufos [15]. Growers are encouraged to apply it at planting time, despite the facts that:
"Terbufos is highly toxic to birds, fish, and aquatic invertebrates [and bees]. [It] shows significant acute mortalities of birds, mammals, reptiles, and fish resulting from broadcast application...In the same study, the application of terbufos as a soil-incorporated treatment to corn...resulted in acute mortalities to birds and reptiles" [16].
Terbufos is strongly systemic, meaning that it is absorbed by the plant roots and could be expected to be expressed in the pollen and nectar.
It can synergize with other pesticides since it ties up the critical CP450 enzymes used in detoxification, to the extent that growers are cautioned that it can cause problems to corn from herbicides [17].
During drought, certain insect pests become more problematic, perhaps resulting in increased exposure to insecticides by bees. For example, drought encourages corn leaf aphids. Read this chilling recommendation for aphids on corn during tasseling (when bees are actively foraging):
If less than 50% of pollination has occurred, aphids and honeydew are covering tassels and plants are stressed, an insecticide may be necessary to ensure adequate pollination, but treatments need to be made within 48 hours of tassel emergence. Asana XL, Brigade, Capture, Cobalt, Dimethoate, Lannate, Lorsban, or Malathion may be used for control [18].
Or this:
Prolonged drought always raises the specter of two-spotted spider mite outbreaks in soybeans and corn. As the 2012 drought intensifies in Minnesota, infestations are reaching treatable levels...The only products that are recommended for spider mites in soybean include insecticides containing chlorpyrifos, dimethoate and bifenthrin[18].
The names of the recommended insecticides above strike fear into the hearts of beekeepers!
Practical application: many "consistently lucky" beekeepers go to great effort to allow their colonies to recover after exposure to pesticides--moving them to unsprayed areas or natural forage, or by immediately feeding protein supplement to stimulate increased broodrearing. Unfortunately, such "recovery" areas are getting harder and harder to find.
The Lynch Mob
Despite the fact that a wide range of bee-toxic insecticides are being applied (often during bloom) to corn, soy, sunflowers, alfalfa, cotton, and other major crops, if you Google anything about insecticide use, you'll quickly find that the blogosphere focuses only upon the putative link between a single class of insecticides--the neonicotinoids-and the demise of pollinators [19].
People look at me incredulously when I point out that there is zero firm evidence to date that the neonic seed treatments are a serious problem! But the notion that all honey bee problems are caused by an insidious new insecticide resonates with a distrustful public [20], and has firmly established itself as "common knowledge." But repeating something does not make it true!
"It's easier to fool people than to convince them that they have been fooled"-Mark Twain
Practical application: the question is, "Are the neonic seed treatments being railroaded into a guilty verdict in the media's kangaroo court of public opinion?"
One group recently brought suit against the EPA to ban the use of the seed treatments clothianidin and thiamethoxam [21], neither of which even make California's top 100 list of pesticides applied [22], nor that have ever been demonstrated to harm colonies feeding on the pollen or nectar of seed-treated plants! A number of people have made up their minds that the neonics are the main cause of colony collapse, and it appears that no amount of facts to the contrary will cause them to reconsider!
Debunking The Myths
As anyone who knows me will tell you, I am a stickler for honesty, accuracy, and factuality. I am concerned about the amount of misinformation and speculation going around about the neonics. So let's look at some of the claims vs. the actual facts.
Arguments Against Neonic Seed Treatments Actual Facts
The neonicotinoids have been "linked" to increased colony mortality. In actuality, such a "link" is merely an urban legend, and has never been demonstrated or confirmed in any study.
On the other hand, the residues of other classes of pesticides are more suspect for causing increased brood or adult bee mortality [24].
The timing of CCD coincides with the introduction of the neonic seed treatments in 2004. CCD started in California bees in the winter of 2004/2005, prior to them ever being exposed to seed-treated crops.
But what else could have changed at that time other than the introduction of neonics? In California, Dr. Eric Mussen [25] determined that the increased colony losses were due to poor summer forage and failure of mite control products (just as this last winter).
There is actually a much stronger association between the incidence of the novel gut parasite Nosema ceranae and increased colony mortality [26].
But the main thing that has changed is the dynamics of the varroa/virus complex, which coincidentally occurred at about the same time that the neonics came into use.
European countries banned the neonics, and the bees recovered after those bans. A few countries placed temporary suspensions on certain seed treatments until planting dust issues were resolved [27]--only Germany has one suspension still in place. The foliar applications were not suspended. The suspensions did not resolve bee health problems.
The European Food Safety Authority recently decided that neonics pose a threat to bees. "The Center for Regulatory Effectiveness (CRE) has recently completed a Data Quality Act (DQA) Alert on the ... (EFSA) report on neonicotinoids which found that neonicotinoids pose a risk to bees. The DQA Alert outlines the serious deficiencies of the EFSA report and demonstrates why the EFSA report violates the DQA...In particular, the EFSA report failed to maximize the objectivity of the data by failing to reconcile numerous studies whose conclusions contradicted the findings of the EFSA report" [28].
Several lab studies have found that neonics affect individual bee behavior, longevity, or immunity. True -- although many studies used unrealistically high doses. The question is whether such artificial studies apply to actual colonies in the field. The numerous field studies to date have failed to find any link between seed treatments and later colony health issues.
It is the seed treatments that make corn a problem. As Bret Adee points out in Buzzkill, corn is replacing pastureland (Fig. 4). Corn, as grown today, is a virtual "bee desert" (similar to the way in which suburban lawns are green bee deserts). And it's not only the bees that this is affecting, the populations of birds and other wildlife are plummeting due to loss of favorable habitat (see my blog on birds and neonics [29]).
A recent survey by Dr. Jerry Bromenshenk found that bees actually avoid field corn pollen, and are exposed to very little of the seed treatment residues [30].
Numerous independent studies, and the experiences of stationary beekeepers throughout the Corn Belt, support the conclusion that colonies can thrive when surrounded by corn, provided that there is some alternative forage within flight range.
As the use of neonic seed treatments increases, bee mortality goes up. In actuality, colony mortality rates go up and down year to year, largely dependent upon weather and varroa mite control. If the neonics were to blame for this winter's bee losses, why didn't they cause similar losses last winter, in which the colony mortality rate was the lowest in years?
French beekeepers also started seeing problems with the introduction of the neonics. I've spoken with beekeepers in France whose apiaries are in pesticide-free areas. They tell me that they experience the same sorts of colony mortality problems as do those in areas exposed to neonics.
Bees in the U.S. are commonly exposed to neonicotinoids. In the most recent USDA survey (100 samples across the country), imidacloprid was only detected in 9% of the samples [31] (although I found some of the residue levels alarmingly high). However, the most common seed treatment, clothianidin (or its degradation products), was not detected at all!
The above real-world data suggests that efforts to ban clothianidin as a seed treatment may be misplaced. It appears that imidacloprid, especially as a foliar application, would be of more concern.
Neonics are the most common pesticides that bees are exposed to. In the above survey, other serious insecticides were more commonly prevalent: chlorpyrifos (in 20% of samples), cyhalothrin (in 7%), and endosulfan (in 11%).
Notably, there was also a high prevalence of beekeeper-applied miticides: fluvalinate (in 38%), coumaphos (in 87%), amitraz (in 27%), fenpyroximate (in 11%), and thymol (in 27%).
There was even higher exposure to fungicides and adjuvants.
It is misleading for the pesticide companies to blame the problems on varroa, nosema, or poor nutrition. The above survey (over 1000 samples) found that the average varroa infestation rate in the U.S. in autumn is above the danger level for virus epidemics!
Sixty to 100% of hives are infected with nosema in December.
Summer drought has historically been associated with high winter mortality.
But didn't the planting dust from corn seeding kill colonies in Ontario? Planting dust is separate issue that clearly needs to be remedied. It does on occasion cause bee kills, for which beekeepers are rarely compensated. This situation must change! All parties are actively working on solutions [32].
Bees in certain agricultural areas tend to go downhill later in the season. This has been observed for a long time--long before the neonics. The question is, which chemicals, chemical synergies, or chemical/nutrient interactions are responsible? The Frazier/Mullin team at Penn State has developed a protocol for helping to figure this out. I strongly support its adoption by the EPA for pesticide risk analysis.
Colonies foraging upon nectar or pollen of seed-treated crops get poisoned. Ask yourself this: if neonic residues were actually so harmful to bees, how is it that the Canadian beekeepers, whose bees forage largely on seed-treated canola, feeding solely upon a diet of canola nectar and pollen with well-documented residues of clothianidin, experience very low winter losses, despite the long Canadian winter (so long as they control varroa and nosema)?
And how is it that the vast majority of beekeepers in the U.S. Corn Belt report that their colonies thrive and that they have far fewer pesticide issues these days than in the past?
The neonicotinoids are "systemic," meaning that they are in the plants all the time! True, but this property is not unique to the neonics--a number of other insecticides also go systemic. In any case, with seed treatment, the concentration of the insecticide in the plant is only high when the plant is young--it gets diluted as the plant grows (e.g., clothianidin in canola is at a level high enough to kill aphids for only about the first 30 days of growth).
The only time that residues in the plant matter to pollinators is when the mature plant flowers. The amount of seed treatment is carefully calibrated so that the residue in the pollen and nectar are below the level that causes demonstrable harm to bees.
In the case of foliar, drench, or chemigation applications prior to bloom, there are greater possibilities for bees to be exposed to toxic levels.
There are fewer butterflies and pollinators in the fields these days. Not surprising, since the new push for "clean farming" has removed the host plants upon which the butterfly larvae feed. Pollinators are forced to subsist upon the stretches of weeds growing along roads at the edges of fields. But surprisingly, pollinators may be abundant there, suggesting that even though populations as a whole are reduced by habitat conversion, it is that, rather than the use of seed treatments, that causes the population declines.
The evil pesticide companies want to kill honey bees. Give me a break! Does anyone truly believe that anyone wants to kill honey bees? What pesticide company would want the bad press of being associated with killing bees? The chemists and biologists on their staffs earnestly work to develop insecticides that are bee friendly.
The EPA is being derelict in their duty to protect pollinators. I have spoken at length with EPA staff, and reviewed their risk assessments, as well as those by, DEFRA, EFSA, PMRA, and other regulatory agencies. I find that the risk assessors have not overlooked any evidence, are well-informed on the subject of neonics, and are justified in their assessments that the on-the-ground evidence (to date) indicates that neonic seed treatments pose acceptable risk to pollinators.
We must all remember that the tobacco industry tried to hide the fact that nicotine was addictive [33]. Spare me! Does anyone seriously think that the EPA is unaware that industry executives may stretch the truth? Of course the EPA is skeptical of any reassuring claims by the pesticide industry--that's why they go over all studies with a fine-toothed comb!
This winter's losses spell the end to commercial beekeeping. The fact of the matter is that many observers note that the bee supply for almonds often follows a boom-bust cycle. Although losses were high this year, the trend for the last decade has been for beekeepers keep ramping up the supply of bees for almonds. So long as growers are willing to pay a profitable rental rate for colonies, market forces will encourage the bee industry to meet the demand (for a detailed analysis, see [34]).
The Precautionary Principal
"But," you say, "shouldn't we exercise precaution due to the lab studies that find adverse effects from the neonics?" Look, I make my living as a beekeeper, I'm not out to sell insecticides, and am as concerned as the next person about the environment and the safety of the food I eat. I've researched the neonics exhaustively, and addressed them in several articles [35]. I am acutely aware that there are suggestions that the neonics may be causing insidious effects in the environment, and I've studied the excellent environmental document Late Lessons from Early Warnings [36], which hammers the message that we should use the "precautionary principle" when dealing with chemicals. The problem is, there is nothing without risk--for example, you have a 1 in 83 chance of being killed in an auto accident in your lifetime. But most people still take the risk of getting into cars, since they feel that the benefit outweighs the clearly high risk!
My practical perspective as both a scientist and a beekeeper: if researchers perform lab studies on any insecticide, they will find that there are all kinds of negative effects upon bees--this should be pretty obvious, since insecticides are specifically designed to harm insects! However, the majority of these studies are taken out of the context of full colonies under field conditions, where bees fly free and choose the flowers upon which they forage. The evidence to date supports the contention that the neonics, properly used as seed treatments, are indeed an improvement over other insecticide options.
As Dr. Eric Mussen succinctly notes:
Nobody's really been able to show that [the neonicotinoids] are more problematic than the rest [of the pesticides to which bees are exposed] [37].
Far be it from me to suggest that the neonics (or any other pesticides) are harmless! But consider this--if the neonic seed treatments were indeed as harmful as some make them out to be, you'd think that after a decade of intense study that at least one researcher could have come up with a single solid piece of field evidence against them!
Let's do a thought experiment. Why doesn't someone simply put a bunch of healthy hives into the middle of seed treated crops and see whether they die afterward? Oh, I forgot--this experiment has already been run by thousands of beekeepers year after year in the Corn Belt and the Canadian prairie! And those beekeepers have invited me to look at their colonies, sent me photos of colonies stacked head high with honey supers, and bragged about their high winter survival!
Some will argue 'til they're blue in the face, but the fact remains that virtually every beekeeper that I've spoken with in the Corn Belt and in canola areas feels that the seed treatments are not a problem [38]. In fact, most tell me that this is the best it's ever been as far as bees and pesticides!
Common sense: I just don't get what is so hard to understand about the reality that there are thousands of colonies thriving year after year in areas of intense seed treatment? To any reasonable person it would suggest that the treatments are causing little noticeable harm other than the occasional planting dust kill, which I have repeatedly stated is a problem that needs to be corrected!
See For Yourself
Let's look at actual independent (from the manufacturer) data from corn and canola areas:
Corn
I asked friends in the Corn Belt if they had any data on winter losses. It so happens that the Michiana Beekeepers Association has been collecting exactly that since the spring of 2010 (Fig. 11).
Figure 11. Percentage of winter losses by the "Michiana" hobby beekeepers. The 2013 figure is as of mid March; it may eventually go down a bit due to a prolonged cold spring. Note that the winter survival rate appears to be linked to average winter temperature. Thanks to beekeeper Danny Slabaugh for sharing the data; temp deviations from [[i]].
[i] http://www.ncdc.noaa.gov/temp-and-precip/maps
How could the above be? Eighty percent winter survival despite sitting in the middle of seed-treated corn and soy? So of course I did a fact check to confirm that those beekeepers were indeed sitting in corn/soy areas (Fig. 12).
Figure 12. USDA land cover categories for the region in which the Michiana hobby beekeepers keep bees--corn and soy acreage is color coded yellow and green, respectively. The selected area is the top half of Indiana and bottom of Michigan, with Lake Michigan at the left. Clearly, these apiaries were exposed to seed-treated corn and soy! I created the map at [[i]].
[i] http://nassgeodata.gmu.edu/CropScape/
The above figures suggest that colony winter survival for stationary hobby beekeepers in the above corn/soy region is higher than the national average, despite the fact that about half of them don't even treat for mites! They also suggest that the neonics or other pesticides used in corn/soy in that region do not cause excessive winter loss. Finally, the data indicate that a main factor for winter loss rates is the winter temperature.
Canola
I've heard some beekeepers saying that their bees crashed after working canola, suspecting that the seed treatments were the problem. So as a reality check I called a Dakota beekeeper who has been running bees to canola for over a decade--some 10,000 hives last season. He tells me that colony strength after canola varies from year to year, but that he sees no problem with the seed treatments. He did point out that beekeepers should be aware that colonies can plug the broodnest on intense canola flows.
The biology: The plugging out of the broodnest during an intense bloom means that three weeks afterward, there will be few emerging workers to take the place of the worn-out foragers, and the colony population will temporarily plummet. Even worse, the remaining mites are then concentrated onto fewer bees--which can initiate virus epidemics. These colonies must then attempt to rebuild from scratch, starting in August, meaning that the weakened, mite-infested colonies faced three long months of drought last summer for that rebuilding process.
Every field study that I've seen for canola also supports the conclusion that the seed-treatments are safe for bees. I joined other beekeepers and regulators in observing a large-scale study of seed-treated canola in Canada [41]. Canola (or rapeseed) is likely the best test crop, since bees eagerly (and virtually exclusively) forage upon it for both pollen and nectar, meaning that every bit of their food supply contains contain easily verifiable residues of the insecticides. The preliminary results indicate that the clothianidin seed treatment did not harm the colonies [42].
Another recent independent long-term field study in Poland [43] came to the same conclusion. In it, the researchers followed 50 colonies for more than two years under field conditions as they foraged on five different large fields of oilseed rape treated with various combinations of five different neonicotinoids applied by seed treatment and spraying. Pollen and nectar samples were taken, and demonstrated that the bees were clearly exposed to normal residues of the insecticides (there was also additional exposure to other common agricultural pesticides). The colonies were monitored for health, brood, strength, nosema, viruses, and winter survival, and compared to two control apiaries set in an area free of the crop. The results?
During the time from the placing of the colonies on the rape fields until wintering, the colonies developed properly in all groups... All colonies overwintered properly... In both years, during the period of being placed in the oilseed rape fields as well as after being moved to the stationary apiary, none of the groups showed disturbances in development or functioning.
Following a paper that suggested that the seed treatments would impair bumblebee colonies' ability to rear queens, DEFRA performed a common-sense field study last year [44]. Their findings:
...the study has shown that bumble bee colonies remained viable and productive in the presence of the neonicotinoid pesticides under these field conditions...The study underlines the importance of taking care in extrapolating laboratory toxicology studies to the field, as well as the great need of further studies under natural conditions.
Sunflowers
Some beekeepers report that their colonies later crashed after they chased sunflowers last summer for honey. One must keep in mind that sunflowers are not a natural food for honey bees, and provide only poor-quality, nutritionally-inadequate pollen [45]. But the main problem with putting bees on sunflowers may be related to the fact that sunflowers are a native plant--meaning that there are a number of native insects that evolved to feed upon it:
Maximum seed yields often require the use of insecticides to protect the crop from insect competitors. Unfortunately, many of the major insect pests of sunflower attack the crop when it is flowering. Thus, insecticides used to control the pest also harm pollinating bees [46].
If sunflowers are the only forage available, colonies may eventually go downhill, due to the one-two punch of poor pollen nutrition coupled with insecticide exposure. And which pesticides would those be? One scary list- Asana XL, Baythroid, endosulfan, Furadan , Lorsban , methyl or ethyl parathion, , Proaxis, Scout X-TRA, Sevin, Warrior, Mustang Max, Declare, Cobalt, Yuma, Delta Gold, and Grizzly Z [47]!
Note that none of the above are neonics, other than seed treatments for wireworms. Surprisingly, field evidence indicates that the seed treatments only "stun" the wireworms for a while [48], which certainly raises the question as to how harmful they might be to bees months later when the plants flower! I will return to sunflowers below.
Be Careful What You Ask For!
Allow me to assure you that I am no pitchman for neonics or any other insecticide--the typical farmer practices far too little integrated pest management, and applies far too many pesticides! All insecticides (and several fungicides and adjuvants) cause problems to pollinators--the neonics are no exception. Any systemic insecticide has the potential to harm bees when applied as foliar applications, by chemigation, or to flowering trees, but it there is no compelling evidence that the neonics are any worse than the alternatives in most applications. On the contrary, there is quite a bit of evidence that they may often be "safer" ("reduced risk").
If the neonic seed treatments were banned, it's not as though all agriculture is suddenly going to go pesticide free--only about 1% of U.S. cropland is registered as "organic"! We must consider the likely alternatives. The products that farmers would then use to control insects would need to be sprayed all over the cropland--we'd then be back to the problem that the bulk of sprayed insecticides go into the environment without ever hitting the intended pest!
I hear from knowledgeable beekeepers that worse than in previous years, some of the new formulations of the spray-applied insecticides [49, 50, 51] can really knock the snot out of bees! One large beekeeper found his hives already dead before moving them away from the fields. Again, this was not a neonicotinoid issue.
Practical application: no one is saying that the neonics are "harmless." The question is whether they are better or worse than the alternatives.
The Effect Of Drought
Let's discuss some of the problems (or suspected problems) with the neonics last season. The record warm and dry spring appeared to exacerbate corn planting dust issues (corn seeds are the worst offender due to their non spherical shape). Beekeepers in some areas of the Corn Belt, the East Coast, and in Ontario suffered from confirmed (in at least some of the cases) planting dust kills (although many went on to make good honey crops after their colonies recovered). The final analysis from Ontario is not yet completed, but dry soil conditions and an early clover bloom likely contributed to the problem. Regulators and the seed companies are working on solutions to the problem [52]. Still, IMHO it is unacceptable to ask beekeepers to bear the burden of bee kills without compensation, and no one could blame the affected beekeepers for being pissed!
Drought-stressed plants
There are a number of advantages to the neonic seed treatments. Besides their safety to the farmer and to most wildlife, there is virtually no way for the farmer to misapply them! The timing of application is only at planting time (when bees normally have little interest in the bare fields), and the dose is determined by the seed-treating company. This means that the applicator can't be tempted to apply at the wrong time, or to over apply too strong a dose (however, their excessive near universal use can be expected to accelerate the development of resistant pests).
That said, beekeeper Bret Adee brought an interesting question to my attention: the dose of seed-applied systemic insecticides (whether neonic or other) is based upon the dilution factor as the plant grows, so that the residues in nectar and pollen will be reduced to below the "no observed adverse effects level." But what happens during drought, when the water-stressed plants only grow knee high before desperately flowering? There would be far less plant biomass in which to dilute the insecticide (assuming that drought-stressed plants absorb the same amount from the seed treatment).
Certain plants (including sunflowers and canola) are known to "hyperaccumulate" toxic metals [53], perhaps more so during drought. Could this also be the case with systemic insecticides? Something that's been stuck in the back of my mind is that Bonmantin [54] found that the concentration of imidacloprid first drops in sunflower plant tissue as it grows, and then reconcentrates in the flower heads.
It occurs to me that the translocation of systemic insecticides is generally studied in plants grown under "normal" conditions. I'd very much like to see data for residues in pollen and nectar from seed-treated plants grown under drought. Had we thought of this earlier, we could have collected pollen and nectar samples from drought-stressed plants last summer. I'm currently trying to track down any data or samples from such plants--if any reader has any such sample analyses, please let me know!
Practical application: the above hypothesis is speculative, but we need actual data from drought-stressed plants to see whether such an effect occurs. If so, it would need to be taken into consideration for the registration of seed treatment products!
Once planting was completed and the drought took its toll, the reports that I've heard are that soybean honey saved a lot of bee operations this season, right in the middle of treated corn/soy farmland. In this case, seed treatment with neonicotinoids may have been a blessing to beekeepers:
The benefits of [seed treatment] not only include the early-season disease control but also suppression of soybean aphids for quite a ways into the growing season. With it, we typically make only one foliar insecticide application for aphid control, usually in August, instead of two applications when [treatment] isn't used. In 2012, with the extremely dry conditions in mid-season, there wasn't as much of an aphid problem, and we treated just 300 acres of soybeans...Last year we sprayed closer to 30,000 acres for aphids [55].
On the other hand, some beekeepers on alfalfa or cotton got hit hard by other classes of insecticides. A hit from a pesticide application can lead to poor subsequent colony performance, queen failure, dwindling, or winter collapse. ABJ published an excellent series of articles on pesticides by Drs. Barbara and Eric Erickson in 1983; Editor Joe Graham has graciously granted me permission to post copies of those articles to my website [56]--I strongly suggest any beekeepers interested in pesticide issues read them! In the second article, the authors discuss both the problems with systemic insecticides and of sublethal effects--note that these articles were written long before the introduction of the neonics!
An anti-pesticide group, along with a handful of beekeepers, recently filed suit against the EPA [57], calling for an immediate ban on the two most common neonicotinoid seed treatments, despite the easily-verifiable fact that hundreds of thousands of colonies thrive in the midst of seed-treated corn, soy, and canola! To me, this suit smacks of being some sort of well-orchestrated publicity stunt, and does not serve the interests of either beekeepers or environmentalism. Worse, it now gives the powerful farm lobby cause to label beekeepers as "radical" enemies.
We don't want this battle: do we really want to take on the farm lobby by backing them into a corner? The French beekeepers took a similar case against fipronil all the way to their supreme court and lost [58, 59]-worth reading]. Agriculture is already positioning itself for a fight [60, 61, 62]. Think about it--the EPA lives in fear of a conservative congress slashing their funding. Does anyone really think that they are going to go against the agricultural lobby without unimpeachable evidence? We should also think twice before calling for a ban on the seed treatments--the alternatives are not pretty!
It disturbs me to hear industry executives and lawyers stretching the truth or misrepresenting data. It disturbs me even more to hear my fellow environmentalists and beekeepers doing so! If we wish to maintain credibility, we should hold ourselves to a higher standard. The question we must ask ourselves the way in which we wish to have pesticide regulation decisions made:
1. By the EPA (the Environmental Protection Agency), whose risk assessors carefully study and weigh all available research and evidence in order to make objective and rational decisions, or
2. To have it decided instead by impassioned, fearful, and often misinformed advocacy groups who hire lawyers and pressure politicians who know little about the subject?
We depend upon the EPA to strike a balance between the availability of cheap food and profitability for those who provide it, versus the risks to human and environmental health and safety. It is good to have activists on both sides of the issues (industry and the anti-pesticide groups) to keep the EPA informed. But I don't feel that either of those groups should be telling the EPA which pesticides to register or to ban! Let the regulators do their job!
Rather than wasting EPA's funding to fight frivolous lawsuits, there are more productive actions that we can take:
Help the EPA to do its job by filing "adverse effects incident reports" if you observe a problem due to pesticides [63]. EPA is begging beekeepers to do this! Unless they have documented reports of pesticide problems, their hands are tied as to restricting the uses of those pesticides!
Support the National Pollinator Defense Fund [64]. Our industry is currently represented by a reasoned and knowledgeable group of (mostly) beekeepers. (Challenge to the pesticide companies: why don't you stand behind the safety of your products and donate? The NPDF is about ensuring that your pesticides are properly applied, so there would be no conflict of interest).
If your local state lead agency is not actively investigating bee kills or enforcing pesticide regulations, then use the local media to embarrass them into action!
Keep pressure on the EPA to resolve corn planting dust problems. Here's a wild idea: I'm not sure of the exact figures, but let's say that 90% of the 95 million acres of corn is grown from neonic-treated seed. If the states were to levy a surcharge of 50 cents per acre (neonic seed treatment adds about $12 per acre to seed costs), they could collect over $42 million each year to fund a pool from which to indemnify the occasional beekeeper who suffers a confirmed kill from planting dust!
Tell Congress that we'd like to see wording added to the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) to specifically protect pollinators. Currently, such protection is nebulous (although the EPA is acutely aware of pollinator issues): "The Administrator shall register a pesticide if... when used in accordance with widespread and commonly recognized practice it will not generally cause unreasonable adverse effects on the environment." Unless there is specific wording to protect pollinators, bee kills may not be considered to be "unreasonable"!
We need far more independent field studies to determine which pesticides and application practices are actually causing harm to pollinators. For pesticides in question, keep pressure on the EPA to require additional field trials to demonstrate whether they are indeed safe for pollinators under field conditions. I'd like to see the establishment of monitoring apiaries (and patches of untilled land) in representative agricultural areas nationwide, with the hives in each apiary to be carefully managed by independent parties. Such apiaries and sites could then be closely monitored each summer to see whether honey bees and other pollinators are able to survive local pesticide practices.
Give farmers workable options! Disseminate and promote bee-friendly agricultural practices that don't hurt the farmers' bottom line. For example, by adopting IPM practices, Arizona cotton growers reduced insecticide spraying from 12.5 times a season to only 1.3 times (cutting insecticide use twentyfold), while using more environmentally-friendly insecticides [65]! Another recent study in Iowa found that adding additional clover or alfalfa rotations in corn/soy farmland was equally profitable, improved the soil, used less energy, used far less pesticides, and decreased water pollution [66].
Business and agriculture respond to consumer demand. Consumer demand stopped most dairymen from injecting their cows with the hormone BST. Consumers could do the same by demanding pasture-fed beef and dairy (which would create more pollinator forage)! I'd also like to see the expansion of consumer choices (other than organic certification) that reward farmers who manage their lands to the benefit of wildlife and pollinators. For ideas, see [67. 68. 69].
Bottom Line
In conclusion, it appears that a perfect storm of a preceding exceptionally warm winter, followed by serious drought across the country, the lack of good mite control, a high prevalence of pathogens, and an unexpected California chill in the orchards prior to bloom, resulted in an unusual degree of colony losses. In other words, rather than one specific cause, there were simply not enough of the good things, and too many of the bad things.
I don't see evidence that pesticides were the major factor in the shortage of bees in almonds this winter, although, as usual, a number of individual beekeepers on certain crops certainly took serious hits.
And how about the fear that there won't be enough bees for almond pollination next year? Beekeepers have already told almond growers to expect higher pollination prices next year (especially since California is again going into serious drought, and beekeepers will be forced to invest extra money in feeding their hives). Most every beekeeper I know is madly making increase right now in anticipation of higher pollination prices next season. The fact of the matter is that should conditions allow beekeepers to successfully rebuild their numbers (following the typical swings of our boom/bust cycle), there could possibly even be a glut of bees for almonds next winter!
Feedback And Corrections
A few countries placed temporary suspensions on certain seed treatments until planting dust issues were resolved [27]--only Germany has one suspension still in place. - Actually there are some more: France (Thiamethoxam in oilseed rape, Imidacloprid in corn and sunflower), Italy (all Neonic seed treatment in corn), and Slovenia (Imidacloprid, Thiamethoxam, and Clothianidin seed treatment in all crops)
French beekeepers also started seeing problems with the introduction of the neonics; I've spoken with beekeepers in France whose apiaries are in pesticide-free areas. They tell me that they experience the same sorts of colony mortality problems as do those in areas exposed to neonics - This is, by the way, likewise confirmed by monitoring results from the French authorities.
In the case of foliar, drench, or chemigation applications prior to bloom, there are greater possibilities for bees to be exposed to toxic levels. - This is not the case for foliar application: as Neonics are xylem-systemic, but hardly mobile in the phloem, they can only be distributed in a plant after root uptake, but not be translocated for instance from a leaf to a later developed flower.
Then, on the topic of systemic residues in plants under drought stress: first, I am quite sure that the decrease of concentration in seed-treated plants over time is not only due to dilution, but also to degradation of the compounds - a factor that is not specifically dependent on water availability for the plants (e.g. photodegradation!); second, even if there would be less dilution in plants under drought stress: the concentrations in nectar and pollen of treated crops are normally so low (when we consider average rather than peak concentrations, and when we consider scenarios where colonies have chronically access exclusively to contaminated nectar/pollen over months unlikely in practice), that even an increased concentration due to drought stress-affected plants should not make a significant difference: if we for instance assume an average concentration of let's say 3-4, or even 5 ppb Clothianidin in corn pollen, and likewise assume a dilution reduced to 50% (which is probably exaggerated), then we would still not end up with excessive residues. And finally, we have residue figures from crops grown in different countries, different climatic conditions, and different agronomic practices; though we have not specifically addressed the drought stress scenario, we have seen that residue figures are quite consistent over all scenarios, and there does not appear to be strong evidence that different environmental conditions would substantially (i.e. by orders of magnitude) and systematically alter residue concentrations.
Dr. Christian Maus
Global Pollinator Safety Manager
Bayer CropScience
/
A ppt on the impact of CRP lands on wildlife in North Dakota
http://www.redriverbasincommission.org/Conference/Proceedings/26th_Proceedings/Kading_RRBC_09.pdf
/
Feedback from a Midwestern apiary inspector:
Just a quick update: This beekeeper who recently told his local newspaper that pesticides were killing his bees, he was making excuses. We examined two of his yards with him yesterday. One yard was showing EFB throughout the whole yard. I think his "mid-summer losses" last year (half of that yard's hives) were EFB kicking in with the mid-summer dearth. In his other yard, most of his dead outs were obvious starve outs. He harvested all of their stores with the first frost, and then didn't feed them. So, in my opinion, and from my observations, pesticides are usually being used responsibly, and aren't killing honey bees. I also think, with the aggressive way bees were on soy fields last summer, the systemic pesticides are not harmful to honeybees. I'm not seeing honey bee problems other than EFB getting the upper hand, due to our cold, late spring. My two cents. Thanks.
References
[1] http://www.frequency.com/video/dan-rather-reports-buzzkill/87705620/-/YouTube
[2] http://www.ars.usda.gov/is/pr/2012/120531.htm and California DPR.
[3] http://www.ncdc.noaa.gov/temp-and-precip/maps.php
[4] Wright, CK & MC Wimberly (2013) Recent land use change in the Western Corn Belt threatens grasslands and wetlands. https://www.motherjones.com/files/pnas201215404_nwow5w1.pdf
[5] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
[6] https://scientificbeekeeping.com/sick-bees-part-2-a-model-of-colony-collapse/
[7] vanEngelsdorp, D, et al (2013) Idiopathic brood disease syndrome and queen events as precursors of colony mortality in migratory beekeeping operations in the eastern United States. Preventive Veterinary Medicine 108(2-3): 225-233. http://www.sciencedirect.com/science/article/pii/S0167587712002656
[8] https://scientificbeekeeping.com/sick-bees-part-18a-colony-collapse-revisited/
[9] http://almondinsights.com/692, http://agfax.com/almonds/2013/reports/03042013-almonds-web.htm
[10] https://scientificbeekeeping.com/sick-bees-part-18a-colony-collaspse-revisited/
[11] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2010-2011-Limited_Survey_Report.pdf
[12] http://www.youtube.com/watch?v=y6B5qm2ut18, http://www.youtube.com/watch?v=PYbLbhZXizY
[13] (Broken Link!) http://www.nccrops.com/2012/07/27/insecticide-recommendations-for-corn-earworm-in-soybeans/
[14] http://www.agriview.com/news/crop/corn-soil-insecticide-use-up-dramatically-to-combat-widespread-rootworm/article_5d09decc-5b40-11e2-b485-001a4bcf887a.html
[15] http://www.amvac-chemical.com/products/documents/Counter20G%20Tech-Sell%20Sheet%20-%202013.pdf
[16] http://pmep.cce.cornell.edu/profiles/insect-mite/propetamphos-zetacyperm/terbufos/insect-prof-terbufos.html
[17] http://www.lewishybrids.com/PDF/3-5-2013Agronomic+ALERT+-+Interaction+between+herbicides+insecticides+corn.pdf
[18] http://pest.ca.uky.edu/EXT/Recs/ENT16-Field%20corn.pdf
[19] (Broken Link!) http://www.soybeans.umn.edu/crop/insects/spider_mites.htm
[20] http://www.nytimes.com/2013/04/07/opinion/sunday/calamity-for-our-most-beneficent-insect.html?nl=todaysheadlines&emc=edit_th_20130407&_r=0
[21] http://www.nytimes.com/2013/04/07/opinion/sunday/calamity-for-our-most-beneficent-insect.html?_r=0
[22] http://www.panna.org/press-release/beekeepers-and-public-interest-groups-sue-epa-over-bee-toxic-pesticides
[23] http://www.cdpr.ca.gov/docs/pur/pur10rep/top_100_ais_lbs10.pdf
[24] http://www.extension.org/pages/60318/pesticides-and-their-involvement-in-colony-collapse-disorder
[25] Mussen, EC (2006) Chaotic almond pollination. http://entomology.ucdavis.edu/faculty/mussen/JanFeb2006.pdf
[26] https://scientificbeekeeping.com/sick-bees-part-18e-colony-collapse-revisited-genetically-modified-plants/
[27] http://www.epa.gov/pesticides/about/intheworks/ccd-european-ban.html
[28] http://www.thecre.com/oira_pd/wp-content/uploads/2013/04/DQA-Alert-EU-Commission-Ban-on-Neonicotinoids-4-10.pdf
[29] https://scientificbeekeeping.com/home/news-and-blogs/
[30] Henderson, CB, JJ Bromenshenk, DL Fischer (2013) Clothianidin exposure levels from bee-collected pollen and nectar in seed-treated corn and canola plantings. Proceedings of the American Bee Research Conference.
[31] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
[32] http://www.ontariograinfarmer.ca/MAGAZINE.aspx?aid=534
[33] http://www.pbs.org/wgbh/pages/frontline/shows/settlement/timelines/april94.html
[34] https://scientificbeekeeping.com/2012-almond-pollination-update/
[35] https://scientificbeekeeping.com/neonicotinoids-trying-to-make-sense-of-the-science/, https://scientificbeekeeping.com/neonicotinoids-trying-to-make-sense-of-the-science-part-2/, https://scientificbeekeeping.com/testing-of-bee-feed-syrups-for-neonicotinoid-residues/
[36] http://www.eea.europa.eu/publications/late-lessons-2
[37] http://www.sciencefriday.com/playlist/#play/segment/9088
[38] https://scientificbeekeeping.com/the-extinction-of-the-honey-bee/
[39] http://www.ncdc.noaa.gov/temp-and-precip/maps
[40] http://nassgeodata.gmu.edu/CropScape/
[41] https://scientificbeekeeping.com/a-new-large-scale-trial-of-clothianidin/
[42] http://www.producer.com/daily/ontario-field-study-finds-no-link-between-seed-treatments-bee-deaths/
[43] Pohorecka, K, et al (2013) Residues of neonicotinoid insecticides in bee collected plant materials from oilseed rape crops and their effect on bee colonies. Journal of Apicultural Science 56(2): 115-134. http://www.degruyter.com/view/j/jas.2012.56.issue-2/v10289-012-0029-3/v10289-012-0029-3.xml?format=INT
[44] http://www.fera.defra.gov.uk/scienceResearch/scienceCapabilities/chemicalsEnvironment/documents/reportPS2371Mar13.pdf
[45] http://repository.up.ac.za/bitstream/handle/2263/20334/Nicolson_Chemical(2012).pdf?sequence=1
[46] (Broken Link!) http://www.ag.ndsu.nodak.edu/aginfo/entomology/entupdates/Sunflower/a1331sunflowerhandbook.pdf
[47] http://www.sunflowernsa.com/growers/approved-chemicals/insecticides-test/
[48] http://www.mydigitalpublication.com/publication/?i=151958&p=41
[49] http://www.sunflowernsa.com/growers/approved-chemicals/insecticides-test/
[50] http://www.farmassist.com/agriedge/images/Resource_PDFs/Soybean/Warrior_Zeon.pdf
[51] http://www2.dupont.com/Production_Agriculture/en_US/assets/downloads/pdfs/K-09315.pdf
[52] http://www.ontariograinfarmer.ca/MAGAZINE.aspx?aid=534
[53] http://en.wikipedia.org/wiki/List_of_hyperaccumulators
[54] Bonmatin, JM, et al (2005) Behaviour of Imidacloprid in Fields. Toxicity for Honey Bees. In Environmental chemistry: green chemistry and pollutants in ecosystems pp. 483-49. http://www.buzzaboutbees.net/support-files/bonmatin2005behaviour-of-imidacloprid-in-fields.pdf
[55] http://cornandsoybeandigest.com/seed/do-soy-seed-treatments-pay?page=2
[56] https://scientificbeekeeping.com/historical-pesticide-overview/
[57] http://www.centerforfoodsafety.org/press-releases/1911/cfs-beekeepers-and-public-interest-groups-sue-epa-over-bee-toxic-pesticides
[58] http://www.theworldlawgroup.com/files/file/docs/Soulier_health_environment_June_2012.pdf
[59] http://www.soulier-avocats.com/upload/documents/Soulier_health_environment_september_2010_F.pdf
[60] http://westernfarmpress.com/government/pesticide-battle-over-honey-bee-health-under-way?page=1
[61] http://westernfarmpress.com/management/total-ag-pesticide-elimination-sought-radicals
[62] http://www.neonicreport.com/home/project-compass/
[63] https://scientificbeekeeping.com/pesticide-incident-reporting/
[64] http://pollinatordefense.org/site/
[65] http://cals.arizona.edu/apmc/docs/IPM_Delivers.pdf
[66] Davis, AS, et al (2012) Increasing cropping system diversity balances productivity, profitability and environmental health. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0047149
[67] http://www.pcl.org/pcl_files/5_Wildlife_Habitat_Farmland.pdf
[68] http://pfspbees.org/
[69] http://www.nwf.org/CertifiedWildlifeHabitat/UserAccount/SignIn
Category: Practical Beekeeping Management, Topics
Tags: beekeeper management, biotic, diseases, drought, environmental, factors, pesticides, randy oliver, varroa | environmental Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/environmental/ |
What Happened To The Bees This Spring? (Part 1 & 2)
First published in: American Bee Journal, June 2013
Part 1: Environmental and Biotic Factors
Setting the Stage
The Lead Up
The Drought
Lack of Good Forage
Varroa
Diseases
Other Indicators of Impending Collapse
An Unexpected Chill
Feedback from Brokers
The Silent Majority
Beekeeper Management
Part 2: The Contribution From Pesticides
The Lynch Mob
Debunking The Myths
The Precautionary Principal
See For Yourself
Be Careful What You Ask For!
The Effect Of Drought
Actions To Take
Bottom Line
References
What Happened To The Bees This Spring?
Part 1: Environmental And Biotic Factors
Randy Oliver
ScientificBeekeeping.com
First published in ABJ June 2013
By now, most everyone has heard that honey bee colonies died in massive numbers this winter. Reporter Dan Rather, in his newscast Buzzkill [1], showed unfortunate beekeepers, some of whom had lost half or more of their colonies, predicting gloom and doom for the bee industry. What were the causes of this year's bee shortage? As Rather says, "Everyone has an opinion." The question is whether those opinions are based upon fact! So let's go over the events leading up to the bee supply debacle.
Setting The Stage
Nearly 800,000 acres of almond trees in California came into bloom this winter--the trees typically start flowering about Valentine's Day, and the bloom lasts for only about two weeks. Almonds require cross fertilization between adjacent rows of varieties (Fig. 1), and honey bees are trucked in from all over the country to do the job (roughly a million and a half colonies). Many large commercial beekeepers move their hives into California in November to overwinter in holding yards; others build them up on winter pollen flows in Florida or Texas, or hold them in temperature-controlled potato cellars until shortly before bloom. The hives are generally placed into the orchards about a week before the first flowers appear. There is virtually no forage in the orchards prior to, or after bloom in many areas.
Figure 1. An almond orchard in late February, showing the flowering of rows of different cultivars required for cross pollination. The bare "late" varieties have not yet bloomed; the green "early" pollenizers have finished bloom. Grading of colonies is normally done during the bloom of the main crop (usually Nonpareil).
The Lead Up
Two seasons ago there was also a shortage of bees in almonds, following the coldest January (2011) in 17 years (cold being a major stressor of wintering bee colonies). Beekeepers then replaced their deadouts with package bees and splits, thus starting a new generation of colonies, which tend to have lower varroa mite levels than established colonies. These colonies entered autumn 2011 in pretty good shape, and then enjoyed the fourth warmest January (2012) on record! As a result, there was the lowest rate of winter mortality in years, and plenty of bees for almonds in 2012 (Fig. 2).
Figure 2. Percent winter losses since the beginning of the national survey--the data is not yet in for 2012/13. Note that there has been a general downward trend, suggesting that whatever caused the high losses in 2007/8 has not been such a problem in recent years. Note also the cyclical nature of colony winter losses, with high losses in 2004/5, 2007/8, 2009/10, and 2012/13 (some data not shown) Data from [[i]].
[i] http://www.ars.usda.gov/is/pr/2012/120531.htm and California DPR.
I was curious as to whether the colony loss rate was linked to the use of neonicotinoid insecticides. There is no recent USDA data, so I went through the California Pesticide Use Reports (data available through 2010). I plotted the amount of imidacloprid applied to crops in California in the preceding year in red (the seed treatment clothianidin didn't even make the top 100 list of pesticides applied). Although there appears to be a possible correlation from 2006 through 2009, the trends were reversed for 2010. I will be curious to add the 2011 data when it becomes available.
In March of 2012 I received a phone call from a California queen producer who had a prescient insight as to a potential brewing disaster. He was receiving calls for queen bees from Northern beekeepers whose bees had already grown to swarming condition due to the unseasonably warm spring weather (Fig. 3).
Figure 3. Last year's warm spring in much of the country lead to early broodrearing, and as a result, early buildup of varroa levels. Note the record warm spring in the Midwest.
The queen producer noted that such early brood rearing also meant early mite buildup, and predicted that since most Midwestern beekeepers treat for mites by the calendar, that they would unknowingly allow mites to build to excessive levels before treatment. This was strike one against the bees.
The Drought
Then it didn't rain-by midsummer, it was clear that the continental U.S. was in serious drought, including California, whose beekeepers supply nearly half the bees for almond pollination. The only ways that we kept our colonies strong was to either feed expensive pollen supplement and sugar syrup, or to move them to elusive better pasture out of state. By late summer, 60% of the U.S. was in drought, meaning that unless your bees were next to soybeans or irrigated crops, there was little forage for them. This lack of good nutrition was strike two against the bees (Fig. 4).
Figure 4. The severe drought in the Midwest really put the hurt to bee pasture in those states in which the majority of commercial hives spend the summer. Source [[i]].
[i] http://www.ncdc.noaa.gov/temp-and-precip/maps.php
Drought not only dries up nectar and pollen sources, but also forces bees to fly further and more frequently for water. Plus it concentrates ag chemicals and pesticides in the few sources of surface water available to bees. The bees started to show the hurt.
Beekeepers tried to move their hives to areas of better forage, sometimes overstocking an area with too many hives, which led to excessive competition for resources, and the spreading of parasites. Others desperately chased less desirable crops such as sunflowers. Colonies in holding yards in California found little to eat, due to our record dry weather. Some beekeepers with winter eucalyptus locations found them crowded with other hives.
Lack Of Good Forage
In Buzzkill, Bret Adee brought up the fact that bee pasture in the Midwest is disappearing under the plow, largely due to our environmentally-irresponsible taxpayer-subsidized policies that encourage farmers to plant every square foot of land into corn (Fig. 5). Bee brokers told me that colonies coming to almonds from the Midwest were in generally poorer shape this year than those coming from the southern states.
Practical application: some Midwestern beekeepers split their operations, hauling some to the South to rebuild over winter, and the rest directly to California-there was a night and day difference as to how the colonies looked in February!
Figure 5. Grasslands and wetlands in the Corn Belt are rapidly being converted to monocultural, heavily herbicided corn/soy, which eliminates virtually all bee and wildlife forage. A new study found that between 2006 and 2011 there was a net loss of 1.3 million acres of grassland. This affects not only bees--the authors [[i]] state that "As a consequence, populations of grassland nesting birds are declining faster than any other group of birds in North America."
[i] Wright, CK & MC Wimberly (2013) Recent land use change in the Western Corn Belt threatens grasslands and wetlands. https://www.motherjones.com/files/pnas201215404_nwow5w1.pdf
To put this loss of bee pasture into perspective, I asked some Dakota beekeepers for estimates of how many acres of CRP grassland are needed to sustain a colony of bees. In recent years, the overall hive density in North Dakota has been more than 10 hives per square mile (less than 64 acres per hive, including wastelands).
Practical application: the best guess by those beekeepers was that each colony of bees requires about 5-15 acres of productive land for forage (late summer forage being the critical factor). If we use the figure of 10 acres per colony, then the conversion of 1.3 million acres of grassland to herbicided cropland suggests that forage for 130,000 colonies of bees has been eliminated in the past five years in the Corn Belt alone! This figure represents nearly 9% of all colonies needed for almond pollination.
Varroa
An excellent window into the causes of colony health problems is the USDA National Honey Bee Pests and Diseases Survey Report [5] (the latest data have not yet been released). It is worrisome that varroa levels appear to be steadily climbing year after year.
And if the drought and forage problems weren't enough, the favored miticide of commercial beekeepers became unavailable for a time last summer, and mite levels built to killing levels in a number of operations. By late July, some of us were already predicting a disaster for the upcoming almond pollination season. Although many beekeepers finally got mite levels down with late-season treatments, the damage had already been done, and there was no turning the colonies around. Strike three for the bees!
In November semi loads of hives started moving into California, or had been placed in potato cellars. Some of the colonies that arrived from the Midwest were in poor shape, or crawling with mites. Oddly, few beekeepers at the time owned up to having problems, despite the reports that I kept hearing of mite and forage issues! I'm not sure whether this was due to denial, wishful thinking, simple lack of lifting the lids, or something else.
Diseases
Nosema infection also runs rampant across the country--70% of colonies were infected in June of last year. The stressful factors leading up to almond bloom apparently put a lot of hives close to the "tip point" at which pathogens can overwhelm the colony immune system and start it going backwards, or initiate the slide into sudden depopulation (detailed at [6]). Few seem to be mentioning signs of CCD-it is unfortunate that the media keep using that term as a catch-all for all hive problems!
One should keep in mind that the winter collapse issue appears to be cyclical, similar to flu or other pathogen epidemics. I have strong reason to suspect that the constantly-evolving viruses are involved in these colony collapse epidemics.
There has also been a strong resurgence of European Foulbrood and other unidentified brood diseases [7] (Figs. 6, 7, and 8). Unlike EFB of old, the new forms don't go away with a nectar flow.
Figure 6. "Shot brood" due to EFB. Note the fat queen near the center. Despite her vigorous egglaying, this colony is unable to pull ahead due to excessive brood mortality. Lots of beekeepers reported EFB symptoms this winter.
Figure 7. You really have to look hard in some colonies with spotty brood to see the cause! Two larvae in this photo show signs of EFB infection.
Figure 8. Dying brood from one of my sick colonies this spring with EFB-like symptoms. Note the "shot" pattern, the twisted larvae, and the dried larval remains. There is also some AFB-like coloration, but lack of roping or AFB odor (this odor is distinct and sour), nor a positive Holst milk test. In this colony, even pupae were dying. I observe these symptoms independent of whether the hives went to almond pollination or not. Colonies with this (or similar) infection cannot grow. Treatment with oxytetracycline generally clears it up.
One thing that I noticed in Buzzkill was the uneaten pollen supplement patties in many of the crashed hives. I've mentioned before [8] that I've found a colony's failure to consume pollen supplement to be a reliable predictor that that colony will later collapse.
Another strong predictor of winter collapse is weak strength in fall (upcoming article), again strongly suggesting that those colonies already have some sort of health issue going into winter. I heard reports from all over the country that bees went into winter in poor condition.
An Unexpected Chill
The final blow to hives in California was a blast of icy weather (Fig. 9). This unexpected chilling compounded all the existing problems! I've previously pointed out that colony collapse often follows unseasonable chills, since it shifts the tip point for virus and nosema epidemics. Clusters that had expanded for broodrearing contracted, resulting in chilled brood and dead young bees on the ground. My own colonies simply shut down broodrearing completely, losing about two weeks of buildup.
Figure 9. Chilling events (blue arrows) in Modesto, California this winter (the dark blue lines represent normal highs and lows). The unusual chilling in late December and early January (hitting the '20's in a number of areas) came at the time when colonies normally begin to build up for almonds. This severe (for California) cold set the already-stressed colonies back hard, and may have allowed nosema and viruses to gain the upper hand. Graph from wunderground.com.
At the national convention in January, the first reports of beekeepers with collapsing operations were heard. But still, the industry was in denial, with an apparent glut of promised bees as late as the end of the month (two weeks before start of bloom)! But when the rubber finally hit the road in mid February, that illusory supply quickly evaporated, with desperate growers and brokers scrambling to obtain bees--some offering obscenely high prices for substandard colonies.
And then, due to the cool spring, the trees held off on blooming for an extra 10-14 days [9]-colonies placed in anticipation of normal start of bloom just sat there starving and shivering on the cold orchard floors.
Practical application: the biology here is that this is the time of the "spring turnover" in bee populations in California, during which the old overwintered adult bees must rear their replacements for the spring buildup of population. The conditions in the almond orchards prior to bloom are miserable for smaller colonies--it is warm enough to encourage them to break winter cluster and expand the broodnest, but overnight frosts on the Valley floor can cause serious chill stress. Furthermore, it is often warm enough to fly at midday, but there is virtually nothing to forage upon until the trees start blooming! Such fruitless foraging further wears out the workers, and allows sick bees to drift to adjacent hives. Worse yet, the desperate foragers rob out any dead or dying colonies in adjacent orchards, rapidly and effectively transmitting mites, nosema, viruses, and anything else harmful in the deadouts.
Many colonies went backwards during this excruciatingly long wait. Some beekeepers told me that hives graded at placement scored better than those graded at bloom (just the opposite of normal)!
I've been carefully observing spring turnover in my "dinks" (weak colonies) in February (Fig. 10). What I find is that the problem is generally not the queen; rather, the colonies are infected with some pathogen- most commonly nosema [10], the paralytic viruses [11], or EFB (or EFB-like brood disease). Those colonies that are able to successfully emerge one solid round of brood are often able to "clear" the infection and completely rebound by April. Those that get hit by frost in February often collapse.
Figure 10. An example of an unsuccessful spring turnover. This colony is in the middle of typical February collapse from nosema or IAPV. You can easily see the outline of the area recently covered with brood, delineated by the crescents of freshly-packed pollen. Colonies undergoing this sort of depopulation tend not to forage for nectar, and do not respond well to supplemental feeding. This colony continued to collapse quickly, and finally died in a cold snap a week later--with only silver-dollar sized patch of dead bees remaining.
Feedback From Brokers
I asked a few of the major pollination brokers for their observations on the colony shortage this season. Their feedback suggested that the causes for the bee shortage were varied and many.
Summary:
Most were able to eventually fill their contracts. Beekeepers often hold colonies in reserve "just in case," or gambling that in "short" years they can rent those last hives at an elevated price. Also, when the offered price went up, hives not originally intended to go to almonds were loaded up at the last minute and shipped to California (I was in Florida at the start of bloom, and had an inspector tell me of certifying colonies for shipment after the bloom had already begun!).
A number of hives received in November were already headed downhill. Some exhibited the symptom of bees not clustering properly (a typical sign preceding sudden colony depopulation/CCD). Some arrived crawling with mites, or with recent mite treatments in place (suggesting that they were treated too late).
Some graders saw piles of dead bees in front of hives--cause unknown. There were reports of some herbicide tank mixes killing bees.
Many of the placed colonies were below standard grade-- growers paid for less than they expected!
Graders told me that there was a huge variation in hive strength from beekeeper to beekeeper. Many hives were strong (12-16 frames of bees) and healthy; other operations graded at zero to three frames of bees (some of the deadouts had spider webs inside, suggesting that they hadn't been occupied by bees for some time).
The unusual winter chill was tough on colonies that had been stimulated into early buildup, and then forced to contract their broodnests. Some colonies kicked out chilled brood and dead bees afterwards.
Many beekeepers watched their colonies go "backward" prior to bloom.
Colonies from the Southern states (especially those delivered in February) were generally in better shape than those from the Midwest.
Midwestern beekeepers blamed drought, mites, poor nutrition.
Several beekeepers said that their best bees came from remote areas, and their worst from ag areas.
A number of beekeepers admitted inadequate mite treatment; mites were a recurrent theme.
There were a number of reports of EFB hitting colonies.
Some had gotten hit last summer with pesticide sprays, and their colonies didn't recover.
"There were good bees and bad bees from every state. They all seemed to have different problems depending on location/state."
Many good beekeepers simply didn't know what happened to their hives; there were lots of lifeless hives delivered. The atmosphere was ripe with speculation as to the actual causes.
"The shortage was also created by beekeepers that chose not to come to California for a variety of reasons. They can make more money with honey, didn't get paid for what they have brought in the past, bees come back home with mites, beetles and whatever else takes a ride on the hives. Beekeepers don't want to risk bee health to chase the dollar." Many out-of-state beekeepers have had bad experiences going to almonds, and simply don't feel that it's worth it. The supply of bees will largely depend upon the price that growers offer for renting them!
The Silent Majority
Buzzkill leaves one with the impression that the entire bee and almond industries are on the verge of collapse. Of course, the news media focus on fear and disaster, so we may consider taking such dire projections with a grain of salt. In the case of Dan Rather, the focus was on the beekeepers with troubles, not upon those who successfully filled their pollination contracts.
So just how severe was the problem? Let's say that there was an overall shortage of 100,000 hives (a figure that I heard floated)--that would represent only about 6% of the total number of hives placed into almond pollination. The other 94% were successfully delivered (although a proportion of those were weak due to the poor season).
Since the debacle, I've heard from plenty of beekeepers whom I'll refer to as the "silent majority," who experienced "normal" colony winter losses in the 5-25% range, and who successfully filled their pollination contracts. Although the hearts of all beekeepers go out to those who suffered severe colony losses, many felt that some of those losses could have been prevented if the afflicted beekeepers had been more proactive than reactive.
And don't forget those upon whom the rest of the industry depends to supply bees for restocking their deadouts! The California package producers, who have been pollinating almonds for decades, are routinely counted on to consistently take strong hives to almonds, and to then shake over a hundred thousand packages of bees for sale afterwards. Few of these major producers experience severe unexplained colony losses.
Beekeeper Management
By no means am I suggesting that those beekeepers who suffered losses engaged in poor beekeeping practices, but I can't help but notice that not all beekeepers were equally affected--a great number provided strong, healthy colonies to almonds. I've spoken to some of them-the common thread is that those who recognized the problems of poor nutrition and mites in August, and took remedial action for the rest of the season, had acceptable winter losses.
Some beekeepers who really put serious effort and money into bee husbandry were even able to sell "shook bees" from their colonies to others in February! For example, watch Keith Jarrett feeding substantial quantities of pollen supplement to very strong colonies in January [12]--Keith consistently brings very strong colonies to almonds every year, and this year was no exception!
Practical application: I'm here to tell you, that one lesson that I've learned during our intense California drought, is that those yards that I fed with protein in late summer before they started going downhill went to almonds much stronger than those that I didn't feed until fall! Proactive is better than reactive--if you wait until colonies are already going downhill, it is much more difficult to turn them around!
I've often been accused of being politically incorrect for speaking frankly. I'd like to make amends at this point by retiring the rude and unsympathetic term "PPB" (Piss Poor Beekeeping). The fact is that the average wintering loss for the past few years has hovered around 30%. So if you experience 30% losses, you can now proudly call yourself an "Average" beekeeper!
But what about those beekeepers who consistently manage to enjoy lower rates of winter loss? I propose that we call them "Lucky" beekeepers, and the best of them, "Consistently Lucky."
Practical application: the harder those beekeepers work, the luckier they get!
But there were clearly "unlucky" beekeepers this year--especially the "big boys" who brought tens of thousands of hives from the drought-ravaged, and corn-converted Midwest to California. California beekeepers are used to summer drought. We have learned to either move our colonies to better (often irrigated) pasture, or to feed expensive pollen supplements. This would be a very expensive proposition to the larger operators, with hives spread all over the place--a cost not covered by current pollination prices.
What Happened To The Bees This Spring?
Part 2: The Contribution From Pesticides
Randy Oliver
ScientificBeekeeping.com
First published in: American Bee Journal, July 2013
It's pretty straightforward to attribute the majority of colony losses this winter to the usual and aforementioned causes, but a number of beekeepers are also pointing the finger at pesticides. There is no doubt that in certain areas pesticides were a serious issue to beekeepers. Colonies set back by pesticide kills may not fully recover over the season, and those going into winter with pesticide residues may go downhill. There is also reason to suspect that pesticides and miticides have something to do with today's high rates of queen failure.
The bees in some drought-stricken areas were forced to forage on irrigated and pesticide-laden crops--the only place in which there was anything to eat. This changes the entire dynamics of pesticide exposure, since residues would no longer be diluted by the pollen and nectar of non crop plants. The lack of good natural forage also suppresses the ability of colonies to deal with the insult of those pesticides. And colonies may be forced, by necessity, to forage upon one treated crop after another, resulting in multiple exposures.
Practical application: under drought conditions, bees may suffer more from pesticides than when times are good.
Due to the current high prices for agricultural commodities, farmers are often applying pesticides indiscriminately as "risk insurance" rather than due to actual need. A chilling recommendation from an extension entomologist reads:
I encourage you to be risk averse and to make an investment that will pay dividends for your valuable crop. Consider applying [flubendiamide, indoxacarb, or spinosad] for corn earworm. If you have stink bugs and are in the [mature plant] stages, you might want to tank mix one of these products with a pyrethroid. A tank mix of a pyrethroid and acephate are an option, but will wipe out all beneficials [13].
The first three insecticides mentioned are considered to be "reduced risk" to bees if residues are allowed to dry for a few hours, but no mention was made to spray at night. Of the five insecticides recommended above for spraying on corn in tassel, at least four are highly toxic to bees if sprayed during the day! No farmer wants to kill bees, but with recommendations like this from state extension agents, well-meaning growers may unwittingly be hurting pollinators.
Bees in agricultural areas are exposed to a vast array of insecticides, miticides, fungicides and surfactants--many of which have clear links to colony health problems. And applications of new mixes of chemicals are up. For example, in addition to the neonicotinoid seed treatments, granular insecticide soil treatments for corn in the Midwest were up by 30% over the previous year [14]. These treatments consist of combinations of organophosphates and pyrethroids.
But I'm not hearing either the bird groups or beekeepers even addressing these treatments! It is scary to read the sales literature for Counter insecticide, the organophosphate terbufos [15]. Growers are encouraged to apply it at planting time, despite the facts that:
"Terbufos is highly toxic to birds, fish, and aquatic invertebrates [and bees]. [It] shows significant acute mortalities of birds, mammals, reptiles, and fish resulting from broadcast application...In the same study, the application of terbufos as a soil-incorporated treatment to corn...resulted in acute mortalities to birds and reptiles" [16].
Terbufos is strongly systemic, meaning that it is absorbed by the plant roots and could be expected to be expressed in the pollen and nectar.
It can synergize with other pesticides since it ties up the critical CP450 enzymes used in detoxification, to the extent that growers are cautioned that it can cause problems to corn from herbicides [17].
During drought, certain insect pests become more problematic, perhaps resulting in increased exposure to insecticides by bees. For example, drought encourages corn leaf aphids. Read this chilling recommendation for aphids on corn during tasseling (when bees are actively foraging):
If less than 50% of pollination has occurred, aphids and honeydew are covering tassels and plants are stressed, an insecticide may be necessary to ensure adequate pollination, but treatments need to be made within 48 hours of tassel emergence. Asana XL, Brigade, Capture, Cobalt, Dimethoate, Lannate, Lorsban, or Malathion may be used for control [18].
Or this:
Prolonged drought always raises the specter of two-spotted spider mite outbreaks in soybeans and corn. As the 2012 drought intensifies in Minnesota, infestations are reaching treatable levels...The only products that are recommended for spider mites in soybean include insecticides containing chlorpyrifos, dimethoate and bifenthrin[18].
The names of the recommended insecticides above strike fear into the hearts of beekeepers!
Practical application: many "consistently lucky" beekeepers go to great effort to allow their colonies to recover after exposure to pesticides--moving them to unsprayed areas or natural forage, or by immediately feeding protein supplement to stimulate increased broodrearing. Unfortunately, such "recovery" areas are getting harder and harder to find.
The Lynch Mob
Despite the fact that a wide range of bee-toxic insecticides are being applied (often during bloom) to corn, soy, sunflowers, alfalfa, cotton, and other major crops, if you Google anything about insecticide use, you'll quickly find that the blogosphere focuses only upon the putative link between a single class of insecticides--the neonicotinoids-and the demise of pollinators [19].
People look at me incredulously when I point out that there is zero firm evidence to date that the neonic seed treatments are a serious problem! But the notion that all honey bee problems are caused by an insidious new insecticide resonates with a distrustful public [20], and has firmly established itself as "common knowledge." But repeating something does not make it true!
"It's easier to fool people than to convince them that they have been fooled"-Mark Twain
Practical application: the question is, "Are the neonic seed treatments being railroaded into a guilty verdict in the media's kangaroo court of public opinion?"
One group recently brought suit against the EPA to ban the use of the seed treatments clothianidin and thiamethoxam [21], neither of which even make California's top 100 list of pesticides applied [22], nor that have ever been demonstrated to harm colonies feeding on the pollen or nectar of seed-treated plants! A number of people have made up their minds that the neonics are the main cause of colony collapse, and it appears that no amount of facts to the contrary will cause them to reconsider!
Debunking The Myths
As anyone who knows me will tell you, I am a stickler for honesty, accuracy, and factuality. I am concerned about the amount of misinformation and speculation going around about the neonics. So let's look at some of the claims vs. the actual facts.
Arguments Against Neonic Seed Treatments Actual Facts
The neonicotinoids have been "linked" to increased colony mortality. In actuality, such a "link" is merely an urban legend, and has never been demonstrated or confirmed in any study.
On the other hand, the residues of other classes of pesticides are more suspect for causing increased brood or adult bee mortality [24].
The timing of CCD coincides with the introduction of the neonic seed treatments in 2004. CCD started in California bees in the winter of 2004/2005, prior to them ever being exposed to seed-treated crops.
But what else could have changed at that time other than the introduction of neonics? In California, Dr. Eric Mussen [25] determined that the increased colony losses were due to poor summer forage and failure of mite control products (just as this last winter).
There is actually a much stronger association between the incidence of the novel gut parasite Nosema ceranae and increased colony mortality [26].
But the main thing that has changed is the dynamics of the varroa/virus complex, which coincidentally occurred at about the same time that the neonics came into use.
European countries banned the neonics, and the bees recovered after those bans. A few countries placed temporary suspensions on certain seed treatments until planting dust issues were resolved [27]--only Germany has one suspension still in place. The foliar applications were not suspended. The suspensions did not resolve bee health problems.
The European Food Safety Authority recently decided that neonics pose a threat to bees. "The Center for Regulatory Effectiveness (CRE) has recently completed a Data Quality Act (DQA) Alert on the ... (EFSA) report on neonicotinoids which found that neonicotinoids pose a risk to bees. The DQA Alert outlines the serious deficiencies of the EFSA report and demonstrates why the EFSA report violates the DQA...In particular, the EFSA report failed to maximize the objectivity of the data by failing to reconcile numerous studies whose conclusions contradicted the findings of the EFSA report" [28].
Several lab studies have found that neonics affect individual bee behavior, longevity, or immunity. True -- although many studies used unrealistically high doses. The question is whether such artificial studies apply to actual colonies in the field. The numerous field studies to date have failed to find any link between seed treatments and later colony health issues.
It is the seed treatments that make corn a problem. As Bret Adee points out in Buzzkill, corn is replacing pastureland (Fig. 4). Corn, as grown today, is a virtual "bee desert" (similar to the way in which suburban lawns are green bee deserts). And it's not only the bees that this is affecting, the populations of birds and other wildlife are plummeting due to loss of favorable habitat (see my blog on birds and neonics [29]).
A recent survey by Dr. Jerry Bromenshenk found that bees actually avoid field corn pollen, and are exposed to very little of the seed treatment residues [30].
Numerous independent studies, and the experiences of stationary beekeepers throughout the Corn Belt, support the conclusion that colonies can thrive when surrounded by corn, provided that there is some alternative forage within flight range.
As the use of neonic seed treatments increases, bee mortality goes up. In actuality, colony mortality rates go up and down year to year, largely dependent upon weather and varroa mite control. If the neonics were to blame for this winter's bee losses, why didn't they cause similar losses last winter, in which the colony mortality rate was the lowest in years?
French beekeepers also started seeing problems with the introduction of the neonics. I've spoken with beekeepers in France whose apiaries are in pesticide-free areas. They tell me that they experience the same sorts of colony mortality problems as do those in areas exposed to neonics.
Bees in the U.S. are commonly exposed to neonicotinoids. In the most recent USDA survey (100 samples across the country), imidacloprid was only detected in 9% of the samples [31] (although I found some of the residue levels alarmingly high). However, the most common seed treatment, clothianidin (or its degradation products), was not detected at all!
The above real-world data suggests that efforts to ban clothianidin as a seed treatment may be misplaced. It appears that imidacloprid, especially as a foliar application, would be of more concern.
Neonics are the most common pesticides that bees are exposed to. In the above survey, other serious insecticides were more commonly prevalent: chlorpyrifos (in 20% of samples), cyhalothrin (in 7%), and endosulfan (in 11%).
Notably, there was also a high prevalence of beekeeper-applied miticides: fluvalinate (in 38%), coumaphos (in 87%), amitraz (in 27%), fenpyroximate (in 11%), and thymol (in 27%).
There was even higher exposure to fungicides and adjuvants.
It is misleading for the pesticide companies to blame the problems on varroa, nosema, or poor nutrition. The above survey (over 1000 samples) found that the average varroa infestation rate in the U.S. in autumn is above the danger level for virus epidemics!
Sixty to 100% of hives are infected with nosema in December.
Summer drought has historically been associated with high winter mortality.
But didn't the planting dust from corn seeding kill colonies in Ontario? Planting dust is separate issue that clearly needs to be remedied. It does on occasion cause bee kills, for which beekeepers are rarely compensated. This situation must change! All parties are actively working on solutions [32].
Bees in certain agricultural areas tend to go downhill later in the season. This has been observed for a long time--long before the neonics. The question is, which chemicals, chemical synergies, or chemical/nutrient interactions are responsible? The Frazier/Mullin team at Penn State has developed a protocol for helping to figure this out. I strongly support its adoption by the EPA for pesticide risk analysis.
Colonies foraging upon nectar or pollen of seed-treated crops get poisoned. Ask yourself this: if neonic residues were actually so harmful to bees, how is it that the Canadian beekeepers, whose bees forage largely on seed-treated canola, feeding solely upon a diet of canola nectar and pollen with well-documented residues of clothianidin, experience very low winter losses, despite the long Canadian winter (so long as they control varroa and nosema)?
And how is it that the vast majority of beekeepers in the U.S. Corn Belt report that their colonies thrive and that they have far fewer pesticide issues these days than in the past?
The neonicotinoids are "systemic," meaning that they are in the plants all the time! True, but this property is not unique to the neonics--a number of other insecticides also go systemic. In any case, with seed treatment, the concentration of the insecticide in the plant is only high when the plant is young--it gets diluted as the plant grows (e.g., clothianidin in canola is at a level high enough to kill aphids for only about the first 30 days of growth).
The only time that residues in the plant matter to pollinators is when the mature plant flowers. The amount of seed treatment is carefully calibrated so that the residue in the pollen and nectar are below the level that causes demonstrable harm to bees.
In the case of foliar, drench, or chemigation applications prior to bloom, there are greater possibilities for bees to be exposed to toxic levels.
There are fewer butterflies and pollinators in the fields these days. Not surprising, since the new push for "clean farming" has removed the host plants upon which the butterfly larvae feed. Pollinators are forced to subsist upon the stretches of weeds growing along roads at the edges of fields. But surprisingly, pollinators may be abundant there, suggesting that even though populations as a whole are reduced by habitat conversion, it is that, rather than the use of seed treatments, that causes the population declines.
The evil pesticide companies want to kill honey bees. Give me a break! Does anyone truly believe that anyone wants to kill honey bees? What pesticide company would want the bad press of being associated with killing bees? The chemists and biologists on their staffs earnestly work to develop insecticides that are bee friendly.
The EPA is being derelict in their duty to protect pollinators. I have spoken at length with EPA staff, and reviewed their risk assessments, as well as those by, DEFRA, EFSA, PMRA, and other regulatory agencies. I find that the risk assessors have not overlooked any evidence, are well-informed on the subject of neonics, and are justified in their assessments that the on-the-ground evidence (to date) indicates that neonic seed treatments pose acceptable risk to pollinators.
We must all remember that the tobacco industry tried to hide the fact that nicotine was addictive [33]. Spare me! Does anyone seriously think that the EPA is unaware that industry executives may stretch the truth? Of course the EPA is skeptical of any reassuring claims by the pesticide industry--that's why they go over all studies with a fine-toothed comb!
This winter's losses spell the end to commercial beekeeping. The fact of the matter is that many observers note that the bee supply for almonds often follows a boom-bust cycle. Although losses were high this year, the trend for the last decade has been for beekeepers keep ramping up the supply of bees for almonds. So long as growers are willing to pay a profitable rental rate for colonies, market forces will encourage the bee industry to meet the demand (for a detailed analysis, see [34]).
The Precautionary Principal
"But," you say, "shouldn't we exercise precaution due to the lab studies that find adverse effects from the neonics?" Look, I make my living as a beekeeper, I'm not out to sell insecticides, and am as concerned as the next person about the environment and the safety of the food I eat. I've researched the neonics exhaustively, and addressed them in several articles [35]. I am acutely aware that there are suggestions that the neonics may be causing insidious effects in the environment, and I've studied the excellent environmental document Late Lessons from Early Warnings [36], which hammers the message that we should use the "precautionary principle" when dealing with chemicals. The problem is, there is nothing without risk--for example, you have a 1 in 83 chance of being killed in an auto accident in your lifetime. But most people still take the risk of getting into cars, since they feel that the benefit outweighs the clearly high risk!
My practical perspective as both a scientist and a beekeeper: if researchers perform lab studies on any insecticide, they will find that there are all kinds of negative effects upon bees--this should be pretty obvious, since insecticides are specifically designed to harm insects! However, the majority of these studies are taken out of the context of full colonies under field conditions, where bees fly free and choose the flowers upon which they forage. The evidence to date supports the contention that the neonics, properly used as seed treatments, are indeed an improvement over other insecticide options.
As Dr. Eric Mussen succinctly notes:
Nobody's really been able to show that [the neonicotinoids] are more problematic than the rest [of the pesticides to which bees are exposed] [37].
Far be it from me to suggest that the neonics (or any other pesticides) are harmless! But consider this--if the neonic seed treatments were indeed as harmful as some make them out to be, you'd think that after a decade of intense study that at least one researcher could have come up with a single solid piece of field evidence against them!
Let's do a thought experiment. Why doesn't someone simply put a bunch of healthy hives into the middle of seed treated crops and see whether they die afterward? Oh, I forgot--this experiment has already been run by thousands of beekeepers year after year in the Corn Belt and the Canadian prairie! And those beekeepers have invited me to look at their colonies, sent me photos of colonies stacked head high with honey supers, and bragged about their high winter survival!
Some will argue 'til they're blue in the face, but the fact remains that virtually every beekeeper that I've spoken with in the Corn Belt and in canola areas feels that the seed treatments are not a problem [38]. In fact, most tell me that this is the best it's ever been as far as bees and pesticides!
Common sense: I just don't get what is so hard to understand about the reality that there are thousands of colonies thriving year after year in areas of intense seed treatment? To any reasonable person it would suggest that the treatments are causing little noticeable harm other than the occasional planting dust kill, which I have repeatedly stated is a problem that needs to be corrected!
See For Yourself
Let's look at actual independent (from the manufacturer) data from corn and canola areas:
Corn
I asked friends in the Corn Belt if they had any data on winter losses. It so happens that the Michiana Beekeepers Association has been collecting exactly that since the spring of 2010 (Fig. 11).
Figure 11. Percentage of winter losses by the "Michiana" hobby beekeepers. The 2013 figure is as of mid March; it may eventually go down a bit due to a prolonged cold spring. Note that the winter survival rate appears to be linked to average winter temperature. Thanks to beekeeper Danny Slabaugh for sharing the data; temp deviations from [[i]].
[i] http://www.ncdc.noaa.gov/temp-and-precip/maps
How could the above be? Eighty percent winter survival despite sitting in the middle of seed-treated corn and soy? So of course I did a fact check to confirm that those beekeepers were indeed sitting in corn/soy areas (Fig. 12).
Figure 12. USDA land cover categories for the region in which the Michiana hobby beekeepers keep bees--corn and soy acreage is color coded yellow and green, respectively. The selected area is the top half of Indiana and bottom of Michigan, with Lake Michigan at the left. Clearly, these apiaries were exposed to seed-treated corn and soy! I created the map at [[i]].
[i] http://nassgeodata.gmu.edu/CropScape/
The above figures suggest that colony winter survival for stationary hobby beekeepers in the above corn/soy region is higher than the national average, despite the fact that about half of them don't even treat for mites! They also suggest that the neonics or other pesticides used in corn/soy in that region do not cause excessive winter loss. Finally, the data indicate that a main factor for winter loss rates is the winter temperature.
Canola
I've heard some beekeepers saying that their bees crashed after working canola, suspecting that the seed treatments were the problem. So as a reality check I called a Dakota beekeeper who has been running bees to canola for over a decade--some 10,000 hives last season. He tells me that colony strength after canola varies from year to year, but that he sees no problem with the seed treatments. He did point out that beekeepers should be aware that colonies can plug the broodnest on intense canola flows.
The biology: The plugging out of the broodnest during an intense bloom means that three weeks afterward, there will be few emerging workers to take the place of the worn-out foragers, and the colony population will temporarily plummet. Even worse, the remaining mites are then concentrated onto fewer bees--which can initiate virus epidemics. These colonies must then attempt to rebuild from scratch, starting in August, meaning that the weakened, mite-infested colonies faced three long months of drought last summer for that rebuilding process.
Every field study that I've seen for canola also supports the conclusion that the seed-treatments are safe for bees. I joined other beekeepers and regulators in observing a large-scale study of seed-treated canola in Canada [41]. Canola (or rapeseed) is likely the best test crop, since bees eagerly (and virtually exclusively) forage upon it for both pollen and nectar, meaning that every bit of their food supply contains contain easily verifiable residues of the insecticides. The preliminary results indicate that the clothianidin seed treatment did not harm the colonies [42].
Another recent independent long-term field study in Poland [43] came to the same conclusion. In it, the researchers followed 50 colonies for more than two years under field conditions as they foraged on five different large fields of oilseed rape treated with various combinations of five different neonicotinoids applied by seed treatment and spraying. Pollen and nectar samples were taken, and demonstrated that the bees were clearly exposed to normal residues of the insecticides (there was also additional exposure to other common agricultural pesticides). The colonies were monitored for health, brood, strength, nosema, viruses, and winter survival, and compared to two control apiaries set in an area free of the crop. The results?
During the time from the placing of the colonies on the rape fields until wintering, the colonies developed properly in all groups... All colonies overwintered properly... In both years, during the period of being placed in the oilseed rape fields as well as after being moved to the stationary apiary, none of the groups showed disturbances in development or functioning.
Following a paper that suggested that the seed treatments would impair bumblebee colonies' ability to rear queens, DEFRA performed a common-sense field study last year [44]. Their findings:
...the study has shown that bumble bee colonies remained viable and productive in the presence of the neonicotinoid pesticides under these field conditions...The study underlines the importance of taking care in extrapolating laboratory toxicology studies to the field, as well as the great need of further studies under natural conditions.
Sunflowers
Some beekeepers report that their colonies later crashed after they chased sunflowers last summer for honey. One must keep in mind that sunflowers are not a natural food for honey bees, and provide only poor-quality, nutritionally-inadequate pollen [45]. But the main problem with putting bees on sunflowers may be related to the fact that sunflowers are a native plant--meaning that there are a number of native insects that evolved to feed upon it:
Maximum seed yields often require the use of insecticides to protect the crop from insect competitors. Unfortunately, many of the major insect pests of sunflower attack the crop when it is flowering. Thus, insecticides used to control the pest also harm pollinating bees [46].
If sunflowers are the only forage available, colonies may eventually go downhill, due to the one-two punch of poor pollen nutrition coupled with insecticide exposure. And which pesticides would those be? One scary list- Asana XL, Baythroid, endosulfan, Furadan , Lorsban , methyl or ethyl parathion, , Proaxis, Scout X-TRA, Sevin, Warrior, Mustang Max, Declare, Cobalt, Yuma, Delta Gold, and Grizzly Z [47]!
Note that none of the above are neonics, other than seed treatments for wireworms. Surprisingly, field evidence indicates that the seed treatments only "stun" the wireworms for a while [48], which certainly raises the question as to how harmful they might be to bees months later when the plants flower! I will return to sunflowers below.
Be Careful What You Ask For!
Allow me to assure you that I am no pitchman for neonics or any other insecticide--the typical farmer practices far too little integrated pest management, and applies far too many pesticides! All insecticides (and several fungicides and adjuvants) cause problems to pollinators--the neonics are no exception. Any systemic insecticide has the potential to harm bees when applied as foliar applications, by chemigation, or to flowering trees, but it there is no compelling evidence that the neonics are any worse than the alternatives in most applications. On the contrary, there is quite a bit of evidence that they may often be "safer" ("reduced risk").
If the neonic seed treatments were banned, it's not as though all agriculture is suddenly going to go pesticide free--only about 1% of U.S. cropland is registered as "organic"! We must consider the likely alternatives. The products that farmers would then use to control insects would need to be sprayed all over the cropland--we'd then be back to the problem that the bulk of sprayed insecticides go into the environment without ever hitting the intended pest!
I hear from knowledgeable beekeepers that worse than in previous years, some of the new formulations of the spray-applied insecticides [49, 50, 51] can really knock the snot out of bees! One large beekeeper found his hives already dead before moving them away from the fields. Again, this was not a neonicotinoid issue.
Practical application: no one is saying that the neonics are "harmless." The question is whether they are better or worse than the alternatives.
The Effect Of Drought
Let's discuss some of the problems (or suspected problems) with the neonics last season. The record warm and dry spring appeared to exacerbate corn planting dust issues (corn seeds are the worst offender due to their non spherical shape). Beekeepers in some areas of the Corn Belt, the East Coast, and in Ontario suffered from confirmed (in at least some of the cases) planting dust kills (although many went on to make good honey crops after their colonies recovered). The final analysis from Ontario is not yet completed, but dry soil conditions and an early clover bloom likely contributed to the problem. Regulators and the seed companies are working on solutions to the problem [52]. Still, IMHO it is unacceptable to ask beekeepers to bear the burden of bee kills without compensation, and no one could blame the affected beekeepers for being pissed!
Drought-stressed plants
There are a number of advantages to the neonic seed treatments. Besides their safety to the farmer and to most wildlife, there is virtually no way for the farmer to misapply them! The timing of application is only at planting time (when bees normally have little interest in the bare fields), and the dose is determined by the seed-treating company. This means that the applicator can't be tempted to apply at the wrong time, or to over apply too strong a dose (however, their excessive near universal use can be expected to accelerate the development of resistant pests).
That said, beekeeper Bret Adee brought an interesting question to my attention: the dose of seed-applied systemic insecticides (whether neonic or other) is based upon the dilution factor as the plant grows, so that the residues in nectar and pollen will be reduced to below the "no observed adverse effects level." But what happens during drought, when the water-stressed plants only grow knee high before desperately flowering? There would be far less plant biomass in which to dilute the insecticide (assuming that drought-stressed plants absorb the same amount from the seed treatment).
Certain plants (including sunflowers and canola) are known to "hyperaccumulate" toxic metals [53], perhaps more so during drought. Could this also be the case with systemic insecticides? Something that's been stuck in the back of my mind is that Bonmantin [54] found that the concentration of imidacloprid first drops in sunflower plant tissue as it grows, and then reconcentrates in the flower heads.
It occurs to me that the translocation of systemic insecticides is generally studied in plants grown under "normal" conditions. I'd very much like to see data for residues in pollen and nectar from seed-treated plants grown under drought. Had we thought of this earlier, we could have collected pollen and nectar samples from drought-stressed plants last summer. I'm currently trying to track down any data or samples from such plants--if any reader has any such sample analyses, please let me know!
Practical application: the above hypothesis is speculative, but we need actual data from drought-stressed plants to see whether such an effect occurs. If so, it would need to be taken into consideration for the registration of seed treatment products!
Once planting was completed and the drought took its toll, the reports that I've heard are that soybean honey saved a lot of bee operations this season, right in the middle of treated corn/soy farmland. In this case, seed treatment with neonicotinoids may have been a blessing to beekeepers:
The benefits of [seed treatment] not only include the early-season disease control but also suppression of soybean aphids for quite a ways into the growing season. With it, we typically make only one foliar insecticide application for aphid control, usually in August, instead of two applications when [treatment] isn't used. In 2012, with the extremely dry conditions in mid-season, there wasn't as much of an aphid problem, and we treated just 300 acres of soybeans...Last year we sprayed closer to 30,000 acres for aphids [55].
On the other hand, some beekeepers on alfalfa or cotton got hit hard by other classes of insecticides. A hit from a pesticide application can lead to poor subsequent colony performance, queen failure, dwindling, or winter collapse. ABJ published an excellent series of articles on pesticides by Drs. Barbara and Eric Erickson in 1983; Editor Joe Graham has graciously granted me permission to post copies of those articles to my website [56]--I strongly suggest any beekeepers interested in pesticide issues read them! In the second article, the authors discuss both the problems with systemic insecticides and of sublethal effects--note that these articles were written long before the introduction of the neonics!
An anti-pesticide group, along with a handful of beekeepers, recently filed suit against the EPA [57], calling for an immediate ban on the two most common neonicotinoid seed treatments, despite the easily-verifiable fact that hundreds of thousands of colonies thrive in the midst of seed-treated corn, soy, and canola! To me, this suit smacks of being some sort of well-orchestrated publicity stunt, and does not serve the interests of either beekeepers or environmentalism. Worse, it now gives the powerful farm lobby cause to label beekeepers as "radical" enemies.
We don't want this battle: do we really want to take on the farm lobby by backing them into a corner? The French beekeepers took a similar case against fipronil all the way to their supreme court and lost [58, 59]-worth reading]. Agriculture is already positioning itself for a fight [60, 61, 62]. Think about it--the EPA lives in fear of a conservative congress slashing their funding. Does anyone really think that they are going to go against the agricultural lobby without unimpeachable evidence? We should also think twice before calling for a ban on the seed treatments--the alternatives are not pretty!
It disturbs me to hear industry executives and lawyers stretching the truth or misrepresenting data. It disturbs me even more to hear my fellow environmentalists and beekeepers doing so! If we wish to maintain credibility, we should hold ourselves to a higher standard. The question we must ask ourselves the way in which we wish to have pesticide regulation decisions made:
1. By the EPA (the Environmental Protection Agency), whose risk assessors carefully study and weigh all available research and evidence in order to make objective and rational decisions, or
2. To have it decided instead by impassioned, fearful, and often misinformed advocacy groups who hire lawyers and pressure politicians who know little about the subject?
We depend upon the EPA to strike a balance between the availability of cheap food and profitability for those who provide it, versus the risks to human and environmental health and safety. It is good to have activists on both sides of the issues (industry and the anti-pesticide groups) to keep the EPA informed. But I don't feel that either of those groups should be telling the EPA which pesticides to register or to ban! Let the regulators do their job!
Rather than wasting EPA's funding to fight frivolous lawsuits, there are more productive actions that we can take:
Help the EPA to do its job by filing "adverse effects incident reports" if you observe a problem due to pesticides [63]. EPA is begging beekeepers to do this! Unless they have documented reports of pesticide problems, their hands are tied as to restricting the uses of those pesticides!
Support the National Pollinator Defense Fund [64]. Our industry is currently represented by a reasoned and knowledgeable group of (mostly) beekeepers. (Challenge to the pesticide companies: why don't you stand behind the safety of your products and donate? The NPDF is about ensuring that your pesticides are properly applied, so there would be no conflict of interest).
If your local state lead agency is not actively investigating bee kills or enforcing pesticide regulations, then use the local media to embarrass them into action!
Keep pressure on the EPA to resolve corn planting dust problems. Here's a wild idea: I'm not sure of the exact figures, but let's say that 90% of the 95 million acres of corn is grown from neonic-treated seed. If the states were to levy a surcharge of 50 cents per acre (neonic seed treatment adds about $12 per acre to seed costs), they could collect over $42 million each year to fund a pool from which to indemnify the occasional beekeeper who suffers a confirmed kill from planting dust!
Tell Congress that we'd like to see wording added to the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) to specifically protect pollinators. Currently, such protection is nebulous (although the EPA is acutely aware of pollinator issues): "The Administrator shall register a pesticide if... when used in accordance with widespread and commonly recognized practice it will not generally cause unreasonable adverse effects on the environment." Unless there is specific wording to protect pollinators, bee kills may not be considered to be "unreasonable"!
We need far more independent field studies to determine which pesticides and application practices are actually causing harm to pollinators. For pesticides in question, keep pressure on the EPA to require additional field trials to demonstrate whether they are indeed safe for pollinators under field conditions. I'd like to see the establishment of monitoring apiaries (and patches of untilled land) in representative agricultural areas nationwide, with the hives in each apiary to be carefully managed by independent parties. Such apiaries and sites could then be closely monitored each summer to see whether honey bees and other pollinators are able to survive local pesticide practices.
Give farmers workable options! Disseminate and promote bee-friendly agricultural practices that don't hurt the farmers' bottom line. For example, by adopting IPM practices, Arizona cotton growers reduced insecticide spraying from 12.5 times a season to only 1.3 times (cutting insecticide use twentyfold), while using more environmentally-friendly insecticides [65]! Another recent study in Iowa found that adding additional clover or alfalfa rotations in corn/soy farmland was equally profitable, improved the soil, used less energy, used far less pesticides, and decreased water pollution [66].
Business and agriculture respond to consumer demand. Consumer demand stopped most dairymen from injecting their cows with the hormone BST. Consumers could do the same by demanding pasture-fed beef and dairy (which would create more pollinator forage)! I'd also like to see the expansion of consumer choices (other than organic certification) that reward farmers who manage their lands to the benefit of wildlife and pollinators. For ideas, see [67. 68. 69].
Bottom Line
In conclusion, it appears that a perfect storm of a preceding exceptionally warm winter, followed by serious drought across the country, the lack of good mite control, a high prevalence of pathogens, and an unexpected California chill in the orchards prior to bloom, resulted in an unusual degree of colony losses. In other words, rather than one specific cause, there were simply not enough of the good things, and too many of the bad things.
I don't see evidence that pesticides were the major factor in the shortage of bees in almonds this winter, although, as usual, a number of individual beekeepers on certain crops certainly took serious hits.
And how about the fear that there won't be enough bees for almond pollination next year? Beekeepers have already told almond growers to expect higher pollination prices next year (especially since California is again going into serious drought, and beekeepers will be forced to invest extra money in feeding their hives). Most every beekeeper I know is madly making increase right now in anticipation of higher pollination prices next season. The fact of the matter is that should conditions allow beekeepers to successfully rebuild their numbers (following the typical swings of our boom/bust cycle), there could possibly even be a glut of bees for almonds next winter!
Feedback And Corrections
A few countries placed temporary suspensions on certain seed treatments until planting dust issues were resolved [27]--only Germany has one suspension still in place. - Actually there are some more: France (Thiamethoxam in oilseed rape, Imidacloprid in corn and sunflower), Italy (all Neonic seed treatment in corn), and Slovenia (Imidacloprid, Thiamethoxam, and Clothianidin seed treatment in all crops)
French beekeepers also started seeing problems with the introduction of the neonics; I've spoken with beekeepers in France whose apiaries are in pesticide-free areas. They tell me that they experience the same sorts of colony mortality problems as do those in areas exposed to neonics - This is, by the way, likewise confirmed by monitoring results from the French authorities.
In the case of foliar, drench, or chemigation applications prior to bloom, there are greater possibilities for bees to be exposed to toxic levels. - This is not the case for foliar application: as Neonics are xylem-systemic, but hardly mobile in the phloem, they can only be distributed in a plant after root uptake, but not be translocated for instance from a leaf to a later developed flower.
Then, on the topic of systemic residues in plants under drought stress: first, I am quite sure that the decrease of concentration in seed-treated plants over time is not only due to dilution, but also to degradation of the compounds - a factor that is not specifically dependent on water availability for the plants (e.g. photodegradation!); second, even if there would be less dilution in plants under drought stress: the concentrations in nectar and pollen of treated crops are normally so low (when we consider average rather than peak concentrations, and when we consider scenarios where colonies have chronically access exclusively to contaminated nectar/pollen over months unlikely in practice), that even an increased concentration due to drought stress-affected plants should not make a significant difference: if we for instance assume an average concentration of let's say 3-4, or even 5 ppb Clothianidin in corn pollen, and likewise assume a dilution reduced to 50% (which is probably exaggerated), then we would still not end up with excessive residues. And finally, we have residue figures from crops grown in different countries, different climatic conditions, and different agronomic practices; though we have not specifically addressed the drought stress scenario, we have seen that residue figures are quite consistent over all scenarios, and there does not appear to be strong evidence that different environmental conditions would substantially (i.e. by orders of magnitude) and systematically alter residue concentrations.
Dr. Christian Maus
Global Pollinator Safety Manager
Bayer CropScience
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A ppt on the impact of CRP lands on wildlife in North Dakota
http://www.redriverbasincommission.org/Conference/Proceedings/26th_Proceedings/Kading_RRBC_09.pdf
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Feedback from a Midwestern apiary inspector:
Just a quick update: This beekeeper who recently told his local newspaper that pesticides were killing his bees, he was making excuses. We examined two of his yards with him yesterday. One yard was showing EFB throughout the whole yard. I think his "mid-summer losses" last year (half of that yard's hives) were EFB kicking in with the mid-summer dearth. In his other yard, most of his dead outs were obvious starve outs. He harvested all of their stores with the first frost, and then didn't feed them. So, in my opinion, and from my observations, pesticides are usually being used responsibly, and aren't killing honey bees. I also think, with the aggressive way bees were on soy fields last summer, the systemic pesticides are not harmful to honeybees. I'm not seeing honey bee problems other than EFB getting the upper hand, due to our cold, late spring. My two cents. Thanks.
References
[1] http://www.frequency.com/video/dan-rather-reports-buzzkill/87705620/-/YouTube
[2] http://www.ars.usda.gov/is/pr/2012/120531.htm and California DPR.
[3] http://www.ncdc.noaa.gov/temp-and-precip/maps.php
[4] Wright, CK & MC Wimberly (2013) Recent land use change in the Western Corn Belt threatens grasslands and wetlands. https://www.motherjones.com/files/pnas201215404_nwow5w1.pdf
[5] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
[6] https://scientificbeekeeping.com/sick-bees-part-2-a-model-of-colony-collapse/
[7] vanEngelsdorp, D, et al (2013) Idiopathic brood disease syndrome and queen events as precursors of colony mortality in migratory beekeeping operations in the eastern United States. Preventive Veterinary Medicine 108(2-3): 225-233. http://www.sciencedirect.com/science/article/pii/S0167587712002656
[8] https://scientificbeekeeping.com/sick-bees-part-18a-colony-collapse-revisited/
[9] http://almondinsights.com/692, http://agfax.com/almonds/2013/reports/03042013-almonds-web.htm
[10] https://scientificbeekeeping.com/sick-bees-part-18a-colony-collaspse-revisited/
[11] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2010-2011-Limited_Survey_Report.pdf
[12] http://www.youtube.com/watch?v=y6B5qm2ut18, http://www.youtube.com/watch?v=PYbLbhZXizY
[13] (Broken Link!) http://www.nccrops.com/2012/07/27/insecticide-recommendations-for-corn-earworm-in-soybeans/
[14] http://www.agriview.com/news/crop/corn-soil-insecticide-use-up-dramatically-to-combat-widespread-rootworm/article_5d09decc-5b40-11e2-b485-001a4bcf887a.html
[15] http://www.amvac-chemical.com/products/documents/Counter20G%20Tech-Sell%20Sheet%20-%202013.pdf
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[17] http://www.lewishybrids.com/PDF/3-5-2013Agronomic+ALERT+-+Interaction+between+herbicides+insecticides+corn.pdf
[18] http://pest.ca.uky.edu/EXT/Recs/ENT16-Field%20corn.pdf
[19] (Broken Link!) http://www.soybeans.umn.edu/crop/insects/spider_mites.htm
[20] http://www.nytimes.com/2013/04/07/opinion/sunday/calamity-for-our-most-beneficent-insect.html?nl=todaysheadlines&emc=edit_th_20130407&_r=0
[21] http://www.nytimes.com/2013/04/07/opinion/sunday/calamity-for-our-most-beneficent-insect.html?_r=0
[22] http://www.panna.org/press-release/beekeepers-and-public-interest-groups-sue-epa-over-bee-toxic-pesticides
[23] http://www.cdpr.ca.gov/docs/pur/pur10rep/top_100_ais_lbs10.pdf
[24] http://www.extension.org/pages/60318/pesticides-and-their-involvement-in-colony-collapse-disorder
[25] Mussen, EC (2006) Chaotic almond pollination. http://entomology.ucdavis.edu/faculty/mussen/JanFeb2006.pdf
[26] https://scientificbeekeeping.com/sick-bees-part-18e-colony-collapse-revisited-genetically-modified-plants/
[27] http://www.epa.gov/pesticides/about/intheworks/ccd-european-ban.html
[28] http://www.thecre.com/oira_pd/wp-content/uploads/2013/04/DQA-Alert-EU-Commission-Ban-on-Neonicotinoids-4-10.pdf
[29] https://scientificbeekeeping.com/home/news-and-blogs/
[30] Henderson, CB, JJ Bromenshenk, DL Fischer (2013) Clothianidin exposure levels from bee-collected pollen and nectar in seed-treated corn and canola plantings. Proceedings of the American Bee Research Conference.
[31] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
[32] http://www.ontariograinfarmer.ca/MAGAZINE.aspx?aid=534
[33] http://www.pbs.org/wgbh/pages/frontline/shows/settlement/timelines/april94.html
[34] https://scientificbeekeeping.com/2012-almond-pollination-update/
[35] https://scientificbeekeeping.com/neonicotinoids-trying-to-make-sense-of-the-science/, https://scientificbeekeeping.com/neonicotinoids-trying-to-make-sense-of-the-science-part-2/, https://scientificbeekeeping.com/testing-of-bee-feed-syrups-for-neonicotinoid-residues/
[36] http://www.eea.europa.eu/publications/late-lessons-2
[37] http://www.sciencefriday.com/playlist/#play/segment/9088
[38] https://scientificbeekeeping.com/the-extinction-of-the-honey-bee/
[39] http://www.ncdc.noaa.gov/temp-and-precip/maps
[40] http://nassgeodata.gmu.edu/CropScape/
[41] https://scientificbeekeeping.com/a-new-large-scale-trial-of-clothianidin/
[42] http://www.producer.com/daily/ontario-field-study-finds-no-link-between-seed-treatments-bee-deaths/
[43] Pohorecka, K, et al (2013) Residues of neonicotinoid insecticides in bee collected plant materials from oilseed rape crops and their effect on bee colonies. Journal of Apicultural Science 56(2): 115-134. http://www.degruyter.com/view/j/jas.2012.56.issue-2/v10289-012-0029-3/v10289-012-0029-3.xml?format=INT
[44] http://www.fera.defra.gov.uk/scienceResearch/scienceCapabilities/chemicalsEnvironment/documents/reportPS2371Mar13.pdf
[45] http://repository.up.ac.za/bitstream/handle/2263/20334/Nicolson_Chemical(2012).pdf?sequence=1
[46] (Broken Link!) http://www.ag.ndsu.nodak.edu/aginfo/entomology/entupdates/Sunflower/a1331sunflowerhandbook.pdf
[47] http://www.sunflowernsa.com/growers/approved-chemicals/insecticides-test/
[48] http://www.mydigitalpublication.com/publication/?i=151958&p=41
[49] http://www.sunflowernsa.com/growers/approved-chemicals/insecticides-test/
[50] http://www.farmassist.com/agriedge/images/Resource_PDFs/Soybean/Warrior_Zeon.pdf
[51] http://www2.dupont.com/Production_Agriculture/en_US/assets/downloads/pdfs/K-09315.pdf
[52] http://www.ontariograinfarmer.ca/MAGAZINE.aspx?aid=534
[53] http://en.wikipedia.org/wiki/List_of_hyperaccumulators
[54] Bonmatin, JM, et al (2005) Behaviour of Imidacloprid in Fields. Toxicity for Honey Bees. In Environmental chemistry: green chemistry and pollutants in ecosystems pp. 483-49. http://www.buzzaboutbees.net/support-files/bonmatin2005behaviour-of-imidacloprid-in-fields.pdf
[55] http://cornandsoybeandigest.com/seed/do-soy-seed-treatments-pay?page=2
[56] https://scientificbeekeeping.com/historical-pesticide-overview/
[57] http://www.centerforfoodsafety.org/press-releases/1911/cfs-beekeepers-and-public-interest-groups-sue-epa-over-bee-toxic-pesticides
[58] http://www.theworldlawgroup.com/files/file/docs/Soulier_health_environment_June_2012.pdf
[59] http://www.soulier-avocats.com/upload/documents/Soulier_health_environment_september_2010_F.pdf
[60] http://westernfarmpress.com/government/pesticide-battle-over-honey-bee-health-under-way?page=1
[61] http://westernfarmpress.com/management/total-ag-pesticide-elimination-sought-radicals
[62] http://www.neonicreport.com/home/project-compass/
[63] https://scientificbeekeeping.com/pesticide-incident-reporting/
[64] http://pollinatordefense.org/site/
[65] http://cals.arizona.edu/apmc/docs/IPM_Delivers.pdf
[66] Davis, AS, et al (2012) Increasing cropping system diversity balances productivity, profitability and environmental health. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0047149
[67] http://www.pcl.org/pcl_files/5_Wildlife_Habitat_Farmland.pdf
[68] http://pfspbees.org/
[69] http://www.nwf.org/CertifiedWildlifeHabitat/UserAccount/SignIn
Category: Practical Beekeeping Management, Topics
Tags: beekeeper management, biotic, diseases, drought, environmental, factors, pesticides, randy oliver, varroa | factors Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/factors/ |
What Happened To The Bees This Spring? (Part 1 & 2)
First published in: American Bee Journal, June 2013
Part 1: Environmental and Biotic Factors
Setting the Stage
The Lead Up
The Drought
Lack of Good Forage
Varroa
Diseases
Other Indicators of Impending Collapse
An Unexpected Chill
Feedback from Brokers
The Silent Majority
Beekeeper Management
Part 2: The Contribution From Pesticides
The Lynch Mob
Debunking The Myths
The Precautionary Principal
See For Yourself
Be Careful What You Ask For!
The Effect Of Drought
Actions To Take
Bottom Line
References
What Happened To The Bees This Spring?
Part 1: Environmental And Biotic Factors
Randy Oliver
ScientificBeekeeping.com
First published in ABJ June 2013
By now, most everyone has heard that honey bee colonies died in massive numbers this winter. Reporter Dan Rather, in his newscast Buzzkill [1], showed unfortunate beekeepers, some of whom had lost half or more of their colonies, predicting gloom and doom for the bee industry. What were the causes of this year's bee shortage? As Rather says, "Everyone has an opinion." The question is whether those opinions are based upon fact! So let's go over the events leading up to the bee supply debacle.
Setting The Stage
Nearly 800,000 acres of almond trees in California came into bloom this winter--the trees typically start flowering about Valentine's Day, and the bloom lasts for only about two weeks. Almonds require cross fertilization between adjacent rows of varieties (Fig. 1), and honey bees are trucked in from all over the country to do the job (roughly a million and a half colonies). Many large commercial beekeepers move their hives into California in November to overwinter in holding yards; others build them up on winter pollen flows in Florida or Texas, or hold them in temperature-controlled potato cellars until shortly before bloom. The hives are generally placed into the orchards about a week before the first flowers appear. There is virtually no forage in the orchards prior to, or after bloom in many areas.
Figure 1. An almond orchard in late February, showing the flowering of rows of different cultivars required for cross pollination. The bare "late" varieties have not yet bloomed; the green "early" pollenizers have finished bloom. Grading of colonies is normally done during the bloom of the main crop (usually Nonpareil).
The Lead Up
Two seasons ago there was also a shortage of bees in almonds, following the coldest January (2011) in 17 years (cold being a major stressor of wintering bee colonies). Beekeepers then replaced their deadouts with package bees and splits, thus starting a new generation of colonies, which tend to have lower varroa mite levels than established colonies. These colonies entered autumn 2011 in pretty good shape, and then enjoyed the fourth warmest January (2012) on record! As a result, there was the lowest rate of winter mortality in years, and plenty of bees for almonds in 2012 (Fig. 2).
Figure 2. Percent winter losses since the beginning of the national survey--the data is not yet in for 2012/13. Note that there has been a general downward trend, suggesting that whatever caused the high losses in 2007/8 has not been such a problem in recent years. Note also the cyclical nature of colony winter losses, with high losses in 2004/5, 2007/8, 2009/10, and 2012/13 (some data not shown) Data from [[i]].
[i] http://www.ars.usda.gov/is/pr/2012/120531.htm and California DPR.
I was curious as to whether the colony loss rate was linked to the use of neonicotinoid insecticides. There is no recent USDA data, so I went through the California Pesticide Use Reports (data available through 2010). I plotted the amount of imidacloprid applied to crops in California in the preceding year in red (the seed treatment clothianidin didn't even make the top 100 list of pesticides applied). Although there appears to be a possible correlation from 2006 through 2009, the trends were reversed for 2010. I will be curious to add the 2011 data when it becomes available.
In March of 2012 I received a phone call from a California queen producer who had a prescient insight as to a potential brewing disaster. He was receiving calls for queen bees from Northern beekeepers whose bees had already grown to swarming condition due to the unseasonably warm spring weather (Fig. 3).
Figure 3. Last year's warm spring in much of the country lead to early broodrearing, and as a result, early buildup of varroa levels. Note the record warm spring in the Midwest.
The queen producer noted that such early brood rearing also meant early mite buildup, and predicted that since most Midwestern beekeepers treat for mites by the calendar, that they would unknowingly allow mites to build to excessive levels before treatment. This was strike one against the bees.
The Drought
Then it didn't rain-by midsummer, it was clear that the continental U.S. was in serious drought, including California, whose beekeepers supply nearly half the bees for almond pollination. The only ways that we kept our colonies strong was to either feed expensive pollen supplement and sugar syrup, or to move them to elusive better pasture out of state. By late summer, 60% of the U.S. was in drought, meaning that unless your bees were next to soybeans or irrigated crops, there was little forage for them. This lack of good nutrition was strike two against the bees (Fig. 4).
Figure 4. The severe drought in the Midwest really put the hurt to bee pasture in those states in which the majority of commercial hives spend the summer. Source [[i]].
[i] http://www.ncdc.noaa.gov/temp-and-precip/maps.php
Drought not only dries up nectar and pollen sources, but also forces bees to fly further and more frequently for water. Plus it concentrates ag chemicals and pesticides in the few sources of surface water available to bees. The bees started to show the hurt.
Beekeepers tried to move their hives to areas of better forage, sometimes overstocking an area with too many hives, which led to excessive competition for resources, and the spreading of parasites. Others desperately chased less desirable crops such as sunflowers. Colonies in holding yards in California found little to eat, due to our record dry weather. Some beekeepers with winter eucalyptus locations found them crowded with other hives.
Lack Of Good Forage
In Buzzkill, Bret Adee brought up the fact that bee pasture in the Midwest is disappearing under the plow, largely due to our environmentally-irresponsible taxpayer-subsidized policies that encourage farmers to plant every square foot of land into corn (Fig. 5). Bee brokers told me that colonies coming to almonds from the Midwest were in generally poorer shape this year than those coming from the southern states.
Practical application: some Midwestern beekeepers split their operations, hauling some to the South to rebuild over winter, and the rest directly to California-there was a night and day difference as to how the colonies looked in February!
Figure 5. Grasslands and wetlands in the Corn Belt are rapidly being converted to monocultural, heavily herbicided corn/soy, which eliminates virtually all bee and wildlife forage. A new study found that between 2006 and 2011 there was a net loss of 1.3 million acres of grassland. This affects not only bees--the authors [[i]] state that "As a consequence, populations of grassland nesting birds are declining faster than any other group of birds in North America."
[i] Wright, CK & MC Wimberly (2013) Recent land use change in the Western Corn Belt threatens grasslands and wetlands. https://www.motherjones.com/files/pnas201215404_nwow5w1.pdf
To put this loss of bee pasture into perspective, I asked some Dakota beekeepers for estimates of how many acres of CRP grassland are needed to sustain a colony of bees. In recent years, the overall hive density in North Dakota has been more than 10 hives per square mile (less than 64 acres per hive, including wastelands).
Practical application: the best guess by those beekeepers was that each colony of bees requires about 5-15 acres of productive land for forage (late summer forage being the critical factor). If we use the figure of 10 acres per colony, then the conversion of 1.3 million acres of grassland to herbicided cropland suggests that forage for 130,000 colonies of bees has been eliminated in the past five years in the Corn Belt alone! This figure represents nearly 9% of all colonies needed for almond pollination.
Varroa
An excellent window into the causes of colony health problems is the USDA National Honey Bee Pests and Diseases Survey Report [5] (the latest data have not yet been released). It is worrisome that varroa levels appear to be steadily climbing year after year.
And if the drought and forage problems weren't enough, the favored miticide of commercial beekeepers became unavailable for a time last summer, and mite levels built to killing levels in a number of operations. By late July, some of us were already predicting a disaster for the upcoming almond pollination season. Although many beekeepers finally got mite levels down with late-season treatments, the damage had already been done, and there was no turning the colonies around. Strike three for the bees!
In November semi loads of hives started moving into California, or had been placed in potato cellars. Some of the colonies that arrived from the Midwest were in poor shape, or crawling with mites. Oddly, few beekeepers at the time owned up to having problems, despite the reports that I kept hearing of mite and forage issues! I'm not sure whether this was due to denial, wishful thinking, simple lack of lifting the lids, or something else.
Diseases
Nosema infection also runs rampant across the country--70% of colonies were infected in June of last year. The stressful factors leading up to almond bloom apparently put a lot of hives close to the "tip point" at which pathogens can overwhelm the colony immune system and start it going backwards, or initiate the slide into sudden depopulation (detailed at [6]). Few seem to be mentioning signs of CCD-it is unfortunate that the media keep using that term as a catch-all for all hive problems!
One should keep in mind that the winter collapse issue appears to be cyclical, similar to flu or other pathogen epidemics. I have strong reason to suspect that the constantly-evolving viruses are involved in these colony collapse epidemics.
There has also been a strong resurgence of European Foulbrood and other unidentified brood diseases [7] (Figs. 6, 7, and 8). Unlike EFB of old, the new forms don't go away with a nectar flow.
Figure 6. "Shot brood" due to EFB. Note the fat queen near the center. Despite her vigorous egglaying, this colony is unable to pull ahead due to excessive brood mortality. Lots of beekeepers reported EFB symptoms this winter.
Figure 7. You really have to look hard in some colonies with spotty brood to see the cause! Two larvae in this photo show signs of EFB infection.
Figure 8. Dying brood from one of my sick colonies this spring with EFB-like symptoms. Note the "shot" pattern, the twisted larvae, and the dried larval remains. There is also some AFB-like coloration, but lack of roping or AFB odor (this odor is distinct and sour), nor a positive Holst milk test. In this colony, even pupae were dying. I observe these symptoms independent of whether the hives went to almond pollination or not. Colonies with this (or similar) infection cannot grow. Treatment with oxytetracycline generally clears it up.
One thing that I noticed in Buzzkill was the uneaten pollen supplement patties in many of the crashed hives. I've mentioned before [8] that I've found a colony's failure to consume pollen supplement to be a reliable predictor that that colony will later collapse.
Another strong predictor of winter collapse is weak strength in fall (upcoming article), again strongly suggesting that those colonies already have some sort of health issue going into winter. I heard reports from all over the country that bees went into winter in poor condition.
An Unexpected Chill
The final blow to hives in California was a blast of icy weather (Fig. 9). This unexpected chilling compounded all the existing problems! I've previously pointed out that colony collapse often follows unseasonable chills, since it shifts the tip point for virus and nosema epidemics. Clusters that had expanded for broodrearing contracted, resulting in chilled brood and dead young bees on the ground. My own colonies simply shut down broodrearing completely, losing about two weeks of buildup.
Figure 9. Chilling events (blue arrows) in Modesto, California this winter (the dark blue lines represent normal highs and lows). The unusual chilling in late December and early January (hitting the '20's in a number of areas) came at the time when colonies normally begin to build up for almonds. This severe (for California) cold set the already-stressed colonies back hard, and may have allowed nosema and viruses to gain the upper hand. Graph from wunderground.com.
At the national convention in January, the first reports of beekeepers with collapsing operations were heard. But still, the industry was in denial, with an apparent glut of promised bees as late as the end of the month (two weeks before start of bloom)! But when the rubber finally hit the road in mid February, that illusory supply quickly evaporated, with desperate growers and brokers scrambling to obtain bees--some offering obscenely high prices for substandard colonies.
And then, due to the cool spring, the trees held off on blooming for an extra 10-14 days [9]-colonies placed in anticipation of normal start of bloom just sat there starving and shivering on the cold orchard floors.
Practical application: the biology here is that this is the time of the "spring turnover" in bee populations in California, during which the old overwintered adult bees must rear their replacements for the spring buildup of population. The conditions in the almond orchards prior to bloom are miserable for smaller colonies--it is warm enough to encourage them to break winter cluster and expand the broodnest, but overnight frosts on the Valley floor can cause serious chill stress. Furthermore, it is often warm enough to fly at midday, but there is virtually nothing to forage upon until the trees start blooming! Such fruitless foraging further wears out the workers, and allows sick bees to drift to adjacent hives. Worse yet, the desperate foragers rob out any dead or dying colonies in adjacent orchards, rapidly and effectively transmitting mites, nosema, viruses, and anything else harmful in the deadouts.
Many colonies went backwards during this excruciatingly long wait. Some beekeepers told me that hives graded at placement scored better than those graded at bloom (just the opposite of normal)!
I've been carefully observing spring turnover in my "dinks" (weak colonies) in February (Fig. 10). What I find is that the problem is generally not the queen; rather, the colonies are infected with some pathogen- most commonly nosema [10], the paralytic viruses [11], or EFB (or EFB-like brood disease). Those colonies that are able to successfully emerge one solid round of brood are often able to "clear" the infection and completely rebound by April. Those that get hit by frost in February often collapse.
Figure 10. An example of an unsuccessful spring turnover. This colony is in the middle of typical February collapse from nosema or IAPV. You can easily see the outline of the area recently covered with brood, delineated by the crescents of freshly-packed pollen. Colonies undergoing this sort of depopulation tend not to forage for nectar, and do not respond well to supplemental feeding. This colony continued to collapse quickly, and finally died in a cold snap a week later--with only silver-dollar sized patch of dead bees remaining.
Feedback From Brokers
I asked a few of the major pollination brokers for their observations on the colony shortage this season. Their feedback suggested that the causes for the bee shortage were varied and many.
Summary:
Most were able to eventually fill their contracts. Beekeepers often hold colonies in reserve "just in case," or gambling that in "short" years they can rent those last hives at an elevated price. Also, when the offered price went up, hives not originally intended to go to almonds were loaded up at the last minute and shipped to California (I was in Florida at the start of bloom, and had an inspector tell me of certifying colonies for shipment after the bloom had already begun!).
A number of hives received in November were already headed downhill. Some exhibited the symptom of bees not clustering properly (a typical sign preceding sudden colony depopulation/CCD). Some arrived crawling with mites, or with recent mite treatments in place (suggesting that they were treated too late).
Some graders saw piles of dead bees in front of hives--cause unknown. There were reports of some herbicide tank mixes killing bees.
Many of the placed colonies were below standard grade-- growers paid for less than they expected!
Graders told me that there was a huge variation in hive strength from beekeeper to beekeeper. Many hives were strong (12-16 frames of bees) and healthy; other operations graded at zero to three frames of bees (some of the deadouts had spider webs inside, suggesting that they hadn't been occupied by bees for some time).
The unusual winter chill was tough on colonies that had been stimulated into early buildup, and then forced to contract their broodnests. Some colonies kicked out chilled brood and dead bees afterwards.
Many beekeepers watched their colonies go "backward" prior to bloom.
Colonies from the Southern states (especially those delivered in February) were generally in better shape than those from the Midwest.
Midwestern beekeepers blamed drought, mites, poor nutrition.
Several beekeepers said that their best bees came from remote areas, and their worst from ag areas.
A number of beekeepers admitted inadequate mite treatment; mites were a recurrent theme.
There were a number of reports of EFB hitting colonies.
Some had gotten hit last summer with pesticide sprays, and their colonies didn't recover.
"There were good bees and bad bees from every state. They all seemed to have different problems depending on location/state."
Many good beekeepers simply didn't know what happened to their hives; there were lots of lifeless hives delivered. The atmosphere was ripe with speculation as to the actual causes.
"The shortage was also created by beekeepers that chose not to come to California for a variety of reasons. They can make more money with honey, didn't get paid for what they have brought in the past, bees come back home with mites, beetles and whatever else takes a ride on the hives. Beekeepers don't want to risk bee health to chase the dollar." Many out-of-state beekeepers have had bad experiences going to almonds, and simply don't feel that it's worth it. The supply of bees will largely depend upon the price that growers offer for renting them!
The Silent Majority
Buzzkill leaves one with the impression that the entire bee and almond industries are on the verge of collapse. Of course, the news media focus on fear and disaster, so we may consider taking such dire projections with a grain of salt. In the case of Dan Rather, the focus was on the beekeepers with troubles, not upon those who successfully filled their pollination contracts.
So just how severe was the problem? Let's say that there was an overall shortage of 100,000 hives (a figure that I heard floated)--that would represent only about 6% of the total number of hives placed into almond pollination. The other 94% were successfully delivered (although a proportion of those were weak due to the poor season).
Since the debacle, I've heard from plenty of beekeepers whom I'll refer to as the "silent majority," who experienced "normal" colony winter losses in the 5-25% range, and who successfully filled their pollination contracts. Although the hearts of all beekeepers go out to those who suffered severe colony losses, many felt that some of those losses could have been prevented if the afflicted beekeepers had been more proactive than reactive.
And don't forget those upon whom the rest of the industry depends to supply bees for restocking their deadouts! The California package producers, who have been pollinating almonds for decades, are routinely counted on to consistently take strong hives to almonds, and to then shake over a hundred thousand packages of bees for sale afterwards. Few of these major producers experience severe unexplained colony losses.
Beekeeper Management
By no means am I suggesting that those beekeepers who suffered losses engaged in poor beekeeping practices, but I can't help but notice that not all beekeepers were equally affected--a great number provided strong, healthy colonies to almonds. I've spoken to some of them-the common thread is that those who recognized the problems of poor nutrition and mites in August, and took remedial action for the rest of the season, had acceptable winter losses.
Some beekeepers who really put serious effort and money into bee husbandry were even able to sell "shook bees" from their colonies to others in February! For example, watch Keith Jarrett feeding substantial quantities of pollen supplement to very strong colonies in January [12]--Keith consistently brings very strong colonies to almonds every year, and this year was no exception!
Practical application: I'm here to tell you, that one lesson that I've learned during our intense California drought, is that those yards that I fed with protein in late summer before they started going downhill went to almonds much stronger than those that I didn't feed until fall! Proactive is better than reactive--if you wait until colonies are already going downhill, it is much more difficult to turn them around!
I've often been accused of being politically incorrect for speaking frankly. I'd like to make amends at this point by retiring the rude and unsympathetic term "PPB" (Piss Poor Beekeeping). The fact is that the average wintering loss for the past few years has hovered around 30%. So if you experience 30% losses, you can now proudly call yourself an "Average" beekeeper!
But what about those beekeepers who consistently manage to enjoy lower rates of winter loss? I propose that we call them "Lucky" beekeepers, and the best of them, "Consistently Lucky."
Practical application: the harder those beekeepers work, the luckier they get!
But there were clearly "unlucky" beekeepers this year--especially the "big boys" who brought tens of thousands of hives from the drought-ravaged, and corn-converted Midwest to California. California beekeepers are used to summer drought. We have learned to either move our colonies to better (often irrigated) pasture, or to feed expensive pollen supplements. This would be a very expensive proposition to the larger operators, with hives spread all over the place--a cost not covered by current pollination prices.
What Happened To The Bees This Spring?
Part 2: The Contribution From Pesticides
Randy Oliver
ScientificBeekeeping.com
First published in: American Bee Journal, July 2013
It's pretty straightforward to attribute the majority of colony losses this winter to the usual and aforementioned causes, but a number of beekeepers are also pointing the finger at pesticides. There is no doubt that in certain areas pesticides were a serious issue to beekeepers. Colonies set back by pesticide kills may not fully recover over the season, and those going into winter with pesticide residues may go downhill. There is also reason to suspect that pesticides and miticides have something to do with today's high rates of queen failure.
The bees in some drought-stricken areas were forced to forage on irrigated and pesticide-laden crops--the only place in which there was anything to eat. This changes the entire dynamics of pesticide exposure, since residues would no longer be diluted by the pollen and nectar of non crop plants. The lack of good natural forage also suppresses the ability of colonies to deal with the insult of those pesticides. And colonies may be forced, by necessity, to forage upon one treated crop after another, resulting in multiple exposures.
Practical application: under drought conditions, bees may suffer more from pesticides than when times are good.
Due to the current high prices for agricultural commodities, farmers are often applying pesticides indiscriminately as "risk insurance" rather than due to actual need. A chilling recommendation from an extension entomologist reads:
I encourage you to be risk averse and to make an investment that will pay dividends for your valuable crop. Consider applying [flubendiamide, indoxacarb, or spinosad] for corn earworm. If you have stink bugs and are in the [mature plant] stages, you might want to tank mix one of these products with a pyrethroid. A tank mix of a pyrethroid and acephate are an option, but will wipe out all beneficials [13].
The first three insecticides mentioned are considered to be "reduced risk" to bees if residues are allowed to dry for a few hours, but no mention was made to spray at night. Of the five insecticides recommended above for spraying on corn in tassel, at least four are highly toxic to bees if sprayed during the day! No farmer wants to kill bees, but with recommendations like this from state extension agents, well-meaning growers may unwittingly be hurting pollinators.
Bees in agricultural areas are exposed to a vast array of insecticides, miticides, fungicides and surfactants--many of which have clear links to colony health problems. And applications of new mixes of chemicals are up. For example, in addition to the neonicotinoid seed treatments, granular insecticide soil treatments for corn in the Midwest were up by 30% over the previous year [14]. These treatments consist of combinations of organophosphates and pyrethroids.
But I'm not hearing either the bird groups or beekeepers even addressing these treatments! It is scary to read the sales literature for Counter insecticide, the organophosphate terbufos [15]. Growers are encouraged to apply it at planting time, despite the facts that:
"Terbufos is highly toxic to birds, fish, and aquatic invertebrates [and bees]. [It] shows significant acute mortalities of birds, mammals, reptiles, and fish resulting from broadcast application...In the same study, the application of terbufos as a soil-incorporated treatment to corn...resulted in acute mortalities to birds and reptiles" [16].
Terbufos is strongly systemic, meaning that it is absorbed by the plant roots and could be expected to be expressed in the pollen and nectar.
It can synergize with other pesticides since it ties up the critical CP450 enzymes used in detoxification, to the extent that growers are cautioned that it can cause problems to corn from herbicides [17].
During drought, certain insect pests become more problematic, perhaps resulting in increased exposure to insecticides by bees. For example, drought encourages corn leaf aphids. Read this chilling recommendation for aphids on corn during tasseling (when bees are actively foraging):
If less than 50% of pollination has occurred, aphids and honeydew are covering tassels and plants are stressed, an insecticide may be necessary to ensure adequate pollination, but treatments need to be made within 48 hours of tassel emergence. Asana XL, Brigade, Capture, Cobalt, Dimethoate, Lannate, Lorsban, or Malathion may be used for control [18].
Or this:
Prolonged drought always raises the specter of two-spotted spider mite outbreaks in soybeans and corn. As the 2012 drought intensifies in Minnesota, infestations are reaching treatable levels...The only products that are recommended for spider mites in soybean include insecticides containing chlorpyrifos, dimethoate and bifenthrin[18].
The names of the recommended insecticides above strike fear into the hearts of beekeepers!
Practical application: many "consistently lucky" beekeepers go to great effort to allow their colonies to recover after exposure to pesticides--moving them to unsprayed areas or natural forage, or by immediately feeding protein supplement to stimulate increased broodrearing. Unfortunately, such "recovery" areas are getting harder and harder to find.
The Lynch Mob
Despite the fact that a wide range of bee-toxic insecticides are being applied (often during bloom) to corn, soy, sunflowers, alfalfa, cotton, and other major crops, if you Google anything about insecticide use, you'll quickly find that the blogosphere focuses only upon the putative link between a single class of insecticides--the neonicotinoids-and the demise of pollinators [19].
People look at me incredulously when I point out that there is zero firm evidence to date that the neonic seed treatments are a serious problem! But the notion that all honey bee problems are caused by an insidious new insecticide resonates with a distrustful public [20], and has firmly established itself as "common knowledge." But repeating something does not make it true!
"It's easier to fool people than to convince them that they have been fooled"-Mark Twain
Practical application: the question is, "Are the neonic seed treatments being railroaded into a guilty verdict in the media's kangaroo court of public opinion?"
One group recently brought suit against the EPA to ban the use of the seed treatments clothianidin and thiamethoxam [21], neither of which even make California's top 100 list of pesticides applied [22], nor that have ever been demonstrated to harm colonies feeding on the pollen or nectar of seed-treated plants! A number of people have made up their minds that the neonics are the main cause of colony collapse, and it appears that no amount of facts to the contrary will cause them to reconsider!
Debunking The Myths
As anyone who knows me will tell you, I am a stickler for honesty, accuracy, and factuality. I am concerned about the amount of misinformation and speculation going around about the neonics. So let's look at some of the claims vs. the actual facts.
Arguments Against Neonic Seed Treatments Actual Facts
The neonicotinoids have been "linked" to increased colony mortality. In actuality, such a "link" is merely an urban legend, and has never been demonstrated or confirmed in any study.
On the other hand, the residues of other classes of pesticides are more suspect for causing increased brood or adult bee mortality [24].
The timing of CCD coincides with the introduction of the neonic seed treatments in 2004. CCD started in California bees in the winter of 2004/2005, prior to them ever being exposed to seed-treated crops.
But what else could have changed at that time other than the introduction of neonics? In California, Dr. Eric Mussen [25] determined that the increased colony losses were due to poor summer forage and failure of mite control products (just as this last winter).
There is actually a much stronger association between the incidence of the novel gut parasite Nosema ceranae and increased colony mortality [26].
But the main thing that has changed is the dynamics of the varroa/virus complex, which coincidentally occurred at about the same time that the neonics came into use.
European countries banned the neonics, and the bees recovered after those bans. A few countries placed temporary suspensions on certain seed treatments until planting dust issues were resolved [27]--only Germany has one suspension still in place. The foliar applications were not suspended. The suspensions did not resolve bee health problems.
The European Food Safety Authority recently decided that neonics pose a threat to bees. "The Center for Regulatory Effectiveness (CRE) has recently completed a Data Quality Act (DQA) Alert on the ... (EFSA) report on neonicotinoids which found that neonicotinoids pose a risk to bees. The DQA Alert outlines the serious deficiencies of the EFSA report and demonstrates why the EFSA report violates the DQA...In particular, the EFSA report failed to maximize the objectivity of the data by failing to reconcile numerous studies whose conclusions contradicted the findings of the EFSA report" [28].
Several lab studies have found that neonics affect individual bee behavior, longevity, or immunity. True -- although many studies used unrealistically high doses. The question is whether such artificial studies apply to actual colonies in the field. The numerous field studies to date have failed to find any link between seed treatments and later colony health issues.
It is the seed treatments that make corn a problem. As Bret Adee points out in Buzzkill, corn is replacing pastureland (Fig. 4). Corn, as grown today, is a virtual "bee desert" (similar to the way in which suburban lawns are green bee deserts). And it's not only the bees that this is affecting, the populations of birds and other wildlife are plummeting due to loss of favorable habitat (see my blog on birds and neonics [29]).
A recent survey by Dr. Jerry Bromenshenk found that bees actually avoid field corn pollen, and are exposed to very little of the seed treatment residues [30].
Numerous independent studies, and the experiences of stationary beekeepers throughout the Corn Belt, support the conclusion that colonies can thrive when surrounded by corn, provided that there is some alternative forage within flight range.
As the use of neonic seed treatments increases, bee mortality goes up. In actuality, colony mortality rates go up and down year to year, largely dependent upon weather and varroa mite control. If the neonics were to blame for this winter's bee losses, why didn't they cause similar losses last winter, in which the colony mortality rate was the lowest in years?
French beekeepers also started seeing problems with the introduction of the neonics. I've spoken with beekeepers in France whose apiaries are in pesticide-free areas. They tell me that they experience the same sorts of colony mortality problems as do those in areas exposed to neonics.
Bees in the U.S. are commonly exposed to neonicotinoids. In the most recent USDA survey (100 samples across the country), imidacloprid was only detected in 9% of the samples [31] (although I found some of the residue levels alarmingly high). However, the most common seed treatment, clothianidin (or its degradation products), was not detected at all!
The above real-world data suggests that efforts to ban clothianidin as a seed treatment may be misplaced. It appears that imidacloprid, especially as a foliar application, would be of more concern.
Neonics are the most common pesticides that bees are exposed to. In the above survey, other serious insecticides were more commonly prevalent: chlorpyrifos (in 20% of samples), cyhalothrin (in 7%), and endosulfan (in 11%).
Notably, there was also a high prevalence of beekeeper-applied miticides: fluvalinate (in 38%), coumaphos (in 87%), amitraz (in 27%), fenpyroximate (in 11%), and thymol (in 27%).
There was even higher exposure to fungicides and adjuvants.
It is misleading for the pesticide companies to blame the problems on varroa, nosema, or poor nutrition. The above survey (over 1000 samples) found that the average varroa infestation rate in the U.S. in autumn is above the danger level for virus epidemics!
Sixty to 100% of hives are infected with nosema in December.
Summer drought has historically been associated with high winter mortality.
But didn't the planting dust from corn seeding kill colonies in Ontario? Planting dust is separate issue that clearly needs to be remedied. It does on occasion cause bee kills, for which beekeepers are rarely compensated. This situation must change! All parties are actively working on solutions [32].
Bees in certain agricultural areas tend to go downhill later in the season. This has been observed for a long time--long before the neonics. The question is, which chemicals, chemical synergies, or chemical/nutrient interactions are responsible? The Frazier/Mullin team at Penn State has developed a protocol for helping to figure this out. I strongly support its adoption by the EPA for pesticide risk analysis.
Colonies foraging upon nectar or pollen of seed-treated crops get poisoned. Ask yourself this: if neonic residues were actually so harmful to bees, how is it that the Canadian beekeepers, whose bees forage largely on seed-treated canola, feeding solely upon a diet of canola nectar and pollen with well-documented residues of clothianidin, experience very low winter losses, despite the long Canadian winter (so long as they control varroa and nosema)?
And how is it that the vast majority of beekeepers in the U.S. Corn Belt report that their colonies thrive and that they have far fewer pesticide issues these days than in the past?
The neonicotinoids are "systemic," meaning that they are in the plants all the time! True, but this property is not unique to the neonics--a number of other insecticides also go systemic. In any case, with seed treatment, the concentration of the insecticide in the plant is only high when the plant is young--it gets diluted as the plant grows (e.g., clothianidin in canola is at a level high enough to kill aphids for only about the first 30 days of growth).
The only time that residues in the plant matter to pollinators is when the mature plant flowers. The amount of seed treatment is carefully calibrated so that the residue in the pollen and nectar are below the level that causes demonstrable harm to bees.
In the case of foliar, drench, or chemigation applications prior to bloom, there are greater possibilities for bees to be exposed to toxic levels.
There are fewer butterflies and pollinators in the fields these days. Not surprising, since the new push for "clean farming" has removed the host plants upon which the butterfly larvae feed. Pollinators are forced to subsist upon the stretches of weeds growing along roads at the edges of fields. But surprisingly, pollinators may be abundant there, suggesting that even though populations as a whole are reduced by habitat conversion, it is that, rather than the use of seed treatments, that causes the population declines.
The evil pesticide companies want to kill honey bees. Give me a break! Does anyone truly believe that anyone wants to kill honey bees? What pesticide company would want the bad press of being associated with killing bees? The chemists and biologists on their staffs earnestly work to develop insecticides that are bee friendly.
The EPA is being derelict in their duty to protect pollinators. I have spoken at length with EPA staff, and reviewed their risk assessments, as well as those by, DEFRA, EFSA, PMRA, and other regulatory agencies. I find that the risk assessors have not overlooked any evidence, are well-informed on the subject of neonics, and are justified in their assessments that the on-the-ground evidence (to date) indicates that neonic seed treatments pose acceptable risk to pollinators.
We must all remember that the tobacco industry tried to hide the fact that nicotine was addictive [33]. Spare me! Does anyone seriously think that the EPA is unaware that industry executives may stretch the truth? Of course the EPA is skeptical of any reassuring claims by the pesticide industry--that's why they go over all studies with a fine-toothed comb!
This winter's losses spell the end to commercial beekeeping. The fact of the matter is that many observers note that the bee supply for almonds often follows a boom-bust cycle. Although losses were high this year, the trend for the last decade has been for beekeepers keep ramping up the supply of bees for almonds. So long as growers are willing to pay a profitable rental rate for colonies, market forces will encourage the bee industry to meet the demand (for a detailed analysis, see [34]).
The Precautionary Principal
"But," you say, "shouldn't we exercise precaution due to the lab studies that find adverse effects from the neonics?" Look, I make my living as a beekeeper, I'm not out to sell insecticides, and am as concerned as the next person about the environment and the safety of the food I eat. I've researched the neonics exhaustively, and addressed them in several articles [35]. I am acutely aware that there are suggestions that the neonics may be causing insidious effects in the environment, and I've studied the excellent environmental document Late Lessons from Early Warnings [36], which hammers the message that we should use the "precautionary principle" when dealing with chemicals. The problem is, there is nothing without risk--for example, you have a 1 in 83 chance of being killed in an auto accident in your lifetime. But most people still take the risk of getting into cars, since they feel that the benefit outweighs the clearly high risk!
My practical perspective as both a scientist and a beekeeper: if researchers perform lab studies on any insecticide, they will find that there are all kinds of negative effects upon bees--this should be pretty obvious, since insecticides are specifically designed to harm insects! However, the majority of these studies are taken out of the context of full colonies under field conditions, where bees fly free and choose the flowers upon which they forage. The evidence to date supports the contention that the neonics, properly used as seed treatments, are indeed an improvement over other insecticide options.
As Dr. Eric Mussen succinctly notes:
Nobody's really been able to show that [the neonicotinoids] are more problematic than the rest [of the pesticides to which bees are exposed] [37].
Far be it from me to suggest that the neonics (or any other pesticides) are harmless! But consider this--if the neonic seed treatments were indeed as harmful as some make them out to be, you'd think that after a decade of intense study that at least one researcher could have come up with a single solid piece of field evidence against them!
Let's do a thought experiment. Why doesn't someone simply put a bunch of healthy hives into the middle of seed treated crops and see whether they die afterward? Oh, I forgot--this experiment has already been run by thousands of beekeepers year after year in the Corn Belt and the Canadian prairie! And those beekeepers have invited me to look at their colonies, sent me photos of colonies stacked head high with honey supers, and bragged about their high winter survival!
Some will argue 'til they're blue in the face, but the fact remains that virtually every beekeeper that I've spoken with in the Corn Belt and in canola areas feels that the seed treatments are not a problem [38]. In fact, most tell me that this is the best it's ever been as far as bees and pesticides!
Common sense: I just don't get what is so hard to understand about the reality that there are thousands of colonies thriving year after year in areas of intense seed treatment? To any reasonable person it would suggest that the treatments are causing little noticeable harm other than the occasional planting dust kill, which I have repeatedly stated is a problem that needs to be corrected!
See For Yourself
Let's look at actual independent (from the manufacturer) data from corn and canola areas:
Corn
I asked friends in the Corn Belt if they had any data on winter losses. It so happens that the Michiana Beekeepers Association has been collecting exactly that since the spring of 2010 (Fig. 11).
Figure 11. Percentage of winter losses by the "Michiana" hobby beekeepers. The 2013 figure is as of mid March; it may eventually go down a bit due to a prolonged cold spring. Note that the winter survival rate appears to be linked to average winter temperature. Thanks to beekeeper Danny Slabaugh for sharing the data; temp deviations from [[i]].
[i] http://www.ncdc.noaa.gov/temp-and-precip/maps
How could the above be? Eighty percent winter survival despite sitting in the middle of seed-treated corn and soy? So of course I did a fact check to confirm that those beekeepers were indeed sitting in corn/soy areas (Fig. 12).
Figure 12. USDA land cover categories for the region in which the Michiana hobby beekeepers keep bees--corn and soy acreage is color coded yellow and green, respectively. The selected area is the top half of Indiana and bottom of Michigan, with Lake Michigan at the left. Clearly, these apiaries were exposed to seed-treated corn and soy! I created the map at [[i]].
[i] http://nassgeodata.gmu.edu/CropScape/
The above figures suggest that colony winter survival for stationary hobby beekeepers in the above corn/soy region is higher than the national average, despite the fact that about half of them don't even treat for mites! They also suggest that the neonics or other pesticides used in corn/soy in that region do not cause excessive winter loss. Finally, the data indicate that a main factor for winter loss rates is the winter temperature.
Canola
I've heard some beekeepers saying that their bees crashed after working canola, suspecting that the seed treatments were the problem. So as a reality check I called a Dakota beekeeper who has been running bees to canola for over a decade--some 10,000 hives last season. He tells me that colony strength after canola varies from year to year, but that he sees no problem with the seed treatments. He did point out that beekeepers should be aware that colonies can plug the broodnest on intense canola flows.
The biology: The plugging out of the broodnest during an intense bloom means that three weeks afterward, there will be few emerging workers to take the place of the worn-out foragers, and the colony population will temporarily plummet. Even worse, the remaining mites are then concentrated onto fewer bees--which can initiate virus epidemics. These colonies must then attempt to rebuild from scratch, starting in August, meaning that the weakened, mite-infested colonies faced three long months of drought last summer for that rebuilding process.
Every field study that I've seen for canola also supports the conclusion that the seed-treatments are safe for bees. I joined other beekeepers and regulators in observing a large-scale study of seed-treated canola in Canada [41]. Canola (or rapeseed) is likely the best test crop, since bees eagerly (and virtually exclusively) forage upon it for both pollen and nectar, meaning that every bit of their food supply contains contain easily verifiable residues of the insecticides. The preliminary results indicate that the clothianidin seed treatment did not harm the colonies [42].
Another recent independent long-term field study in Poland [43] came to the same conclusion. In it, the researchers followed 50 colonies for more than two years under field conditions as they foraged on five different large fields of oilseed rape treated with various combinations of five different neonicotinoids applied by seed treatment and spraying. Pollen and nectar samples were taken, and demonstrated that the bees were clearly exposed to normal residues of the insecticides (there was also additional exposure to other common agricultural pesticides). The colonies were monitored for health, brood, strength, nosema, viruses, and winter survival, and compared to two control apiaries set in an area free of the crop. The results?
During the time from the placing of the colonies on the rape fields until wintering, the colonies developed properly in all groups... All colonies overwintered properly... In both years, during the period of being placed in the oilseed rape fields as well as after being moved to the stationary apiary, none of the groups showed disturbances in development or functioning.
Following a paper that suggested that the seed treatments would impair bumblebee colonies' ability to rear queens, DEFRA performed a common-sense field study last year [44]. Their findings:
...the study has shown that bumble bee colonies remained viable and productive in the presence of the neonicotinoid pesticides under these field conditions...The study underlines the importance of taking care in extrapolating laboratory toxicology studies to the field, as well as the great need of further studies under natural conditions.
Sunflowers
Some beekeepers report that their colonies later crashed after they chased sunflowers last summer for honey. One must keep in mind that sunflowers are not a natural food for honey bees, and provide only poor-quality, nutritionally-inadequate pollen [45]. But the main problem with putting bees on sunflowers may be related to the fact that sunflowers are a native plant--meaning that there are a number of native insects that evolved to feed upon it:
Maximum seed yields often require the use of insecticides to protect the crop from insect competitors. Unfortunately, many of the major insect pests of sunflower attack the crop when it is flowering. Thus, insecticides used to control the pest also harm pollinating bees [46].
If sunflowers are the only forage available, colonies may eventually go downhill, due to the one-two punch of poor pollen nutrition coupled with insecticide exposure. And which pesticides would those be? One scary list- Asana XL, Baythroid, endosulfan, Furadan , Lorsban , methyl or ethyl parathion, , Proaxis, Scout X-TRA, Sevin, Warrior, Mustang Max, Declare, Cobalt, Yuma, Delta Gold, and Grizzly Z [47]!
Note that none of the above are neonics, other than seed treatments for wireworms. Surprisingly, field evidence indicates that the seed treatments only "stun" the wireworms for a while [48], which certainly raises the question as to how harmful they might be to bees months later when the plants flower! I will return to sunflowers below.
Be Careful What You Ask For!
Allow me to assure you that I am no pitchman for neonics or any other insecticide--the typical farmer practices far too little integrated pest management, and applies far too many pesticides! All insecticides (and several fungicides and adjuvants) cause problems to pollinators--the neonics are no exception. Any systemic insecticide has the potential to harm bees when applied as foliar applications, by chemigation, or to flowering trees, but it there is no compelling evidence that the neonics are any worse than the alternatives in most applications. On the contrary, there is quite a bit of evidence that they may often be "safer" ("reduced risk").
If the neonic seed treatments were banned, it's not as though all agriculture is suddenly going to go pesticide free--only about 1% of U.S. cropland is registered as "organic"! We must consider the likely alternatives. The products that farmers would then use to control insects would need to be sprayed all over the cropland--we'd then be back to the problem that the bulk of sprayed insecticides go into the environment without ever hitting the intended pest!
I hear from knowledgeable beekeepers that worse than in previous years, some of the new formulations of the spray-applied insecticides [49, 50, 51] can really knock the snot out of bees! One large beekeeper found his hives already dead before moving them away from the fields. Again, this was not a neonicotinoid issue.
Practical application: no one is saying that the neonics are "harmless." The question is whether they are better or worse than the alternatives.
The Effect Of Drought
Let's discuss some of the problems (or suspected problems) with the neonics last season. The record warm and dry spring appeared to exacerbate corn planting dust issues (corn seeds are the worst offender due to their non spherical shape). Beekeepers in some areas of the Corn Belt, the East Coast, and in Ontario suffered from confirmed (in at least some of the cases) planting dust kills (although many went on to make good honey crops after their colonies recovered). The final analysis from Ontario is not yet completed, but dry soil conditions and an early clover bloom likely contributed to the problem. Regulators and the seed companies are working on solutions to the problem [52]. Still, IMHO it is unacceptable to ask beekeepers to bear the burden of bee kills without compensation, and no one could blame the affected beekeepers for being pissed!
Drought-stressed plants
There are a number of advantages to the neonic seed treatments. Besides their safety to the farmer and to most wildlife, there is virtually no way for the farmer to misapply them! The timing of application is only at planting time (when bees normally have little interest in the bare fields), and the dose is determined by the seed-treating company. This means that the applicator can't be tempted to apply at the wrong time, or to over apply too strong a dose (however, their excessive near universal use can be expected to accelerate the development of resistant pests).
That said, beekeeper Bret Adee brought an interesting question to my attention: the dose of seed-applied systemic insecticides (whether neonic or other) is based upon the dilution factor as the plant grows, so that the residues in nectar and pollen will be reduced to below the "no observed adverse effects level." But what happens during drought, when the water-stressed plants only grow knee high before desperately flowering? There would be far less plant biomass in which to dilute the insecticide (assuming that drought-stressed plants absorb the same amount from the seed treatment).
Certain plants (including sunflowers and canola) are known to "hyperaccumulate" toxic metals [53], perhaps more so during drought. Could this also be the case with systemic insecticides? Something that's been stuck in the back of my mind is that Bonmantin [54] found that the concentration of imidacloprid first drops in sunflower plant tissue as it grows, and then reconcentrates in the flower heads.
It occurs to me that the translocation of systemic insecticides is generally studied in plants grown under "normal" conditions. I'd very much like to see data for residues in pollen and nectar from seed-treated plants grown under drought. Had we thought of this earlier, we could have collected pollen and nectar samples from drought-stressed plants last summer. I'm currently trying to track down any data or samples from such plants--if any reader has any such sample analyses, please let me know!
Practical application: the above hypothesis is speculative, but we need actual data from drought-stressed plants to see whether such an effect occurs. If so, it would need to be taken into consideration for the registration of seed treatment products!
Once planting was completed and the drought took its toll, the reports that I've heard are that soybean honey saved a lot of bee operations this season, right in the middle of treated corn/soy farmland. In this case, seed treatment with neonicotinoids may have been a blessing to beekeepers:
The benefits of [seed treatment] not only include the early-season disease control but also suppression of soybean aphids for quite a ways into the growing season. With it, we typically make only one foliar insecticide application for aphid control, usually in August, instead of two applications when [treatment] isn't used. In 2012, with the extremely dry conditions in mid-season, there wasn't as much of an aphid problem, and we treated just 300 acres of soybeans...Last year we sprayed closer to 30,000 acres for aphids [55].
On the other hand, some beekeepers on alfalfa or cotton got hit hard by other classes of insecticides. A hit from a pesticide application can lead to poor subsequent colony performance, queen failure, dwindling, or winter collapse. ABJ published an excellent series of articles on pesticides by Drs. Barbara and Eric Erickson in 1983; Editor Joe Graham has graciously granted me permission to post copies of those articles to my website [56]--I strongly suggest any beekeepers interested in pesticide issues read them! In the second article, the authors discuss both the problems with systemic insecticides and of sublethal effects--note that these articles were written long before the introduction of the neonics!
An anti-pesticide group, along with a handful of beekeepers, recently filed suit against the EPA [57], calling for an immediate ban on the two most common neonicotinoid seed treatments, despite the easily-verifiable fact that hundreds of thousands of colonies thrive in the midst of seed-treated corn, soy, and canola! To me, this suit smacks of being some sort of well-orchestrated publicity stunt, and does not serve the interests of either beekeepers or environmentalism. Worse, it now gives the powerful farm lobby cause to label beekeepers as "radical" enemies.
We don't want this battle: do we really want to take on the farm lobby by backing them into a corner? The French beekeepers took a similar case against fipronil all the way to their supreme court and lost [58, 59]-worth reading]. Agriculture is already positioning itself for a fight [60, 61, 62]. Think about it--the EPA lives in fear of a conservative congress slashing their funding. Does anyone really think that they are going to go against the agricultural lobby without unimpeachable evidence? We should also think twice before calling for a ban on the seed treatments--the alternatives are not pretty!
It disturbs me to hear industry executives and lawyers stretching the truth or misrepresenting data. It disturbs me even more to hear my fellow environmentalists and beekeepers doing so! If we wish to maintain credibility, we should hold ourselves to a higher standard. The question we must ask ourselves the way in which we wish to have pesticide regulation decisions made:
1. By the EPA (the Environmental Protection Agency), whose risk assessors carefully study and weigh all available research and evidence in order to make objective and rational decisions, or
2. To have it decided instead by impassioned, fearful, and often misinformed advocacy groups who hire lawyers and pressure politicians who know little about the subject?
We depend upon the EPA to strike a balance between the availability of cheap food and profitability for those who provide it, versus the risks to human and environmental health and safety. It is good to have activists on both sides of the issues (industry and the anti-pesticide groups) to keep the EPA informed. But I don't feel that either of those groups should be telling the EPA which pesticides to register or to ban! Let the regulators do their job!
Rather than wasting EPA's funding to fight frivolous lawsuits, there are more productive actions that we can take:
Help the EPA to do its job by filing "adverse effects incident reports" if you observe a problem due to pesticides [63]. EPA is begging beekeepers to do this! Unless they have documented reports of pesticide problems, their hands are tied as to restricting the uses of those pesticides!
Support the National Pollinator Defense Fund [64]. Our industry is currently represented by a reasoned and knowledgeable group of (mostly) beekeepers. (Challenge to the pesticide companies: why don't you stand behind the safety of your products and donate? The NPDF is about ensuring that your pesticides are properly applied, so there would be no conflict of interest).
If your local state lead agency is not actively investigating bee kills or enforcing pesticide regulations, then use the local media to embarrass them into action!
Keep pressure on the EPA to resolve corn planting dust problems. Here's a wild idea: I'm not sure of the exact figures, but let's say that 90% of the 95 million acres of corn is grown from neonic-treated seed. If the states were to levy a surcharge of 50 cents per acre (neonic seed treatment adds about $12 per acre to seed costs), they could collect over $42 million each year to fund a pool from which to indemnify the occasional beekeeper who suffers a confirmed kill from planting dust!
Tell Congress that we'd like to see wording added to the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) to specifically protect pollinators. Currently, such protection is nebulous (although the EPA is acutely aware of pollinator issues): "The Administrator shall register a pesticide if... when used in accordance with widespread and commonly recognized practice it will not generally cause unreasonable adverse effects on the environment." Unless there is specific wording to protect pollinators, bee kills may not be considered to be "unreasonable"!
We need far more independent field studies to determine which pesticides and application practices are actually causing harm to pollinators. For pesticides in question, keep pressure on the EPA to require additional field trials to demonstrate whether they are indeed safe for pollinators under field conditions. I'd like to see the establishment of monitoring apiaries (and patches of untilled land) in representative agricultural areas nationwide, with the hives in each apiary to be carefully managed by independent parties. Such apiaries and sites could then be closely monitored each summer to see whether honey bees and other pollinators are able to survive local pesticide practices.
Give farmers workable options! Disseminate and promote bee-friendly agricultural practices that don't hurt the farmers' bottom line. For example, by adopting IPM practices, Arizona cotton growers reduced insecticide spraying from 12.5 times a season to only 1.3 times (cutting insecticide use twentyfold), while using more environmentally-friendly insecticides [65]! Another recent study in Iowa found that adding additional clover or alfalfa rotations in corn/soy farmland was equally profitable, improved the soil, used less energy, used far less pesticides, and decreased water pollution [66].
Business and agriculture respond to consumer demand. Consumer demand stopped most dairymen from injecting their cows with the hormone BST. Consumers could do the same by demanding pasture-fed beef and dairy (which would create more pollinator forage)! I'd also like to see the expansion of consumer choices (other than organic certification) that reward farmers who manage their lands to the benefit of wildlife and pollinators. For ideas, see [67. 68. 69].
Bottom Line
In conclusion, it appears that a perfect storm of a preceding exceptionally warm winter, followed by serious drought across the country, the lack of good mite control, a high prevalence of pathogens, and an unexpected California chill in the orchards prior to bloom, resulted in an unusual degree of colony losses. In other words, rather than one specific cause, there were simply not enough of the good things, and too many of the bad things.
I don't see evidence that pesticides were the major factor in the shortage of bees in almonds this winter, although, as usual, a number of individual beekeepers on certain crops certainly took serious hits.
And how about the fear that there won't be enough bees for almond pollination next year? Beekeepers have already told almond growers to expect higher pollination prices next year (especially since California is again going into serious drought, and beekeepers will be forced to invest extra money in feeding their hives). Most every beekeeper I know is madly making increase right now in anticipation of higher pollination prices next season. The fact of the matter is that should conditions allow beekeepers to successfully rebuild their numbers (following the typical swings of our boom/bust cycle), there could possibly even be a glut of bees for almonds next winter!
Feedback And Corrections
A few countries placed temporary suspensions on certain seed treatments until planting dust issues were resolved [27]--only Germany has one suspension still in place. - Actually there are some more: France (Thiamethoxam in oilseed rape, Imidacloprid in corn and sunflower), Italy (all Neonic seed treatment in corn), and Slovenia (Imidacloprid, Thiamethoxam, and Clothianidin seed treatment in all crops)
French beekeepers also started seeing problems with the introduction of the neonics; I've spoken with beekeepers in France whose apiaries are in pesticide-free areas. They tell me that they experience the same sorts of colony mortality problems as do those in areas exposed to neonics - This is, by the way, likewise confirmed by monitoring results from the French authorities.
In the case of foliar, drench, or chemigation applications prior to bloom, there are greater possibilities for bees to be exposed to toxic levels. - This is not the case for foliar application: as Neonics are xylem-systemic, but hardly mobile in the phloem, they can only be distributed in a plant after root uptake, but not be translocated for instance from a leaf to a later developed flower.
Then, on the topic of systemic residues in plants under drought stress: first, I am quite sure that the decrease of concentration in seed-treated plants over time is not only due to dilution, but also to degradation of the compounds - a factor that is not specifically dependent on water availability for the plants (e.g. photodegradation!); second, even if there would be less dilution in plants under drought stress: the concentrations in nectar and pollen of treated crops are normally so low (when we consider average rather than peak concentrations, and when we consider scenarios where colonies have chronically access exclusively to contaminated nectar/pollen over months unlikely in practice), that even an increased concentration due to drought stress-affected plants should not make a significant difference: if we for instance assume an average concentration of let's say 3-4, or even 5 ppb Clothianidin in corn pollen, and likewise assume a dilution reduced to 50% (which is probably exaggerated), then we would still not end up with excessive residues. And finally, we have residue figures from crops grown in different countries, different climatic conditions, and different agronomic practices; though we have not specifically addressed the drought stress scenario, we have seen that residue figures are quite consistent over all scenarios, and there does not appear to be strong evidence that different environmental conditions would substantially (i.e. by orders of magnitude) and systematically alter residue concentrations.
Dr. Christian Maus
Global Pollinator Safety Manager
Bayer CropScience
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A ppt on the impact of CRP lands on wildlife in North Dakota
http://www.redriverbasincommission.org/Conference/Proceedings/26th_Proceedings/Kading_RRBC_09.pdf
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Feedback from a Midwestern apiary inspector:
Just a quick update: This beekeeper who recently told his local newspaper that pesticides were killing his bees, he was making excuses. We examined two of his yards with him yesterday. One yard was showing EFB throughout the whole yard. I think his "mid-summer losses" last year (half of that yard's hives) were EFB kicking in with the mid-summer dearth. In his other yard, most of his dead outs were obvious starve outs. He harvested all of their stores with the first frost, and then didn't feed them. So, in my opinion, and from my observations, pesticides are usually being used responsibly, and aren't killing honey bees. I also think, with the aggressive way bees were on soy fields last summer, the systemic pesticides are not harmful to honeybees. I'm not seeing honey bee problems other than EFB getting the upper hand, due to our cold, late spring. My two cents. Thanks.
References
[1] http://www.frequency.com/video/dan-rather-reports-buzzkill/87705620/-/YouTube
[2] http://www.ars.usda.gov/is/pr/2012/120531.htm and California DPR.
[3] http://www.ncdc.noaa.gov/temp-and-precip/maps.php
[4] Wright, CK & MC Wimberly (2013) Recent land use change in the Western Corn Belt threatens grasslands and wetlands. https://www.motherjones.com/files/pnas201215404_nwow5w1.pdf
[5] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
[6] https://scientificbeekeeping.com/sick-bees-part-2-a-model-of-colony-collapse/
[7] vanEngelsdorp, D, et al (2013) Idiopathic brood disease syndrome and queen events as precursors of colony mortality in migratory beekeeping operations in the eastern United States. Preventive Veterinary Medicine 108(2-3): 225-233. http://www.sciencedirect.com/science/article/pii/S0167587712002656
[8] https://scientificbeekeeping.com/sick-bees-part-18a-colony-collapse-revisited/
[9] http://almondinsights.com/692, http://agfax.com/almonds/2013/reports/03042013-almonds-web.htm
[10] https://scientificbeekeeping.com/sick-bees-part-18a-colony-collaspse-revisited/
[11] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2010-2011-Limited_Survey_Report.pdf
[12] http://www.youtube.com/watch?v=y6B5qm2ut18, http://www.youtube.com/watch?v=PYbLbhZXizY
[13] (Broken Link!) http://www.nccrops.com/2012/07/27/insecticide-recommendations-for-corn-earworm-in-soybeans/
[14] http://www.agriview.com/news/crop/corn-soil-insecticide-use-up-dramatically-to-combat-widespread-rootworm/article_5d09decc-5b40-11e2-b485-001a4bcf887a.html
[15] http://www.amvac-chemical.com/products/documents/Counter20G%20Tech-Sell%20Sheet%20-%202013.pdf
[16] http://pmep.cce.cornell.edu/profiles/insect-mite/propetamphos-zetacyperm/terbufos/insect-prof-terbufos.html
[17] http://www.lewishybrids.com/PDF/3-5-2013Agronomic+ALERT+-+Interaction+between+herbicides+insecticides+corn.pdf
[18] http://pest.ca.uky.edu/EXT/Recs/ENT16-Field%20corn.pdf
[19] (Broken Link!) http://www.soybeans.umn.edu/crop/insects/spider_mites.htm
[20] http://www.nytimes.com/2013/04/07/opinion/sunday/calamity-for-our-most-beneficent-insect.html?nl=todaysheadlines&emc=edit_th_20130407&_r=0
[21] http://www.nytimes.com/2013/04/07/opinion/sunday/calamity-for-our-most-beneficent-insect.html?_r=0
[22] http://www.panna.org/press-release/beekeepers-and-public-interest-groups-sue-epa-over-bee-toxic-pesticides
[23] http://www.cdpr.ca.gov/docs/pur/pur10rep/top_100_ais_lbs10.pdf
[24] http://www.extension.org/pages/60318/pesticides-and-their-involvement-in-colony-collapse-disorder
[25] Mussen, EC (2006) Chaotic almond pollination. http://entomology.ucdavis.edu/faculty/mussen/JanFeb2006.pdf
[26] https://scientificbeekeeping.com/sick-bees-part-18e-colony-collapse-revisited-genetically-modified-plants/
[27] http://www.epa.gov/pesticides/about/intheworks/ccd-european-ban.html
[28] http://www.thecre.com/oira_pd/wp-content/uploads/2013/04/DQA-Alert-EU-Commission-Ban-on-Neonicotinoids-4-10.pdf
[29] https://scientificbeekeeping.com/home/news-and-blogs/
[30] Henderson, CB, JJ Bromenshenk, DL Fischer (2013) Clothianidin exposure levels from bee-collected pollen and nectar in seed-treated corn and canola plantings. Proceedings of the American Bee Research Conference.
[31] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
[32] http://www.ontariograinfarmer.ca/MAGAZINE.aspx?aid=534
[33] http://www.pbs.org/wgbh/pages/frontline/shows/settlement/timelines/april94.html
[34] https://scientificbeekeeping.com/2012-almond-pollination-update/
[35] https://scientificbeekeeping.com/neonicotinoids-trying-to-make-sense-of-the-science/, https://scientificbeekeeping.com/neonicotinoids-trying-to-make-sense-of-the-science-part-2/, https://scientificbeekeeping.com/testing-of-bee-feed-syrups-for-neonicotinoid-residues/
[36] http://www.eea.europa.eu/publications/late-lessons-2
[37] http://www.sciencefriday.com/playlist/#play/segment/9088
[38] https://scientificbeekeeping.com/the-extinction-of-the-honey-bee/
[39] http://www.ncdc.noaa.gov/temp-and-precip/maps
[40] http://nassgeodata.gmu.edu/CropScape/
[41] https://scientificbeekeeping.com/a-new-large-scale-trial-of-clothianidin/
[42] http://www.producer.com/daily/ontario-field-study-finds-no-link-between-seed-treatments-bee-deaths/
[43] Pohorecka, K, et al (2013) Residues of neonicotinoid insecticides in bee collected plant materials from oilseed rape crops and their effect on bee colonies. Journal of Apicultural Science 56(2): 115-134. http://www.degruyter.com/view/j/jas.2012.56.issue-2/v10289-012-0029-3/v10289-012-0029-3.xml?format=INT
[44] http://www.fera.defra.gov.uk/scienceResearch/scienceCapabilities/chemicalsEnvironment/documents/reportPS2371Mar13.pdf
[45] http://repository.up.ac.za/bitstream/handle/2263/20334/Nicolson_Chemical(2012).pdf?sequence=1
[46] (Broken Link!) http://www.ag.ndsu.nodak.edu/aginfo/entomology/entupdates/Sunflower/a1331sunflowerhandbook.pdf
[47] http://www.sunflowernsa.com/growers/approved-chemicals/insecticides-test/
[48] http://www.mydigitalpublication.com/publication/?i=151958&p=41
[49] http://www.sunflowernsa.com/growers/approved-chemicals/insecticides-test/
[50] http://www.farmassist.com/agriedge/images/Resource_PDFs/Soybean/Warrior_Zeon.pdf
[51] http://www2.dupont.com/Production_Agriculture/en_US/assets/downloads/pdfs/K-09315.pdf
[52] http://www.ontariograinfarmer.ca/MAGAZINE.aspx?aid=534
[53] http://en.wikipedia.org/wiki/List_of_hyperaccumulators
[54] Bonmatin, JM, et al (2005) Behaviour of Imidacloprid in Fields. Toxicity for Honey Bees. In Environmental chemistry: green chemistry and pollutants in ecosystems pp. 483-49. http://www.buzzaboutbees.net/support-files/bonmatin2005behaviour-of-imidacloprid-in-fields.pdf
[55] http://cornandsoybeandigest.com/seed/do-soy-seed-treatments-pay?page=2
[56] https://scientificbeekeeping.com/historical-pesticide-overview/
[57] http://www.centerforfoodsafety.org/press-releases/1911/cfs-beekeepers-and-public-interest-groups-sue-epa-over-bee-toxic-pesticides
[58] http://www.theworldlawgroup.com/files/file/docs/Soulier_health_environment_June_2012.pdf
[59] http://www.soulier-avocats.com/upload/documents/Soulier_health_environment_september_2010_F.pdf
[60] http://westernfarmpress.com/government/pesticide-battle-over-honey-bee-health-under-way?page=1
[61] http://westernfarmpress.com/management/total-ag-pesticide-elimination-sought-radicals
[62] http://www.neonicreport.com/home/project-compass/
[63] https://scientificbeekeeping.com/pesticide-incident-reporting/
[64] http://pollinatordefense.org/site/
[65] http://cals.arizona.edu/apmc/docs/IPM_Delivers.pdf
[66] Davis, AS, et al (2012) Increasing cropping system diversity balances productivity, profitability and environmental health. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0047149
[67] http://www.pcl.org/pcl_files/5_Wildlife_Habitat_Farmland.pdf
[68] http://pfspbees.org/
[69] http://www.nwf.org/CertifiedWildlifeHabitat/UserAccount/SignIn
Category: Practical Beekeeping Management, Topics
Tags: beekeeper management, biotic, diseases, drought, environmental, factors, pesticides, randy oliver, varroa | beekeeper management Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/beekeeper-management/ |
What Happened To The Bees This Spring? (Part 1 & 2)
First published in: American Bee Journal, June 2013
Part 1: Environmental and Biotic Factors
Setting the Stage
The Lead Up
The Drought
Lack of Good Forage
Varroa
Diseases
Other Indicators of Impending Collapse
An Unexpected Chill
Feedback from Brokers
The Silent Majority
Beekeeper Management
Part 2: The Contribution From Pesticides
The Lynch Mob
Debunking The Myths
The Precautionary Principal
See For Yourself
Be Careful What You Ask For!
The Effect Of Drought
Actions To Take
Bottom Line
References
What Happened To The Bees This Spring?
Part 1: Environmental And Biotic Factors
Randy Oliver
ScientificBeekeeping.com
First published in ABJ June 2013
By now, most everyone has heard that honey bee colonies died in massive numbers this winter. Reporter Dan Rather, in his newscast Buzzkill [1], showed unfortunate beekeepers, some of whom had lost half or more of their colonies, predicting gloom and doom for the bee industry. What were the causes of this year's bee shortage? As Rather says, "Everyone has an opinion." The question is whether those opinions are based upon fact! So let's go over the events leading up to the bee supply debacle.
Setting The Stage
Nearly 800,000 acres of almond trees in California came into bloom this winter--the trees typically start flowering about Valentine's Day, and the bloom lasts for only about two weeks. Almonds require cross fertilization between adjacent rows of varieties (Fig. 1), and honey bees are trucked in from all over the country to do the job (roughly a million and a half colonies). Many large commercial beekeepers move their hives into California in November to overwinter in holding yards; others build them up on winter pollen flows in Florida or Texas, or hold them in temperature-controlled potato cellars until shortly before bloom. The hives are generally placed into the orchards about a week before the first flowers appear. There is virtually no forage in the orchards prior to, or after bloom in many areas.
Figure 1. An almond orchard in late February, showing the flowering of rows of different cultivars required for cross pollination. The bare "late" varieties have not yet bloomed; the green "early" pollenizers have finished bloom. Grading of colonies is normally done during the bloom of the main crop (usually Nonpareil).
The Lead Up
Two seasons ago there was also a shortage of bees in almonds, following the coldest January (2011) in 17 years (cold being a major stressor of wintering bee colonies). Beekeepers then replaced their deadouts with package bees and splits, thus starting a new generation of colonies, which tend to have lower varroa mite levels than established colonies. These colonies entered autumn 2011 in pretty good shape, and then enjoyed the fourth warmest January (2012) on record! As a result, there was the lowest rate of winter mortality in years, and plenty of bees for almonds in 2012 (Fig. 2).
Figure 2. Percent winter losses since the beginning of the national survey--the data is not yet in for 2012/13. Note that there has been a general downward trend, suggesting that whatever caused the high losses in 2007/8 has not been such a problem in recent years. Note also the cyclical nature of colony winter losses, with high losses in 2004/5, 2007/8, 2009/10, and 2012/13 (some data not shown) Data from [[i]].
[i] http://www.ars.usda.gov/is/pr/2012/120531.htm and California DPR.
I was curious as to whether the colony loss rate was linked to the use of neonicotinoid insecticides. There is no recent USDA data, so I went through the California Pesticide Use Reports (data available through 2010). I plotted the amount of imidacloprid applied to crops in California in the preceding year in red (the seed treatment clothianidin didn't even make the top 100 list of pesticides applied). Although there appears to be a possible correlation from 2006 through 2009, the trends were reversed for 2010. I will be curious to add the 2011 data when it becomes available.
In March of 2012 I received a phone call from a California queen producer who had a prescient insight as to a potential brewing disaster. He was receiving calls for queen bees from Northern beekeepers whose bees had already grown to swarming condition due to the unseasonably warm spring weather (Fig. 3).
Figure 3. Last year's warm spring in much of the country lead to early broodrearing, and as a result, early buildup of varroa levels. Note the record warm spring in the Midwest.
The queen producer noted that such early brood rearing also meant early mite buildup, and predicted that since most Midwestern beekeepers treat for mites by the calendar, that they would unknowingly allow mites to build to excessive levels before treatment. This was strike one against the bees.
The Drought
Then it didn't rain-by midsummer, it was clear that the continental U.S. was in serious drought, including California, whose beekeepers supply nearly half the bees for almond pollination. The only ways that we kept our colonies strong was to either feed expensive pollen supplement and sugar syrup, or to move them to elusive better pasture out of state. By late summer, 60% of the U.S. was in drought, meaning that unless your bees were next to soybeans or irrigated crops, there was little forage for them. This lack of good nutrition was strike two against the bees (Fig. 4).
Figure 4. The severe drought in the Midwest really put the hurt to bee pasture in those states in which the majority of commercial hives spend the summer. Source [[i]].
[i] http://www.ncdc.noaa.gov/temp-and-precip/maps.php
Drought not only dries up nectar and pollen sources, but also forces bees to fly further and more frequently for water. Plus it concentrates ag chemicals and pesticides in the few sources of surface water available to bees. The bees started to show the hurt.
Beekeepers tried to move their hives to areas of better forage, sometimes overstocking an area with too many hives, which led to excessive competition for resources, and the spreading of parasites. Others desperately chased less desirable crops such as sunflowers. Colonies in holding yards in California found little to eat, due to our record dry weather. Some beekeepers with winter eucalyptus locations found them crowded with other hives.
Lack Of Good Forage
In Buzzkill, Bret Adee brought up the fact that bee pasture in the Midwest is disappearing under the plow, largely due to our environmentally-irresponsible taxpayer-subsidized policies that encourage farmers to plant every square foot of land into corn (Fig. 5). Bee brokers told me that colonies coming to almonds from the Midwest were in generally poorer shape this year than those coming from the southern states.
Practical application: some Midwestern beekeepers split their operations, hauling some to the South to rebuild over winter, and the rest directly to California-there was a night and day difference as to how the colonies looked in February!
Figure 5. Grasslands and wetlands in the Corn Belt are rapidly being converted to monocultural, heavily herbicided corn/soy, which eliminates virtually all bee and wildlife forage. A new study found that between 2006 and 2011 there was a net loss of 1.3 million acres of grassland. This affects not only bees--the authors [[i]] state that "As a consequence, populations of grassland nesting birds are declining faster than any other group of birds in North America."
[i] Wright, CK & MC Wimberly (2013) Recent land use change in the Western Corn Belt threatens grasslands and wetlands. https://www.motherjones.com/files/pnas201215404_nwow5w1.pdf
To put this loss of bee pasture into perspective, I asked some Dakota beekeepers for estimates of how many acres of CRP grassland are needed to sustain a colony of bees. In recent years, the overall hive density in North Dakota has been more than 10 hives per square mile (less than 64 acres per hive, including wastelands).
Practical application: the best guess by those beekeepers was that each colony of bees requires about 5-15 acres of productive land for forage (late summer forage being the critical factor). If we use the figure of 10 acres per colony, then the conversion of 1.3 million acres of grassland to herbicided cropland suggests that forage for 130,000 colonies of bees has been eliminated in the past five years in the Corn Belt alone! This figure represents nearly 9% of all colonies needed for almond pollination.
Varroa
An excellent window into the causes of colony health problems is the USDA National Honey Bee Pests and Diseases Survey Report [5] (the latest data have not yet been released). It is worrisome that varroa levels appear to be steadily climbing year after year.
And if the drought and forage problems weren't enough, the favored miticide of commercial beekeepers became unavailable for a time last summer, and mite levels built to killing levels in a number of operations. By late July, some of us were already predicting a disaster for the upcoming almond pollination season. Although many beekeepers finally got mite levels down with late-season treatments, the damage had already been done, and there was no turning the colonies around. Strike three for the bees!
In November semi loads of hives started moving into California, or had been placed in potato cellars. Some of the colonies that arrived from the Midwest were in poor shape, or crawling with mites. Oddly, few beekeepers at the time owned up to having problems, despite the reports that I kept hearing of mite and forage issues! I'm not sure whether this was due to denial, wishful thinking, simple lack of lifting the lids, or something else.
Diseases
Nosema infection also runs rampant across the country--70% of colonies were infected in June of last year. The stressful factors leading up to almond bloom apparently put a lot of hives close to the "tip point" at which pathogens can overwhelm the colony immune system and start it going backwards, or initiate the slide into sudden depopulation (detailed at [6]). Few seem to be mentioning signs of CCD-it is unfortunate that the media keep using that term as a catch-all for all hive problems!
One should keep in mind that the winter collapse issue appears to be cyclical, similar to flu or other pathogen epidemics. I have strong reason to suspect that the constantly-evolving viruses are involved in these colony collapse epidemics.
There has also been a strong resurgence of European Foulbrood and other unidentified brood diseases [7] (Figs. 6, 7, and 8). Unlike EFB of old, the new forms don't go away with a nectar flow.
Figure 6. "Shot brood" due to EFB. Note the fat queen near the center. Despite her vigorous egglaying, this colony is unable to pull ahead due to excessive brood mortality. Lots of beekeepers reported EFB symptoms this winter.
Figure 7. You really have to look hard in some colonies with spotty brood to see the cause! Two larvae in this photo show signs of EFB infection.
Figure 8. Dying brood from one of my sick colonies this spring with EFB-like symptoms. Note the "shot" pattern, the twisted larvae, and the dried larval remains. There is also some AFB-like coloration, but lack of roping or AFB odor (this odor is distinct and sour), nor a positive Holst milk test. In this colony, even pupae were dying. I observe these symptoms independent of whether the hives went to almond pollination or not. Colonies with this (or similar) infection cannot grow. Treatment with oxytetracycline generally clears it up.
One thing that I noticed in Buzzkill was the uneaten pollen supplement patties in many of the crashed hives. I've mentioned before [8] that I've found a colony's failure to consume pollen supplement to be a reliable predictor that that colony will later collapse.
Another strong predictor of winter collapse is weak strength in fall (upcoming article), again strongly suggesting that those colonies already have some sort of health issue going into winter. I heard reports from all over the country that bees went into winter in poor condition.
An Unexpected Chill
The final blow to hives in California was a blast of icy weather (Fig. 9). This unexpected chilling compounded all the existing problems! I've previously pointed out that colony collapse often follows unseasonable chills, since it shifts the tip point for virus and nosema epidemics. Clusters that had expanded for broodrearing contracted, resulting in chilled brood and dead young bees on the ground. My own colonies simply shut down broodrearing completely, losing about two weeks of buildup.
Figure 9. Chilling events (blue arrows) in Modesto, California this winter (the dark blue lines represent normal highs and lows). The unusual chilling in late December and early January (hitting the '20's in a number of areas) came at the time when colonies normally begin to build up for almonds. This severe (for California) cold set the already-stressed colonies back hard, and may have allowed nosema and viruses to gain the upper hand. Graph from wunderground.com.
At the national convention in January, the first reports of beekeepers with collapsing operations were heard. But still, the industry was in denial, with an apparent glut of promised bees as late as the end of the month (two weeks before start of bloom)! But when the rubber finally hit the road in mid February, that illusory supply quickly evaporated, with desperate growers and brokers scrambling to obtain bees--some offering obscenely high prices for substandard colonies.
And then, due to the cool spring, the trees held off on blooming for an extra 10-14 days [9]-colonies placed in anticipation of normal start of bloom just sat there starving and shivering on the cold orchard floors.
Practical application: the biology here is that this is the time of the "spring turnover" in bee populations in California, during which the old overwintered adult bees must rear their replacements for the spring buildup of population. The conditions in the almond orchards prior to bloom are miserable for smaller colonies--it is warm enough to encourage them to break winter cluster and expand the broodnest, but overnight frosts on the Valley floor can cause serious chill stress. Furthermore, it is often warm enough to fly at midday, but there is virtually nothing to forage upon until the trees start blooming! Such fruitless foraging further wears out the workers, and allows sick bees to drift to adjacent hives. Worse yet, the desperate foragers rob out any dead or dying colonies in adjacent orchards, rapidly and effectively transmitting mites, nosema, viruses, and anything else harmful in the deadouts.
Many colonies went backwards during this excruciatingly long wait. Some beekeepers told me that hives graded at placement scored better than those graded at bloom (just the opposite of normal)!
I've been carefully observing spring turnover in my "dinks" (weak colonies) in February (Fig. 10). What I find is that the problem is generally not the queen; rather, the colonies are infected with some pathogen- most commonly nosema [10], the paralytic viruses [11], or EFB (or EFB-like brood disease). Those colonies that are able to successfully emerge one solid round of brood are often able to "clear" the infection and completely rebound by April. Those that get hit by frost in February often collapse.
Figure 10. An example of an unsuccessful spring turnover. This colony is in the middle of typical February collapse from nosema or IAPV. You can easily see the outline of the area recently covered with brood, delineated by the crescents of freshly-packed pollen. Colonies undergoing this sort of depopulation tend not to forage for nectar, and do not respond well to supplemental feeding. This colony continued to collapse quickly, and finally died in a cold snap a week later--with only silver-dollar sized patch of dead bees remaining.
Feedback From Brokers
I asked a few of the major pollination brokers for their observations on the colony shortage this season. Their feedback suggested that the causes for the bee shortage were varied and many.
Summary:
Most were able to eventually fill their contracts. Beekeepers often hold colonies in reserve "just in case," or gambling that in "short" years they can rent those last hives at an elevated price. Also, when the offered price went up, hives not originally intended to go to almonds were loaded up at the last minute and shipped to California (I was in Florida at the start of bloom, and had an inspector tell me of certifying colonies for shipment after the bloom had already begun!).
A number of hives received in November were already headed downhill. Some exhibited the symptom of bees not clustering properly (a typical sign preceding sudden colony depopulation/CCD). Some arrived crawling with mites, or with recent mite treatments in place (suggesting that they were treated too late).
Some graders saw piles of dead bees in front of hives--cause unknown. There were reports of some herbicide tank mixes killing bees.
Many of the placed colonies were below standard grade-- growers paid for less than they expected!
Graders told me that there was a huge variation in hive strength from beekeeper to beekeeper. Many hives were strong (12-16 frames of bees) and healthy; other operations graded at zero to three frames of bees (some of the deadouts had spider webs inside, suggesting that they hadn't been occupied by bees for some time).
The unusual winter chill was tough on colonies that had been stimulated into early buildup, and then forced to contract their broodnests. Some colonies kicked out chilled brood and dead bees afterwards.
Many beekeepers watched their colonies go "backward" prior to bloom.
Colonies from the Southern states (especially those delivered in February) were generally in better shape than those from the Midwest.
Midwestern beekeepers blamed drought, mites, poor nutrition.
Several beekeepers said that their best bees came from remote areas, and their worst from ag areas.
A number of beekeepers admitted inadequate mite treatment; mites were a recurrent theme.
There were a number of reports of EFB hitting colonies.
Some had gotten hit last summer with pesticide sprays, and their colonies didn't recover.
"There were good bees and bad bees from every state. They all seemed to have different problems depending on location/state."
Many good beekeepers simply didn't know what happened to their hives; there were lots of lifeless hives delivered. The atmosphere was ripe with speculation as to the actual causes.
"The shortage was also created by beekeepers that chose not to come to California for a variety of reasons. They can make more money with honey, didn't get paid for what they have brought in the past, bees come back home with mites, beetles and whatever else takes a ride on the hives. Beekeepers don't want to risk bee health to chase the dollar." Many out-of-state beekeepers have had bad experiences going to almonds, and simply don't feel that it's worth it. The supply of bees will largely depend upon the price that growers offer for renting them!
The Silent Majority
Buzzkill leaves one with the impression that the entire bee and almond industries are on the verge of collapse. Of course, the news media focus on fear and disaster, so we may consider taking such dire projections with a grain of salt. In the case of Dan Rather, the focus was on the beekeepers with troubles, not upon those who successfully filled their pollination contracts.
So just how severe was the problem? Let's say that there was an overall shortage of 100,000 hives (a figure that I heard floated)--that would represent only about 6% of the total number of hives placed into almond pollination. The other 94% were successfully delivered (although a proportion of those were weak due to the poor season).
Since the debacle, I've heard from plenty of beekeepers whom I'll refer to as the "silent majority," who experienced "normal" colony winter losses in the 5-25% range, and who successfully filled their pollination contracts. Although the hearts of all beekeepers go out to those who suffered severe colony losses, many felt that some of those losses could have been prevented if the afflicted beekeepers had been more proactive than reactive.
And don't forget those upon whom the rest of the industry depends to supply bees for restocking their deadouts! The California package producers, who have been pollinating almonds for decades, are routinely counted on to consistently take strong hives to almonds, and to then shake over a hundred thousand packages of bees for sale afterwards. Few of these major producers experience severe unexplained colony losses.
Beekeeper Management
By no means am I suggesting that those beekeepers who suffered losses engaged in poor beekeeping practices, but I can't help but notice that not all beekeepers were equally affected--a great number provided strong, healthy colonies to almonds. I've spoken to some of them-the common thread is that those who recognized the problems of poor nutrition and mites in August, and took remedial action for the rest of the season, had acceptable winter losses.
Some beekeepers who really put serious effort and money into bee husbandry were even able to sell "shook bees" from their colonies to others in February! For example, watch Keith Jarrett feeding substantial quantities of pollen supplement to very strong colonies in January [12]--Keith consistently brings very strong colonies to almonds every year, and this year was no exception!
Practical application: I'm here to tell you, that one lesson that I've learned during our intense California drought, is that those yards that I fed with protein in late summer before they started going downhill went to almonds much stronger than those that I didn't feed until fall! Proactive is better than reactive--if you wait until colonies are already going downhill, it is much more difficult to turn them around!
I've often been accused of being politically incorrect for speaking frankly. I'd like to make amends at this point by retiring the rude and unsympathetic term "PPB" (Piss Poor Beekeeping). The fact is that the average wintering loss for the past few years has hovered around 30%. So if you experience 30% losses, you can now proudly call yourself an "Average" beekeeper!
But what about those beekeepers who consistently manage to enjoy lower rates of winter loss? I propose that we call them "Lucky" beekeepers, and the best of them, "Consistently Lucky."
Practical application: the harder those beekeepers work, the luckier they get!
But there were clearly "unlucky" beekeepers this year--especially the "big boys" who brought tens of thousands of hives from the drought-ravaged, and corn-converted Midwest to California. California beekeepers are used to summer drought. We have learned to either move our colonies to better (often irrigated) pasture, or to feed expensive pollen supplements. This would be a very expensive proposition to the larger operators, with hives spread all over the place--a cost not covered by current pollination prices.
What Happened To The Bees This Spring?
Part 2: The Contribution From Pesticides
Randy Oliver
ScientificBeekeeping.com
First published in: American Bee Journal, July 2013
It's pretty straightforward to attribute the majority of colony losses this winter to the usual and aforementioned causes, but a number of beekeepers are also pointing the finger at pesticides. There is no doubt that in certain areas pesticides were a serious issue to beekeepers. Colonies set back by pesticide kills may not fully recover over the season, and those going into winter with pesticide residues may go downhill. There is also reason to suspect that pesticides and miticides have something to do with today's high rates of queen failure.
The bees in some drought-stricken areas were forced to forage on irrigated and pesticide-laden crops--the only place in which there was anything to eat. This changes the entire dynamics of pesticide exposure, since residues would no longer be diluted by the pollen and nectar of non crop plants. The lack of good natural forage also suppresses the ability of colonies to deal with the insult of those pesticides. And colonies may be forced, by necessity, to forage upon one treated crop after another, resulting in multiple exposures.
Practical application: under drought conditions, bees may suffer more from pesticides than when times are good.
Due to the current high prices for agricultural commodities, farmers are often applying pesticides indiscriminately as "risk insurance" rather than due to actual need. A chilling recommendation from an extension entomologist reads:
I encourage you to be risk averse and to make an investment that will pay dividends for your valuable crop. Consider applying [flubendiamide, indoxacarb, or spinosad] for corn earworm. If you have stink bugs and are in the [mature plant] stages, you might want to tank mix one of these products with a pyrethroid. A tank mix of a pyrethroid and acephate are an option, but will wipe out all beneficials [13].
The first three insecticides mentioned are considered to be "reduced risk" to bees if residues are allowed to dry for a few hours, but no mention was made to spray at night. Of the five insecticides recommended above for spraying on corn in tassel, at least four are highly toxic to bees if sprayed during the day! No farmer wants to kill bees, but with recommendations like this from state extension agents, well-meaning growers may unwittingly be hurting pollinators.
Bees in agricultural areas are exposed to a vast array of insecticides, miticides, fungicides and surfactants--many of which have clear links to colony health problems. And applications of new mixes of chemicals are up. For example, in addition to the neonicotinoid seed treatments, granular insecticide soil treatments for corn in the Midwest were up by 30% over the previous year [14]. These treatments consist of combinations of organophosphates and pyrethroids.
But I'm not hearing either the bird groups or beekeepers even addressing these treatments! It is scary to read the sales literature for Counter insecticide, the organophosphate terbufos [15]. Growers are encouraged to apply it at planting time, despite the facts that:
"Terbufos is highly toxic to birds, fish, and aquatic invertebrates [and bees]. [It] shows significant acute mortalities of birds, mammals, reptiles, and fish resulting from broadcast application...In the same study, the application of terbufos as a soil-incorporated treatment to corn...resulted in acute mortalities to birds and reptiles" [16].
Terbufos is strongly systemic, meaning that it is absorbed by the plant roots and could be expected to be expressed in the pollen and nectar.
It can synergize with other pesticides since it ties up the critical CP450 enzymes used in detoxification, to the extent that growers are cautioned that it can cause problems to corn from herbicides [17].
During drought, certain insect pests become more problematic, perhaps resulting in increased exposure to insecticides by bees. For example, drought encourages corn leaf aphids. Read this chilling recommendation for aphids on corn during tasseling (when bees are actively foraging):
If less than 50% of pollination has occurred, aphids and honeydew are covering tassels and plants are stressed, an insecticide may be necessary to ensure adequate pollination, but treatments need to be made within 48 hours of tassel emergence. Asana XL, Brigade, Capture, Cobalt, Dimethoate, Lannate, Lorsban, or Malathion may be used for control [18].
Or this:
Prolonged drought always raises the specter of two-spotted spider mite outbreaks in soybeans and corn. As the 2012 drought intensifies in Minnesota, infestations are reaching treatable levels...The only products that are recommended for spider mites in soybean include insecticides containing chlorpyrifos, dimethoate and bifenthrin[18].
The names of the recommended insecticides above strike fear into the hearts of beekeepers!
Practical application: many "consistently lucky" beekeepers go to great effort to allow their colonies to recover after exposure to pesticides--moving them to unsprayed areas or natural forage, or by immediately feeding protein supplement to stimulate increased broodrearing. Unfortunately, such "recovery" areas are getting harder and harder to find.
The Lynch Mob
Despite the fact that a wide range of bee-toxic insecticides are being applied (often during bloom) to corn, soy, sunflowers, alfalfa, cotton, and other major crops, if you Google anything about insecticide use, you'll quickly find that the blogosphere focuses only upon the putative link between a single class of insecticides--the neonicotinoids-and the demise of pollinators [19].
People look at me incredulously when I point out that there is zero firm evidence to date that the neonic seed treatments are a serious problem! But the notion that all honey bee problems are caused by an insidious new insecticide resonates with a distrustful public [20], and has firmly established itself as "common knowledge." But repeating something does not make it true!
"It's easier to fool people than to convince them that they have been fooled"-Mark Twain
Practical application: the question is, "Are the neonic seed treatments being railroaded into a guilty verdict in the media's kangaroo court of public opinion?"
One group recently brought suit against the EPA to ban the use of the seed treatments clothianidin and thiamethoxam [21], neither of which even make California's top 100 list of pesticides applied [22], nor that have ever been demonstrated to harm colonies feeding on the pollen or nectar of seed-treated plants! A number of people have made up their minds that the neonics are the main cause of colony collapse, and it appears that no amount of facts to the contrary will cause them to reconsider!
Debunking The Myths
As anyone who knows me will tell you, I am a stickler for honesty, accuracy, and factuality. I am concerned about the amount of misinformation and speculation going around about the neonics. So let's look at some of the claims vs. the actual facts.
Arguments Against Neonic Seed Treatments Actual Facts
The neonicotinoids have been "linked" to increased colony mortality. In actuality, such a "link" is merely an urban legend, and has never been demonstrated or confirmed in any study.
On the other hand, the residues of other classes of pesticides are more suspect for causing increased brood or adult bee mortality [24].
The timing of CCD coincides with the introduction of the neonic seed treatments in 2004. CCD started in California bees in the winter of 2004/2005, prior to them ever being exposed to seed-treated crops.
But what else could have changed at that time other than the introduction of neonics? In California, Dr. Eric Mussen [25] determined that the increased colony losses were due to poor summer forage and failure of mite control products (just as this last winter).
There is actually a much stronger association between the incidence of the novel gut parasite Nosema ceranae and increased colony mortality [26].
But the main thing that has changed is the dynamics of the varroa/virus complex, which coincidentally occurred at about the same time that the neonics came into use.
European countries banned the neonics, and the bees recovered after those bans. A few countries placed temporary suspensions on certain seed treatments until planting dust issues were resolved [27]--only Germany has one suspension still in place. The foliar applications were not suspended. The suspensions did not resolve bee health problems.
The European Food Safety Authority recently decided that neonics pose a threat to bees. "The Center for Regulatory Effectiveness (CRE) has recently completed a Data Quality Act (DQA) Alert on the ... (EFSA) report on neonicotinoids which found that neonicotinoids pose a risk to bees. The DQA Alert outlines the serious deficiencies of the EFSA report and demonstrates why the EFSA report violates the DQA...In particular, the EFSA report failed to maximize the objectivity of the data by failing to reconcile numerous studies whose conclusions contradicted the findings of the EFSA report" [28].
Several lab studies have found that neonics affect individual bee behavior, longevity, or immunity. True -- although many studies used unrealistically high doses. The question is whether such artificial studies apply to actual colonies in the field. The numerous field studies to date have failed to find any link between seed treatments and later colony health issues.
It is the seed treatments that make corn a problem. As Bret Adee points out in Buzzkill, corn is replacing pastureland (Fig. 4). Corn, as grown today, is a virtual "bee desert" (similar to the way in which suburban lawns are green bee deserts). And it's not only the bees that this is affecting, the populations of birds and other wildlife are plummeting due to loss of favorable habitat (see my blog on birds and neonics [29]).
A recent survey by Dr. Jerry Bromenshenk found that bees actually avoid field corn pollen, and are exposed to very little of the seed treatment residues [30].
Numerous independent studies, and the experiences of stationary beekeepers throughout the Corn Belt, support the conclusion that colonies can thrive when surrounded by corn, provided that there is some alternative forage within flight range.
As the use of neonic seed treatments increases, bee mortality goes up. In actuality, colony mortality rates go up and down year to year, largely dependent upon weather and varroa mite control. If the neonics were to blame for this winter's bee losses, why didn't they cause similar losses last winter, in which the colony mortality rate was the lowest in years?
French beekeepers also started seeing problems with the introduction of the neonics. I've spoken with beekeepers in France whose apiaries are in pesticide-free areas. They tell me that they experience the same sorts of colony mortality problems as do those in areas exposed to neonics.
Bees in the U.S. are commonly exposed to neonicotinoids. In the most recent USDA survey (100 samples across the country), imidacloprid was only detected in 9% of the samples [31] (although I found some of the residue levels alarmingly high). However, the most common seed treatment, clothianidin (or its degradation products), was not detected at all!
The above real-world data suggests that efforts to ban clothianidin as a seed treatment may be misplaced. It appears that imidacloprid, especially as a foliar application, would be of more concern.
Neonics are the most common pesticides that bees are exposed to. In the above survey, other serious insecticides were more commonly prevalent: chlorpyrifos (in 20% of samples), cyhalothrin (in 7%), and endosulfan (in 11%).
Notably, there was also a high prevalence of beekeeper-applied miticides: fluvalinate (in 38%), coumaphos (in 87%), amitraz (in 27%), fenpyroximate (in 11%), and thymol (in 27%).
There was even higher exposure to fungicides and adjuvants.
It is misleading for the pesticide companies to blame the problems on varroa, nosema, or poor nutrition. The above survey (over 1000 samples) found that the average varroa infestation rate in the U.S. in autumn is above the danger level for virus epidemics!
Sixty to 100% of hives are infected with nosema in December.
Summer drought has historically been associated with high winter mortality.
But didn't the planting dust from corn seeding kill colonies in Ontario? Planting dust is separate issue that clearly needs to be remedied. It does on occasion cause bee kills, for which beekeepers are rarely compensated. This situation must change! All parties are actively working on solutions [32].
Bees in certain agricultural areas tend to go downhill later in the season. This has been observed for a long time--long before the neonics. The question is, which chemicals, chemical synergies, or chemical/nutrient interactions are responsible? The Frazier/Mullin team at Penn State has developed a protocol for helping to figure this out. I strongly support its adoption by the EPA for pesticide risk analysis.
Colonies foraging upon nectar or pollen of seed-treated crops get poisoned. Ask yourself this: if neonic residues were actually so harmful to bees, how is it that the Canadian beekeepers, whose bees forage largely on seed-treated canola, feeding solely upon a diet of canola nectar and pollen with well-documented residues of clothianidin, experience very low winter losses, despite the long Canadian winter (so long as they control varroa and nosema)?
And how is it that the vast majority of beekeepers in the U.S. Corn Belt report that their colonies thrive and that they have far fewer pesticide issues these days than in the past?
The neonicotinoids are "systemic," meaning that they are in the plants all the time! True, but this property is not unique to the neonics--a number of other insecticides also go systemic. In any case, with seed treatment, the concentration of the insecticide in the plant is only high when the plant is young--it gets diluted as the plant grows (e.g., clothianidin in canola is at a level high enough to kill aphids for only about the first 30 days of growth).
The only time that residues in the plant matter to pollinators is when the mature plant flowers. The amount of seed treatment is carefully calibrated so that the residue in the pollen and nectar are below the level that causes demonstrable harm to bees.
In the case of foliar, drench, or chemigation applications prior to bloom, there are greater possibilities for bees to be exposed to toxic levels.
There are fewer butterflies and pollinators in the fields these days. Not surprising, since the new push for "clean farming" has removed the host plants upon which the butterfly larvae feed. Pollinators are forced to subsist upon the stretches of weeds growing along roads at the edges of fields. But surprisingly, pollinators may be abundant there, suggesting that even though populations as a whole are reduced by habitat conversion, it is that, rather than the use of seed treatments, that causes the population declines.
The evil pesticide companies want to kill honey bees. Give me a break! Does anyone truly believe that anyone wants to kill honey bees? What pesticide company would want the bad press of being associated with killing bees? The chemists and biologists on their staffs earnestly work to develop insecticides that are bee friendly.
The EPA is being derelict in their duty to protect pollinators. I have spoken at length with EPA staff, and reviewed their risk assessments, as well as those by, DEFRA, EFSA, PMRA, and other regulatory agencies. I find that the risk assessors have not overlooked any evidence, are well-informed on the subject of neonics, and are justified in their assessments that the on-the-ground evidence (to date) indicates that neonic seed treatments pose acceptable risk to pollinators.
We must all remember that the tobacco industry tried to hide the fact that nicotine was addictive [33]. Spare me! Does anyone seriously think that the EPA is unaware that industry executives may stretch the truth? Of course the EPA is skeptical of any reassuring claims by the pesticide industry--that's why they go over all studies with a fine-toothed comb!
This winter's losses spell the end to commercial beekeeping. The fact of the matter is that many observers note that the bee supply for almonds often follows a boom-bust cycle. Although losses were high this year, the trend for the last decade has been for beekeepers keep ramping up the supply of bees for almonds. So long as growers are willing to pay a profitable rental rate for colonies, market forces will encourage the bee industry to meet the demand (for a detailed analysis, see [34]).
The Precautionary Principal
"But," you say, "shouldn't we exercise precaution due to the lab studies that find adverse effects from the neonics?" Look, I make my living as a beekeeper, I'm not out to sell insecticides, and am as concerned as the next person about the environment and the safety of the food I eat. I've researched the neonics exhaustively, and addressed them in several articles [35]. I am acutely aware that there are suggestions that the neonics may be causing insidious effects in the environment, and I've studied the excellent environmental document Late Lessons from Early Warnings [36], which hammers the message that we should use the "precautionary principle" when dealing with chemicals. The problem is, there is nothing without risk--for example, you have a 1 in 83 chance of being killed in an auto accident in your lifetime. But most people still take the risk of getting into cars, since they feel that the benefit outweighs the clearly high risk!
My practical perspective as both a scientist and a beekeeper: if researchers perform lab studies on any insecticide, they will find that there are all kinds of negative effects upon bees--this should be pretty obvious, since insecticides are specifically designed to harm insects! However, the majority of these studies are taken out of the context of full colonies under field conditions, where bees fly free and choose the flowers upon which they forage. The evidence to date supports the contention that the neonics, properly used as seed treatments, are indeed an improvement over other insecticide options.
As Dr. Eric Mussen succinctly notes:
Nobody's really been able to show that [the neonicotinoids] are more problematic than the rest [of the pesticides to which bees are exposed] [37].
Far be it from me to suggest that the neonics (or any other pesticides) are harmless! But consider this--if the neonic seed treatments were indeed as harmful as some make them out to be, you'd think that after a decade of intense study that at least one researcher could have come up with a single solid piece of field evidence against them!
Let's do a thought experiment. Why doesn't someone simply put a bunch of healthy hives into the middle of seed treated crops and see whether they die afterward? Oh, I forgot--this experiment has already been run by thousands of beekeepers year after year in the Corn Belt and the Canadian prairie! And those beekeepers have invited me to look at their colonies, sent me photos of colonies stacked head high with honey supers, and bragged about their high winter survival!
Some will argue 'til they're blue in the face, but the fact remains that virtually every beekeeper that I've spoken with in the Corn Belt and in canola areas feels that the seed treatments are not a problem [38]. In fact, most tell me that this is the best it's ever been as far as bees and pesticides!
Common sense: I just don't get what is so hard to understand about the reality that there are thousands of colonies thriving year after year in areas of intense seed treatment? To any reasonable person it would suggest that the treatments are causing little noticeable harm other than the occasional planting dust kill, which I have repeatedly stated is a problem that needs to be corrected!
See For Yourself
Let's look at actual independent (from the manufacturer) data from corn and canola areas:
Corn
I asked friends in the Corn Belt if they had any data on winter losses. It so happens that the Michiana Beekeepers Association has been collecting exactly that since the spring of 2010 (Fig. 11).
Figure 11. Percentage of winter losses by the "Michiana" hobby beekeepers. The 2013 figure is as of mid March; it may eventually go down a bit due to a prolonged cold spring. Note that the winter survival rate appears to be linked to average winter temperature. Thanks to beekeeper Danny Slabaugh for sharing the data; temp deviations from [[i]].
[i] http://www.ncdc.noaa.gov/temp-and-precip/maps
How could the above be? Eighty percent winter survival despite sitting in the middle of seed-treated corn and soy? So of course I did a fact check to confirm that those beekeepers were indeed sitting in corn/soy areas (Fig. 12).
Figure 12. USDA land cover categories for the region in which the Michiana hobby beekeepers keep bees--corn and soy acreage is color coded yellow and green, respectively. The selected area is the top half of Indiana and bottom of Michigan, with Lake Michigan at the left. Clearly, these apiaries were exposed to seed-treated corn and soy! I created the map at [[i]].
[i] http://nassgeodata.gmu.edu/CropScape/
The above figures suggest that colony winter survival for stationary hobby beekeepers in the above corn/soy region is higher than the national average, despite the fact that about half of them don't even treat for mites! They also suggest that the neonics or other pesticides used in corn/soy in that region do not cause excessive winter loss. Finally, the data indicate that a main factor for winter loss rates is the winter temperature.
Canola
I've heard some beekeepers saying that their bees crashed after working canola, suspecting that the seed treatments were the problem. So as a reality check I called a Dakota beekeeper who has been running bees to canola for over a decade--some 10,000 hives last season. He tells me that colony strength after canola varies from year to year, but that he sees no problem with the seed treatments. He did point out that beekeepers should be aware that colonies can plug the broodnest on intense canola flows.
The biology: The plugging out of the broodnest during an intense bloom means that three weeks afterward, there will be few emerging workers to take the place of the worn-out foragers, and the colony population will temporarily plummet. Even worse, the remaining mites are then concentrated onto fewer bees--which can initiate virus epidemics. These colonies must then attempt to rebuild from scratch, starting in August, meaning that the weakened, mite-infested colonies faced three long months of drought last summer for that rebuilding process.
Every field study that I've seen for canola also supports the conclusion that the seed-treatments are safe for bees. I joined other beekeepers and regulators in observing a large-scale study of seed-treated canola in Canada [41]. Canola (or rapeseed) is likely the best test crop, since bees eagerly (and virtually exclusively) forage upon it for both pollen and nectar, meaning that every bit of their food supply contains contain easily verifiable residues of the insecticides. The preliminary results indicate that the clothianidin seed treatment did not harm the colonies [42].
Another recent independent long-term field study in Poland [43] came to the same conclusion. In it, the researchers followed 50 colonies for more than two years under field conditions as they foraged on five different large fields of oilseed rape treated with various combinations of five different neonicotinoids applied by seed treatment and spraying. Pollen and nectar samples were taken, and demonstrated that the bees were clearly exposed to normal residues of the insecticides (there was also additional exposure to other common agricultural pesticides). The colonies were monitored for health, brood, strength, nosema, viruses, and winter survival, and compared to two control apiaries set in an area free of the crop. The results?
During the time from the placing of the colonies on the rape fields until wintering, the colonies developed properly in all groups... All colonies overwintered properly... In both years, during the period of being placed in the oilseed rape fields as well as after being moved to the stationary apiary, none of the groups showed disturbances in development or functioning.
Following a paper that suggested that the seed treatments would impair bumblebee colonies' ability to rear queens, DEFRA performed a common-sense field study last year [44]. Their findings:
...the study has shown that bumble bee colonies remained viable and productive in the presence of the neonicotinoid pesticides under these field conditions...The study underlines the importance of taking care in extrapolating laboratory toxicology studies to the field, as well as the great need of further studies under natural conditions.
Sunflowers
Some beekeepers report that their colonies later crashed after they chased sunflowers last summer for honey. One must keep in mind that sunflowers are not a natural food for honey bees, and provide only poor-quality, nutritionally-inadequate pollen [45]. But the main problem with putting bees on sunflowers may be related to the fact that sunflowers are a native plant--meaning that there are a number of native insects that evolved to feed upon it:
Maximum seed yields often require the use of insecticides to protect the crop from insect competitors. Unfortunately, many of the major insect pests of sunflower attack the crop when it is flowering. Thus, insecticides used to control the pest also harm pollinating bees [46].
If sunflowers are the only forage available, colonies may eventually go downhill, due to the one-two punch of poor pollen nutrition coupled with insecticide exposure. And which pesticides would those be? One scary list- Asana XL, Baythroid, endosulfan, Furadan , Lorsban , methyl or ethyl parathion, , Proaxis, Scout X-TRA, Sevin, Warrior, Mustang Max, Declare, Cobalt, Yuma, Delta Gold, and Grizzly Z [47]!
Note that none of the above are neonics, other than seed treatments for wireworms. Surprisingly, field evidence indicates that the seed treatments only "stun" the wireworms for a while [48], which certainly raises the question as to how harmful they might be to bees months later when the plants flower! I will return to sunflowers below.
Be Careful What You Ask For!
Allow me to assure you that I am no pitchman for neonics or any other insecticide--the typical farmer practices far too little integrated pest management, and applies far too many pesticides! All insecticides (and several fungicides and adjuvants) cause problems to pollinators--the neonics are no exception. Any systemic insecticide has the potential to harm bees when applied as foliar applications, by chemigation, or to flowering trees, but it there is no compelling evidence that the neonics are any worse than the alternatives in most applications. On the contrary, there is quite a bit of evidence that they may often be "safer" ("reduced risk").
If the neonic seed treatments were banned, it's not as though all agriculture is suddenly going to go pesticide free--only about 1% of U.S. cropland is registered as "organic"! We must consider the likely alternatives. The products that farmers would then use to control insects would need to be sprayed all over the cropland--we'd then be back to the problem that the bulk of sprayed insecticides go into the environment without ever hitting the intended pest!
I hear from knowledgeable beekeepers that worse than in previous years, some of the new formulations of the spray-applied insecticides [49, 50, 51] can really knock the snot out of bees! One large beekeeper found his hives already dead before moving them away from the fields. Again, this was not a neonicotinoid issue.
Practical application: no one is saying that the neonics are "harmless." The question is whether they are better or worse than the alternatives.
The Effect Of Drought
Let's discuss some of the problems (or suspected problems) with the neonics last season. The record warm and dry spring appeared to exacerbate corn planting dust issues (corn seeds are the worst offender due to their non spherical shape). Beekeepers in some areas of the Corn Belt, the East Coast, and in Ontario suffered from confirmed (in at least some of the cases) planting dust kills (although many went on to make good honey crops after their colonies recovered). The final analysis from Ontario is not yet completed, but dry soil conditions and an early clover bloom likely contributed to the problem. Regulators and the seed companies are working on solutions to the problem [52]. Still, IMHO it is unacceptable to ask beekeepers to bear the burden of bee kills without compensation, and no one could blame the affected beekeepers for being pissed!
Drought-stressed plants
There are a number of advantages to the neonic seed treatments. Besides their safety to the farmer and to most wildlife, there is virtually no way for the farmer to misapply them! The timing of application is only at planting time (when bees normally have little interest in the bare fields), and the dose is determined by the seed-treating company. This means that the applicator can't be tempted to apply at the wrong time, or to over apply too strong a dose (however, their excessive near universal use can be expected to accelerate the development of resistant pests).
That said, beekeeper Bret Adee brought an interesting question to my attention: the dose of seed-applied systemic insecticides (whether neonic or other) is based upon the dilution factor as the plant grows, so that the residues in nectar and pollen will be reduced to below the "no observed adverse effects level." But what happens during drought, when the water-stressed plants only grow knee high before desperately flowering? There would be far less plant biomass in which to dilute the insecticide (assuming that drought-stressed plants absorb the same amount from the seed treatment).
Certain plants (including sunflowers and canola) are known to "hyperaccumulate" toxic metals [53], perhaps more so during drought. Could this also be the case with systemic insecticides? Something that's been stuck in the back of my mind is that Bonmantin [54] found that the concentration of imidacloprid first drops in sunflower plant tissue as it grows, and then reconcentrates in the flower heads.
It occurs to me that the translocation of systemic insecticides is generally studied in plants grown under "normal" conditions. I'd very much like to see data for residues in pollen and nectar from seed-treated plants grown under drought. Had we thought of this earlier, we could have collected pollen and nectar samples from drought-stressed plants last summer. I'm currently trying to track down any data or samples from such plants--if any reader has any such sample analyses, please let me know!
Practical application: the above hypothesis is speculative, but we need actual data from drought-stressed plants to see whether such an effect occurs. If so, it would need to be taken into consideration for the registration of seed treatment products!
Once planting was completed and the drought took its toll, the reports that I've heard are that soybean honey saved a lot of bee operations this season, right in the middle of treated corn/soy farmland. In this case, seed treatment with neonicotinoids may have been a blessing to beekeepers:
The benefits of [seed treatment] not only include the early-season disease control but also suppression of soybean aphids for quite a ways into the growing season. With it, we typically make only one foliar insecticide application for aphid control, usually in August, instead of two applications when [treatment] isn't used. In 2012, with the extremely dry conditions in mid-season, there wasn't as much of an aphid problem, and we treated just 300 acres of soybeans...Last year we sprayed closer to 30,000 acres for aphids [55].
On the other hand, some beekeepers on alfalfa or cotton got hit hard by other classes of insecticides. A hit from a pesticide application can lead to poor subsequent colony performance, queen failure, dwindling, or winter collapse. ABJ published an excellent series of articles on pesticides by Drs. Barbara and Eric Erickson in 1983; Editor Joe Graham has graciously granted me permission to post copies of those articles to my website [56]--I strongly suggest any beekeepers interested in pesticide issues read them! In the second article, the authors discuss both the problems with systemic insecticides and of sublethal effects--note that these articles were written long before the introduction of the neonics!
An anti-pesticide group, along with a handful of beekeepers, recently filed suit against the EPA [57], calling for an immediate ban on the two most common neonicotinoid seed treatments, despite the easily-verifiable fact that hundreds of thousands of colonies thrive in the midst of seed-treated corn, soy, and canola! To me, this suit smacks of being some sort of well-orchestrated publicity stunt, and does not serve the interests of either beekeepers or environmentalism. Worse, it now gives the powerful farm lobby cause to label beekeepers as "radical" enemies.
We don't want this battle: do we really want to take on the farm lobby by backing them into a corner? The French beekeepers took a similar case against fipronil all the way to their supreme court and lost [58, 59]-worth reading]. Agriculture is already positioning itself for a fight [60, 61, 62]. Think about it--the EPA lives in fear of a conservative congress slashing their funding. Does anyone really think that they are going to go against the agricultural lobby without unimpeachable evidence? We should also think twice before calling for a ban on the seed treatments--the alternatives are not pretty!
It disturbs me to hear industry executives and lawyers stretching the truth or misrepresenting data. It disturbs me even more to hear my fellow environmentalists and beekeepers doing so! If we wish to maintain credibility, we should hold ourselves to a higher standard. The question we must ask ourselves the way in which we wish to have pesticide regulation decisions made:
1. By the EPA (the Environmental Protection Agency), whose risk assessors carefully study and weigh all available research and evidence in order to make objective and rational decisions, or
2. To have it decided instead by impassioned, fearful, and often misinformed advocacy groups who hire lawyers and pressure politicians who know little about the subject?
We depend upon the EPA to strike a balance between the availability of cheap food and profitability for those who provide it, versus the risks to human and environmental health and safety. It is good to have activists on both sides of the issues (industry and the anti-pesticide groups) to keep the EPA informed. But I don't feel that either of those groups should be telling the EPA which pesticides to register or to ban! Let the regulators do their job!
Rather than wasting EPA's funding to fight frivolous lawsuits, there are more productive actions that we can take:
Help the EPA to do its job by filing "adverse effects incident reports" if you observe a problem due to pesticides [63]. EPA is begging beekeepers to do this! Unless they have documented reports of pesticide problems, their hands are tied as to restricting the uses of those pesticides!
Support the National Pollinator Defense Fund [64]. Our industry is currently represented by a reasoned and knowledgeable group of (mostly) beekeepers. (Challenge to the pesticide companies: why don't you stand behind the safety of your products and donate? The NPDF is about ensuring that your pesticides are properly applied, so there would be no conflict of interest).
If your local state lead agency is not actively investigating bee kills or enforcing pesticide regulations, then use the local media to embarrass them into action!
Keep pressure on the EPA to resolve corn planting dust problems. Here's a wild idea: I'm not sure of the exact figures, but let's say that 90% of the 95 million acres of corn is grown from neonic-treated seed. If the states were to levy a surcharge of 50 cents per acre (neonic seed treatment adds about $12 per acre to seed costs), they could collect over $42 million each year to fund a pool from which to indemnify the occasional beekeeper who suffers a confirmed kill from planting dust!
Tell Congress that we'd like to see wording added to the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) to specifically protect pollinators. Currently, such protection is nebulous (although the EPA is acutely aware of pollinator issues): "The Administrator shall register a pesticide if... when used in accordance with widespread and commonly recognized practice it will not generally cause unreasonable adverse effects on the environment." Unless there is specific wording to protect pollinators, bee kills may not be considered to be "unreasonable"!
We need far more independent field studies to determine which pesticides and application practices are actually causing harm to pollinators. For pesticides in question, keep pressure on the EPA to require additional field trials to demonstrate whether they are indeed safe for pollinators under field conditions. I'd like to see the establishment of monitoring apiaries (and patches of untilled land) in representative agricultural areas nationwide, with the hives in each apiary to be carefully managed by independent parties. Such apiaries and sites could then be closely monitored each summer to see whether honey bees and other pollinators are able to survive local pesticide practices.
Give farmers workable options! Disseminate and promote bee-friendly agricultural practices that don't hurt the farmers' bottom line. For example, by adopting IPM practices, Arizona cotton growers reduced insecticide spraying from 12.5 times a season to only 1.3 times (cutting insecticide use twentyfold), while using more environmentally-friendly insecticides [65]! Another recent study in Iowa found that adding additional clover or alfalfa rotations in corn/soy farmland was equally profitable, improved the soil, used less energy, used far less pesticides, and decreased water pollution [66].
Business and agriculture respond to consumer demand. Consumer demand stopped most dairymen from injecting their cows with the hormone BST. Consumers could do the same by demanding pasture-fed beef and dairy (which would create more pollinator forage)! I'd also like to see the expansion of consumer choices (other than organic certification) that reward farmers who manage their lands to the benefit of wildlife and pollinators. For ideas, see [67. 68. 69].
Bottom Line
In conclusion, it appears that a perfect storm of a preceding exceptionally warm winter, followed by serious drought across the country, the lack of good mite control, a high prevalence of pathogens, and an unexpected California chill in the orchards prior to bloom, resulted in an unusual degree of colony losses. In other words, rather than one specific cause, there were simply not enough of the good things, and too many of the bad things.
I don't see evidence that pesticides were the major factor in the shortage of bees in almonds this winter, although, as usual, a number of individual beekeepers on certain crops certainly took serious hits.
And how about the fear that there won't be enough bees for almond pollination next year? Beekeepers have already told almond growers to expect higher pollination prices next year (especially since California is again going into serious drought, and beekeepers will be forced to invest extra money in feeding their hives). Most every beekeeper I know is madly making increase right now in anticipation of higher pollination prices next season. The fact of the matter is that should conditions allow beekeepers to successfully rebuild their numbers (following the typical swings of our boom/bust cycle), there could possibly even be a glut of bees for almonds next winter!
Feedback And Corrections
A few countries placed temporary suspensions on certain seed treatments until planting dust issues were resolved [27]--only Germany has one suspension still in place. - Actually there are some more: France (Thiamethoxam in oilseed rape, Imidacloprid in corn and sunflower), Italy (all Neonic seed treatment in corn), and Slovenia (Imidacloprid, Thiamethoxam, and Clothianidin seed treatment in all crops)
French beekeepers also started seeing problems with the introduction of the neonics; I've spoken with beekeepers in France whose apiaries are in pesticide-free areas. They tell me that they experience the same sorts of colony mortality problems as do those in areas exposed to neonics - This is, by the way, likewise confirmed by monitoring results from the French authorities.
In the case of foliar, drench, or chemigation applications prior to bloom, there are greater possibilities for bees to be exposed to toxic levels. - This is not the case for foliar application: as Neonics are xylem-systemic, but hardly mobile in the phloem, they can only be distributed in a plant after root uptake, but not be translocated for instance from a leaf to a later developed flower.
Then, on the topic of systemic residues in plants under drought stress: first, I am quite sure that the decrease of concentration in seed-treated plants over time is not only due to dilution, but also to degradation of the compounds - a factor that is not specifically dependent on water availability for the plants (e.g. photodegradation!); second, even if there would be less dilution in plants under drought stress: the concentrations in nectar and pollen of treated crops are normally so low (when we consider average rather than peak concentrations, and when we consider scenarios where colonies have chronically access exclusively to contaminated nectar/pollen over months unlikely in practice), that even an increased concentration due to drought stress-affected plants should not make a significant difference: if we for instance assume an average concentration of let's say 3-4, or even 5 ppb Clothianidin in corn pollen, and likewise assume a dilution reduced to 50% (which is probably exaggerated), then we would still not end up with excessive residues. And finally, we have residue figures from crops grown in different countries, different climatic conditions, and different agronomic practices; though we have not specifically addressed the drought stress scenario, we have seen that residue figures are quite consistent over all scenarios, and there does not appear to be strong evidence that different environmental conditions would substantially (i.e. by orders of magnitude) and systematically alter residue concentrations.
Dr. Christian Maus
Global Pollinator Safety Manager
Bayer CropScience
/
A ppt on the impact of CRP lands on wildlife in North Dakota
http://www.redriverbasincommission.org/Conference/Proceedings/26th_Proceedings/Kading_RRBC_09.pdf
/
Feedback from a Midwestern apiary inspector:
Just a quick update: This beekeeper who recently told his local newspaper that pesticides were killing his bees, he was making excuses. We examined two of his yards with him yesterday. One yard was showing EFB throughout the whole yard. I think his "mid-summer losses" last year (half of that yard's hives) were EFB kicking in with the mid-summer dearth. In his other yard, most of his dead outs were obvious starve outs. He harvested all of their stores with the first frost, and then didn't feed them. So, in my opinion, and from my observations, pesticides are usually being used responsibly, and aren't killing honey bees. I also think, with the aggressive way bees were on soy fields last summer, the systemic pesticides are not harmful to honeybees. I'm not seeing honey bee problems other than EFB getting the upper hand, due to our cold, late spring. My two cents. Thanks.
References
[1] http://www.frequency.com/video/dan-rather-reports-buzzkill/87705620/-/YouTube
[2] http://www.ars.usda.gov/is/pr/2012/120531.htm and California DPR.
[3] http://www.ncdc.noaa.gov/temp-and-precip/maps.php
[4] Wright, CK & MC Wimberly (2013) Recent land use change in the Western Corn Belt threatens grasslands and wetlands. https://www.motherjones.com/files/pnas201215404_nwow5w1.pdf
[5] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
[6] https://scientificbeekeeping.com/sick-bees-part-2-a-model-of-colony-collapse/
[7] vanEngelsdorp, D, et al (2013) Idiopathic brood disease syndrome and queen events as precursors of colony mortality in migratory beekeeping operations in the eastern United States. Preventive Veterinary Medicine 108(2-3): 225-233. http://www.sciencedirect.com/science/article/pii/S0167587712002656
[8] https://scientificbeekeeping.com/sick-bees-part-18a-colony-collapse-revisited/
[9] http://almondinsights.com/692, http://agfax.com/almonds/2013/reports/03042013-almonds-web.htm
[10] https://scientificbeekeeping.com/sick-bees-part-18a-colony-collaspse-revisited/
[11] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2010-2011-Limited_Survey_Report.pdf
[12] http://www.youtube.com/watch?v=y6B5qm2ut18, http://www.youtube.com/watch?v=PYbLbhZXizY
[13] (Broken Link!) http://www.nccrops.com/2012/07/27/insecticide-recommendations-for-corn-earworm-in-soybeans/
[14] http://www.agriview.com/news/crop/corn-soil-insecticide-use-up-dramatically-to-combat-widespread-rootworm/article_5d09decc-5b40-11e2-b485-001a4bcf887a.html
[15] http://www.amvac-chemical.com/products/documents/Counter20G%20Tech-Sell%20Sheet%20-%202013.pdf
[16] http://pmep.cce.cornell.edu/profiles/insect-mite/propetamphos-zetacyperm/terbufos/insect-prof-terbufos.html
[17] http://www.lewishybrids.com/PDF/3-5-2013Agronomic+ALERT+-+Interaction+between+herbicides+insecticides+corn.pdf
[18] http://pest.ca.uky.edu/EXT/Recs/ENT16-Field%20corn.pdf
[19] (Broken Link!) http://www.soybeans.umn.edu/crop/insects/spider_mites.htm
[20] http://www.nytimes.com/2013/04/07/opinion/sunday/calamity-for-our-most-beneficent-insect.html?nl=todaysheadlines&emc=edit_th_20130407&_r=0
[21] http://www.nytimes.com/2013/04/07/opinion/sunday/calamity-for-our-most-beneficent-insect.html?_r=0
[22] http://www.panna.org/press-release/beekeepers-and-public-interest-groups-sue-epa-over-bee-toxic-pesticides
[23] http://www.cdpr.ca.gov/docs/pur/pur10rep/top_100_ais_lbs10.pdf
[24] http://www.extension.org/pages/60318/pesticides-and-their-involvement-in-colony-collapse-disorder
[25] Mussen, EC (2006) Chaotic almond pollination. http://entomology.ucdavis.edu/faculty/mussen/JanFeb2006.pdf
[26] https://scientificbeekeeping.com/sick-bees-part-18e-colony-collapse-revisited-genetically-modified-plants/
[27] http://www.epa.gov/pesticides/about/intheworks/ccd-european-ban.html
[28] http://www.thecre.com/oira_pd/wp-content/uploads/2013/04/DQA-Alert-EU-Commission-Ban-on-Neonicotinoids-4-10.pdf
[29] https://scientificbeekeeping.com/home/news-and-blogs/
[30] Henderson, CB, JJ Bromenshenk, DL Fischer (2013) Clothianidin exposure levels from bee-collected pollen and nectar in seed-treated corn and canola plantings. Proceedings of the American Bee Research Conference.
[31] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
[32] http://www.ontariograinfarmer.ca/MAGAZINE.aspx?aid=534
[33] http://www.pbs.org/wgbh/pages/frontline/shows/settlement/timelines/april94.html
[34] https://scientificbeekeeping.com/2012-almond-pollination-update/
[35] https://scientificbeekeeping.com/neonicotinoids-trying-to-make-sense-of-the-science/, https://scientificbeekeeping.com/neonicotinoids-trying-to-make-sense-of-the-science-part-2/, https://scientificbeekeeping.com/testing-of-bee-feed-syrups-for-neonicotinoid-residues/
[36] http://www.eea.europa.eu/publications/late-lessons-2
[37] http://www.sciencefriday.com/playlist/#play/segment/9088
[38] https://scientificbeekeeping.com/the-extinction-of-the-honey-bee/
[39] http://www.ncdc.noaa.gov/temp-and-precip/maps
[40] http://nassgeodata.gmu.edu/CropScape/
[41] https://scientificbeekeeping.com/a-new-large-scale-trial-of-clothianidin/
[42] http://www.producer.com/daily/ontario-field-study-finds-no-link-between-seed-treatments-bee-deaths/
[43] Pohorecka, K, et al (2013) Residues of neonicotinoid insecticides in bee collected plant materials from oilseed rape crops and their effect on bee colonies. Journal of Apicultural Science 56(2): 115-134. http://www.degruyter.com/view/j/jas.2012.56.issue-2/v10289-012-0029-3/v10289-012-0029-3.xml?format=INT
[44] http://www.fera.defra.gov.uk/scienceResearch/scienceCapabilities/chemicalsEnvironment/documents/reportPS2371Mar13.pdf
[45] http://repository.up.ac.za/bitstream/handle/2263/20334/Nicolson_Chemical(2012).pdf?sequence=1
[46] (Broken Link!) http://www.ag.ndsu.nodak.edu/aginfo/entomology/entupdates/Sunflower/a1331sunflowerhandbook.pdf
[47] http://www.sunflowernsa.com/growers/approved-chemicals/insecticides-test/
[48] http://www.mydigitalpublication.com/publication/?i=151958&p=41
[49] http://www.sunflowernsa.com/growers/approved-chemicals/insecticides-test/
[50] http://www.farmassist.com/agriedge/images/Resource_PDFs/Soybean/Warrior_Zeon.pdf
[51] http://www2.dupont.com/Production_Agriculture/en_US/assets/downloads/pdfs/K-09315.pdf
[52] http://www.ontariograinfarmer.ca/MAGAZINE.aspx?aid=534
[53] http://en.wikipedia.org/wiki/List_of_hyperaccumulators
[54] Bonmatin, JM, et al (2005) Behaviour of Imidacloprid in Fields. Toxicity for Honey Bees. In Environmental chemistry: green chemistry and pollutants in ecosystems pp. 483-49. http://www.buzzaboutbees.net/support-files/bonmatin2005behaviour-of-imidacloprid-in-fields.pdf
[55] http://cornandsoybeandigest.com/seed/do-soy-seed-treatments-pay?page=2
[56] https://scientificbeekeeping.com/historical-pesticide-overview/
[57] http://www.centerforfoodsafety.org/press-releases/1911/cfs-beekeepers-and-public-interest-groups-sue-epa-over-bee-toxic-pesticides
[58] http://www.theworldlawgroup.com/files/file/docs/Soulier_health_environment_June_2012.pdf
[59] http://www.soulier-avocats.com/upload/documents/Soulier_health_environment_september_2010_F.pdf
[60] http://westernfarmpress.com/government/pesticide-battle-over-honey-bee-health-under-way?page=1
[61] http://westernfarmpress.com/management/total-ag-pesticide-elimination-sought-radicals
[62] http://www.neonicreport.com/home/project-compass/
[63] https://scientificbeekeeping.com/pesticide-incident-reporting/
[64] http://pollinatordefense.org/site/
[65] http://cals.arizona.edu/apmc/docs/IPM_Delivers.pdf
[66] Davis, AS, et al (2012) Increasing cropping system diversity balances productivity, profitability and environmental health. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0047149
[67] http://www.pcl.org/pcl_files/5_Wildlife_Habitat_Farmland.pdf
[68] http://pfspbees.org/
[69] http://www.nwf.org/CertifiedWildlifeHabitat/UserAccount/SignIn
Category: Practical Beekeeping Management, Topics
Tags: beekeeper management, biotic, diseases, drought, environmental, factors, pesticides, randy oliver, varroa | biotic Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/biotic/ |
Sick Bees Part 18F9: Colony Collapse Revisited - The Bee/Pesticide Problem Complex
First published in: American Bee Journal, January 2014
Sick Bees Part 18F9:
Colony Collapse Revisited - The Bee/Pesticide Problem Complex
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in January 2014
Examples Of Improved Technology
The Transition
The "Bee/Pesticide Problem Complex"
Pesticide Hazard Quotients
A More Relevant Figure?
Wrap Up
Acknowledgements
Citations and Footnotes
Part 1
In my lifetime I've witnessed a wholesale shift in our attitudes toward pesticides. We've gone from the arrogant and unrealistic expectation that we could conquer all of our self-created "pest" problems via chemistry, to realizing that it's a bit more complicated than that, and that we are going to have to learn to work with Nature. I came of age just as Rachel Carson published Silent Spring, which led to a complete overhaul in the way in which we regulate the poisons that we introduce into the environment. But our transition continues to be a work in progress; we still rely upon an ever evolving arsenal of toxic substances to solve our problems (our own industry being an exemplary case in point).
However, I'm heartened by the fact that society's 21st century values are shifting toward a more sustainable model of environmental stewardship. Both industry and our government are being reluctantly dragged in that direction; none too soon for those species that are forced to eke out a living in areas of intense agriculture. The populations of many species of life, both plant and animal, are rapidly declining. Our current agricultural practices are often at odds with the needs of pollinators, which must forage in the "wild" for a safe and continuous food supply.
It is clearly time for environmental action; however, we are most effective when we base our arguments and protests upon facts and scientific data. Unfortunately, such facts are often difficult to sort from popular myths. For example, take the story of the unfortunate Chinese pear growers of Sichuan province [1] who are forced to hand pollinate their trees due to all the bees being killed off by pesticides--indeed a dreadfully grim image! In reality, this compelling story turns out to be an exaggeration of the facts, as detailed by Mark Grossman in an engrossing and thought-provoking essay [2] (I'm not going to spoil the story--read it yourself).
But I will quote excerpts from Grossman's conclusion:
Many articles about declining bee populations have a theme and tone that reminds me of those old sci-fi movies from the 1950's. Somehow, human technological tampering with nature is punished in some awful (and bizarre) way. You can almost read this theme between the lines of more than a few articles -- an echoed suggestion that some technological tinkering has angered Mother Nature... And we are being punished by the disappearance of our bees. Then, domino-like, all of modern civilization will fall to ruins...
The inaccurate impression of the Sichuan Province as the scene of a bee extinction fits almost too neatly into an increasingly pervasive, though less than articulate, mythology -- the mythology of the bee apocalypse...the mythology of our current bee die-off as divine retribution from God or Gaea, heaven or earth, conceals the actual problem by confusing it with our own most personal hopes and fears about both our technology and our future. Our bees and our agriculture -- our food supply -- are in real danger. This should drive us directly toward an understanding of the problem and, then, to a solution. And, most certainly, that solution will be technological and require more technology...
If we are to save our bees, we need to forget the myths and fables and remember the technology. Yes, in some way, almost every technological advance brings with it both a blessing and a curse. So, even if our technology is, in some measure, responsible for the problem of declining honeybee populations, that same technology will most certainly be the source of the solution.
The fact is that technological advances in agriculture have allowed the human population to explode. And it's going to take more technological advances to deal with the consequences. There is no going back to "the old ways"--it is politically unpopular to allow millions of people to starve. As James McWilliams observes [3]:
Currently, there are two paradigms of agriculture being widely promoted: local and organic systems versus globalized and industrialized agriculture. Each has fervent followers and critics. Genuine discourse has broken down: You're either with Michael Pollan or you're with Monsanto. But neither of these paradigms, standing alone, can fully meet our needs.
So should we dismiss organic agriculture outright? Absolutely not. Organic may not be "the" solution to global food demand, but it can certainly be part of it. As Jason Clay, senior vice president of the World Wildlife Fund, writes [4], "I think we need a new kind of agriculture--kind of a third agriculture, between the big agribusiness, commercial approach to agriculture, and the lessons from organic and local systems." With enhanced investment in agricultural research, there's every reason to hope that organic yields will improve and that the organic model will become more prominent. The fact that we're not yet there... doesn't mean we should abandon the quest for agricultural systems that are both high yielding and as ecologically responsible as they can be.
Amen! By promoting a sustainable mixture of traditional practices and new technology we may be able to halt our indefensible destruction of the environment. And we are slowly making progress. The concept of agroecology is catching on, as well as integrated pest management, eco-friendly advances in biotechnology, and the development of "greener" pesticides.
Examples Of Improved Technology
It's bad enough when one's bees get killed by a careful application of pesticides. But it gets a beekeeper's blood boiling when such a kill is due to carelessness or from the intentional disregard of label restrictions [5]. And this is where new robotic and GPS technology may help (Fig. 1).
Figure 1. Beekeeper Steven Coy tells me that in Mississippi, cotton receives up to 14 aerial spraying a season! To that State Lead Agency's credit, all aerial applications of pesticides require GPS tracking to confirm that the pesticide was applied accurately. In the image above, the red lines track the route of the applicator; the white bars where the spray valves were open. Such a record documents what actually took place! Image courtesy Tommy McDaniel, Director, Mississippi Pesticide Division.
But why stop at airplanes? Aerial applications have the great advantage of not needing to drive over the crop, are quick and relatively cheap. But most of an applied insecticide never hits its intended target insect, and any sort of wind results in pesticide drift off the field. The other problem is that pilots don't want to fly at night, the best time to apply pesticides if one wishes to minimize their impact upon pollinators.
We now have the technology to build GPS-guided robotic sprayers that could accurately spray fields during the night, when there is little wind, and bees are safe in the hive. Such a device would allow growers to spray their orchards while they sleep [6].
This is not pie in the sky--the WeedseekerO is already on the market [7]. This device mounts on a tractor herbicide spray rig. It optically recognizes the difference between crop plants and weeds, and then spot sprays only the intended weeds. This reduces herbicide application by up to 90%, and, of more import to the grower, quickly pays for itself.
Despite a frenzy of protests, eco-friendly biotechnology is clearly the wave of the future [8]. Genetically-engineered crops got off to a bad start in the public's eye due to their association with giant agribusinesses and the fact that the two flagship GM crops both have something to do with pesticides [9]. Engineered plant cultivars already in development stand to save the orange juice industry from citrus greening disease [10], and the world's wheat production from a devastating fungus [11]--both would greatly reduce pesticide applications.
And all the major [12], and number of startup, pesticide companies are jumping on the "biorational" pesticide bandwagon. California-based Marrone Bio Innovations, Inc. produces state of the art naturally-derived biopesticides [13], including the bee-friendly insecticide GrandevoO and fungicide RegaliaO.
With all this talk of agricultural innovations, I can't help but comment that other than the addition of motors to my vehicles and extractor, my own bee operation runs on technology that hasn't changed since the 1850's.
The Transition
The transition to agroecological practices won't be easy--the chemical companies are very good at selling pesticides to farmers, and they have much larger budgets than do the extension agronomists who are doggedly attempting to promote IPM. American consumers have gotten used to cheap meat and grain, and cosmetically-perfect produce. Few farmers would willingly take the chance of losing their crop to some bug. The powerful farm lobby rewards those politicians who write the rules. I've come to accept that pesticides are going to be part of beekeeping for the rest of my lifetime.
A thoughtful perspective on pesticide issues can be found at [14], from which I'll share a couple of excerpts:
...many people today think that pesticides are unacceptably dangerous to the environment or to man. Citizens want to know more about pesticides, their benefits, their risks, and the ways government regulates them. With good information, citizens are better able to analyze the arguments of both opponents and supporters of pesticide use. Pesticide policies should be formulated based on facts and reason instead of false perceptions and hysteria. Any rational approach to pesticide use should include a risk-benefit comparison...Pesticides are poisons and can be hazardous. Fortunately, research, education, and government agencies are constantly reducing the risk of using pesticides by producing "safer" chemicals, pest-specific pesticides, better application methods, and tougher pesticide laws. The result is a constantly improving risk-benefit ratio.
The above is good news for both bees and beekeepers. Beekeepers from every region tell me that pesticide issues have improved since the Bad Old Days of the 1960's and '70's. But that's not to say that pesticides aren't still widely applied, nor that they are not still a problem for bees in some areas. What is devilishly difficult to figure out is exactly why it is, that despite such exposure, bees can thrive in some ag areas, yet perish in others. Perhaps by carefully examining the kinds of pesticides to which bees are most exposed in each area, we can start to make some sense of it all.
The "Bee/Pesticide Problem Complex"
Although the bulk of chemicals are applied to the environmentally-devastating vast corn and soy monocultures in the Midwest, pesticides are often more of a problem for those beekeepers in other areas; such as for those being paid for pollination services, whether that be for melons in California, seed crops in Oregon, apples in New York, or pumpkins in Pennsylvania. These pollination-dependent crops are often grown in areas consisting of a patchwork of different crops, many of which are not dependent upon bees, but upon and around which one's bees may nevertheless forage (Fig. 2).
Figure 2. Look at this color-coded patchwork of different crops in California's San Joaquin Valley. Note the scale of the map, and just how many different crops may be within flight range of any hive. When I ask beekeepers in the Valley which crops are most problematic, it is often not the crop for which they are being paid to pollinate (such as vine crops)-their bees instead get hit by pesticide applications on nearby corn, tomatoes, cotton, and alfalfa. You can download a similar map for any agricultural area from the NASS CropScape website [[i]].
[i] http://nassgeodata.gmu.edu/CropScape/
Since bees don't pay attention to property lines, the beekeeper has no control over where his bees will actually forage. A number of times I've watched a grower write me a pollination check while he was watching the bees fly out of my hives and in a direction away from his orchard. Bees go wherever they get the best return on investment. If attractive flowers are blooming anywhere within flight range, then that's where the bees will go. It is nearly impossible for the beekeeper to keep track of all the different pesticides that may be applied within that area, which could easily encompass anywhere from 12 to 50 square miles.
The result is that colonies are typically exposed to a greater diversity of pesticides than that applied to the crop upon which they are placed. The Ericksons [16] termed this stew of toxin exposure, coupled with environmental factors, "the bee/pesticide problem complex" (complex: a group or system of different things that are linked in a close or complicated way; emphasis on the word "complicated").
The diversity of pesticides in pollen is staggering. The Fraziers [17] documented 52 pesticide residues from colonies placed on nine different crops; Pettis [18] found 35 in pollen taken from hives in 7 different crops; Stoner [19] detected well over 60 pesticides from 5 apiaries in Connecticut. An important observation is that two colonies side by side may bring back entirely different pollen loads, with different pesticide residues, none associated with the crop upon which they are placed!
And keep in mind that the Fraziers [20] found that residues may be detected to a greater extent in dead or dying bees as opposed to in the hive matrices. This finding suggests that colonies are losing their field force without leaving residues in the hive (the lesser of two evils), but suggesting that the impacts of some pesticides may be underestimated by samples taken from the combs-they found field forces to be significantly reduced in colonies pollinating cotton, corn, and alfalfa.
Dr. Jim Frazier explains that it is impossible for us to figure out how all the different combinations of pesticides interact with colony health [21], especially when we throw in any contribution from the unlabeled adjuvants, which can be even more toxic to bees than the pesticide active ingredient itself [22].
This is likely the reason that despite beekeepers clearly being able to see that colonies suffer after certain ag exposures, that no one has been able to link any specific pesticide as being the cause of colony losses (other than in the case of outright bee kills). This is of course extremely frustrating to beekeepers who want the EPA to "do something" (and to the EPA, which does want to do something!).
Pesticide Hazard Quotients
Even more frustrating to the beekeeper is that when he is given the results of pesticide analyses, all that he sees are a bunch of nearly meaningless numbers. In order to make any sense of the detect results, he must then search for published LD50 (lethal dose) figures for oral, contact, and chronic exposure (unfortunately, these figures are all over the page, depending upon who did the lab testing; the figures may be in ug/kg, ppm, nanograms/g, ppb, or ppt; and for many pesticides, published figures are either nonexistent or highly suspect). Then he must calculate/guesstimate how much nectar, pollen, or dust a bee actually consumed or to which it was exposed. I've done these calculations time and again--believe me, it's a pain!
Drs. Kimberly Stoner and Brian Eitzer [23] propose that researchers save beekeepers from all that work and confusion by reporting detected concentrations not only in ppb's, but also as "hazard quotients" [24]. This would really help the beekeeper to put the numbers into context.
The way that they calculated their Pollen Hazard Quotient (PHQ) was to take the concentration of the pesticide residue in the sample (in ppb), and then divide the result by the most appropriate available oral LD50 figure. For example, the maximum residue of phosmet in their samples was 16,556 ppb, and the published oral LD50 is 0.37 ug/bee, resulting in a pollen hazard quotient of 44,746 (they could also calculate nectar hazard quotients).
How About A More Meaningful Figure?
Unfortunately, the above figure (PHQ of 44,746) is, in my book, still just another big, scary, confusing number to the beekeeper. So let's go a step better...
Regulatory Terms
Pesticide regulators use the term Acceptable Daily Intake (ADI) to quantify the amount of a pesticide that can be ingested daily over a lifetime without appreciable risk (they typically throw in a 10x safety factor to be on the safe side). If the concentration of that pesticide in food exceeds the ADI, then it is said to pose a "consumption hazard." In the above study, Stoner and Eitzer not only calculated the Pollen Hazard Quotient, but also what I consider to be an even more meaningful figure--the percentage of the oral LD50 consumed per day [25]:
I suggest that we give this figure a catchy name such as the "Daily Consumption Hazard" (DCH). The DCH would be eminently simple to interpret: a DCH of 1 would mean that a bee would consume 100% of a lethal dose over the course of a day; a DCH of 0.50 would mean that it would consume 50% of a lethal dose.
For example, at the highest concentration of phosmet found in their pollen samples, the Daily Consumption Hazard would be calculated thusly [26]:
Now that's a figure that anyone can understand! A typical nurse bee, if eating the phosmet-contaminated pollen, would be consuming an alarming 42% of the lethal oral dose of phosmet per day. This would clearly be a figure of concern to the beekeeper!
Although they didn't use that term, the authors calculated the DCH to nurse bees for the highest detect of each pesticide found in their pollen samples (Table 1):
Pesticide Maximum residue (ppb) Percentage of oral LD50
("Daily Consumption Hazard")
Phosmet 16556 42.5
Imidacloprid 70 17.1
Indoxacarb 417 2.0
Fibronil 3.5 0.8
Thiamethoxam 4.1 0.8
Dinotefuran 7.6 0.3
Chlorpyrifos 25.2 0.1
Diazinon 18 0.1
Methomyl 24 0.1
Dimethoate 4.2 0.1
Table 1. The "Daily Consumption Hazard" to nurse bees consuming beebread containing the maximum residue concentrations of various pesticides in pollen samples collected over several years from 5 apiaries in Connecticut. The concentration of phosmet approached half the oral lethal dose. For most pesticides, the DCH was less than 1% of the lethal dose, so likely not of serious concern. After Stoner and Eitzen, cited above.
It is important to note that in order to save costs, the authors omitted performing analyses for two pesticides of concern--the pyrethroids and the fungicide chlorothalanil. I suspect that those two would have ranked high on the list.
Curious, I calculated Daily Consumption Hazards from the data of the aforementioned study by Pettis [[i]], in which the researchers collected beebread samples from hives placed in seven major crops. The pesticides with the highest DCH's were, in order, the organophosphate phosmet, six different pyrethroids, followed by the neonicotinoid imidacloprid.
Note that the above rankings for toxic risk are based upon the maximum levels of residues detected, not the averages. I suspect that it is this sort of sporadic high-but-not-quite lethal exposure that may help to explain some of the colony morbidity in agricultural areas. In none of these studies did the authors mention observing overt bee kills.
Practical application: the main value to calculating Daily Consumption Hazards is that it quickly brings to our attention those pesticides that are most likely to be affecting bees due to residues in the pollen. On the other hand, it also allows us to judge which pesticide residues are not likely to be of biological significance.
Limitations Of Hazard Quotients
Although readily understandable, calculations of daily consumption hazards are limited by our lack of knowledge and data. The meaningfulness of any hazard quotient is based upon any number of assumptions about the actual toxicity of a substance. It is troubling that researchers have found that, "All in all, it seems that there is no clear correlation between acute and chronic toxicity" [28]. Unfortunately, until recently, regulators have not been calling for 10-day chronic toxicity data, so we simply do not have those figures at our disposal for many pesticides [29]. Heck, for many pesticides, we don't even have oral toxicity figures, only contact LD50's!
The quotients based upon residues in pollen would only apply to toxicity to nurse bees, since foragers typically do not consume pollen. For older bees we would need to calculate "nectar toxicities," based upon feeding studies with spiked syrup. And then for nurse bees we would need to add this figure to the toxic load that they receive from their consumption of pollen.
The quotient does not take into account environmental factors (such as temperature or humidity), colony nutritional stress, or parasite loads.
The quotient does not automatically calculate the additive risk of pesticides with similar modes of action, such as that from any pyrethroid exposure on top of the "foundation" of fluvalinate contamination of most beeswax.
Nor does the quotient take into account potential chemical synergies between pesticides or other toxins (including beekeeper-applied miticides). Such synergies would greatly increase the DCH of certain pesticides.
Do not expect the actual testing labs to calculate hazard quotients, since such interpretation would by necessity be based upon the research and assumptions of others (for food consumption rates, LD50's, and LC50's).
Luckily, regulatory agencies across the world are adopting more stringent testing requirements for pesticides, so we will likely have better toxicity figures to work with in the future.
Wrap Up
Beekeepers are drowning in data that makes little sense to them. I commend Drs. Stoner and Eitzen for formally proposing that researchers present their pesticide residue data in a more "user-friendly" way. I feel that the most meaningful figure to beekeepers would be what I've termed the "Daily Consumption Hazard" (there may well be a better name), as this would let them know which pesticides in their area would most likely be affecting their bees.
In fact, that is such a good idea, that I may do so myself in the next article, in which I will look at which pesticides are applied in which parts of the U.S., and their known effects upon bees.
Acknowledgements
As always, I'm deeply indebted to my partner in the mission to get accurate scientific information to beekeepers, Pete Borst. I also appreciate James Fischer's research skills in his posts to Bee-L. And of course, my hat is off to the scientists whom I cite, most of whom have taken the time to share their thoughts with me.
Citations And Footnotes
1 http://thebeephotographer.photoshelter.com/gallery/-/G0000M46TBQX4Odc/
2 http://marklgrossmann.wordpress.com/2013/09/26/thursday-bees-who-needs-em-the-sichuan-sentence-the-bee-apocalypse/
3 McWilliams, JE (2011) Organic Crops Alone Can't Feed the World. http://www.slate.com/articles/health_and_science/green_room/2011/03/organic_crops_alone_cant_feed_the_world.html
4 http://dotearth.blogs.nytimes.com/2011/03/03/a-hybrid-path-to-feeding-9-billion-on-a-still-green-planet/?_r=1
5 http://grist.org/news/farm-kills-millions-of-bees-with-illegal-pesticide-spraying-gets-slap-on-wrist/
6 http://www.kgw.com/lifestyle/Robot-pesticide-sprayer-future-of-farming-219504211.html,
(Broken Link!) http://www.crophuggerreport.com/2011/02/micothon-developes-new-pesticide.html
7 (Broken Link!) http://www.cropoptics.com.au/weedseeker.html
http://www.cals.arizona.edu/pubs/general/resrpt2008/article3.pdf
8 http://www.forbes.com/forbes/2010/0301/opinions-gmos-crops-genetics-monsato-ideas-opinions.html
9 http://www.slate.com/articles/life/food/2013/07/a_hippie_s_defense_of_gmos_why_genetically_modified_food_isn_t_necessarily.single.html
10 http://www.nytimes.com/2013/07/28/science/a-race-to-save-the-orange-by-altering-its-dna.html?_r=1&
11 http://www.k-state.edu/media/newsreleases/jun13/sr3562713.html
12 http://www.cropscience.bayer.com/en/Products-and-Innovation/Brands/Biologicals.aspx
1 http://www.marronebioinnovations.com/agriculture/products/, http://www.marronebioinnovations.com/biopesticides
14 Pesticide Usage in the United States: History, Benefits, Risks, and Trends http://ipm.ncsu.edu/safety/factsheets/pestuse.pdf
15 http://nassgeodata.gmu.edu/CropScape/
16 https://scientificbeekeeping.com/historical-pesticide-overview/
17 Frazier, M.T., S. Ashcraft, W. Zhu & J. Frazier (2011) - Assessing the reduction of field populations in honey bee colonies pollinating nine different crops http://www.extension.org/pages/58650/proceedings-of-the-american-bee-research-conference-2011#.UhDTZX-aucw
18 Pettis JS, et al. (2013) Crop pollination exposes honey bees to pesticides which alters their susceptibility to the gut pathogen Nosema ceranae. PLoS ONE 8(7): e70182. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0070182
19 Stoner KA, Eitzer BD (2013) Using a hazard quotient to evaluate pesticide residues detected in pollen trapped from honey bees (Apis mellifera) in Connecticut . PLoS ONE http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0077550
20 Frazier, M.T., et al. (2011) Op. cit.
21 Presentation at the Monsanto Honey Bee Health Summit.
22 Mullin, CA, et al (2011) A primer on pesticide formulation 'inerts' and honey bees. 2011 American Bee Research Conference. http://www.extension.org/pages/58650/proceedings-of-the-american-bee-research-conference-2011#.Ulq6D1Mgvd5
23 Stoner KA, Eitzer BD (2013) Op. cit.
24 http://www.epa.gov/R5Super/ecology/erasteps/erastep2.html#hazquot
25 In the right-hand column of their Table 3, with the heading "Percentage of oral LD50."
26 I simplified the calculation in the text. The actual calculation would be:
For the first term, I converted ppb to a rate. For the second, I used the authors' reasonable estimate that a nurse bee would consume 9.5 mg of pollen per day, and converted the published LD50 of 0.37 ug/bee to 0.00037 mg/bee. The final resulting "Daily Consumption Hazard" is in essence the inverse of the "margin of safety," or the Toxicity Exposure Ratio (TER)--the smaller the TER, the more toxic the exposure, approaching lethality as the TER approaches a value of 1.
27 Pettis JS, et al. (2013) Op. cit.
28 Simon-Delso, N, et al (2011) Risk assessment of pesticides on bees: evaluating risk coefficients for assessing acute and chronic toxicity. 11th International Symposium of the ICP-BR Bee Protection Group, Wageningen (The Netherlands). (Broken Link!) http://pub.jki.bund.de/index.php/JKA/article/view/1934/2310
29 What we need are figures for the chronic LC50--the lethal concentration of a pesticide in pollen or nectar that causes mortality or morbidity in 10-day feeding studies.
Category: Pesticide Issues
Tags: colony collapse, pesticides, sick bees | colony collapse Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/colony-collapse/ |
What's Happening To The Bees? - Part 1
First published in: American Bee Journal, February 2014
What's Happening To The Bees?
Originally published in ABJ Feb 2014
Randy Oliver
ScientificBeekeeping.com
I'm realizing that what I thought was going to be a quick review of CCD has turned into a very long series of detailed articles, and I'm not even near reaching the conclusion. So on this 20th anniversary of my first seeing the parasite that changed beekeeping worldwide, I thought that I'd interrupt the Sick Bees series and attempt to explain, more briefly (hah!), and from an ecological perspective, what's happening to the bees these days, and how beekeepers are being forced to adapt.
One Wild Ride!
In 1994 I saw my first varroa mite--on a stickyboard that had been placed by the county bee inspector under one of my hives. Little did I know how much that little maroon speck was about to change my life!
Varroa clobbered me (or more precisely my bees). And then did it again; and then again. I finally got pissed off and decided that I should either give up beekeeping altogether, or dust off my scientific training and really learn about bee and mite biology, and how to apply it to practical beekeeping.
What's interesting is that my very first article (on almond pollination), in the fall of 2006, was published just as Dave Hackenberg's colonies began to collapse from CCD. The occurrence of CCD put the bee research community into high gear to try to figure out what the heck was happening. And that created a "niche" for a practical beekeeper with a biological background, willing to act as a translator of the scientific findings to an alarmed beekeeping community. I unwittingly stepped into that niche, and it swallowed me up. A mere seven years later, and to my utter surprise, I've gone from being an obscure sideline beekeeper to a globetrotting speaker on bee health and management.
I've now been fortunate enough to visit both professional and recreational beekeepers in every part of North America and in several other countries. I've seen many styles of beekeeping, from the tropics to the Arctic, heard the local problems and concerns, and had the chance to learn from some very smart and successful beekeepers. I've attended scores of conferences, read countless scientific papers, and picked the brains of the world's best apicultural researchers. Then I've done my best to share what I've learned with others. I've met scores of wonderful people and made a lot of new friends, and I'd like to take this opportunity to thank you all for the appreciative and effusive support!
How We've Benefitted From CCD
CCD has been a mixed blessing to beekeepers. It brought grown men and women to tears (see the film The Last Beekeeper [1]), and the elevated rate of colony mortality in recent years has made it difficult to keep our operations in the black. But it also pushed our scientific community to learn more about the biology of the honey bee than they had in a great many years. And many of us are much the better beekeepers for it.
Unlike that of other livestock, the true contribution of pollinators to U.S. agricultural production is not reflected by farm gate sales figures, so bees have traditionally not received their fair share of USDA research funding, nor does the beekeeping industry have the lobbying clout of the cattle, poultry, or pork producers. But we've benefitted from the public awareness of the plight of pollinators, which has resulted in the shifting of some funding our way [2] (although bees still only get about a tenth the amount of money set aside for research on beef production). In addition, universities, grantors, and other governments have recently supported a great deal of research into honey bee and pollinator health (I only wish that the millions who signed the internet petitions to "save the bees" had instead each donated a single dollar toward bee research).
Misunderstanding And Misinformation
Although CCD refers to a specific set of symptoms [3], the media soon began to use the term for any sort of honey bee mortality (as did many beekeepers). And although the epizootic appears to have largely run its course, speculation ran rampant as to the cause(s) of "CCD," and continues to do so with every new "documentary" and press release. Although "CCD" remains the poster child of colony losses, a blue-ribbon group of bee researchers cautions:
During the winter of 2008/2009, ~10% of the 2.3million managed honey bee colonies in the US died with "CCD-like symptoms", and US beekeepers self-diagnosed CCD as only the 8th most important contributor to colony mortality, behind starvation, queen-related issues, and parasites. The point is, honey bees die from many things. We must be careful to not synonymize CCD with all honey bee losses [4] (emphasis mine).
I'm typing these words as I fly over the beautiful jigsaw-puzzle-like frozen Manitoba landscape on my return from a speaking engagement in Sweden, where the film More than Honey had been recently shown. To my considerable surprise, the Swedish beekeepers (Fig. 1), after viewing the movie, were under the very strong impression that the bee problems in the U.S. were due to our brutal commercial beekeeping practices, and the moving of hives to the deadly almond orchards in California.
Figure 1. Beekeeper Goran Sundstrom at one of his apiaries in Sweden. Goran typically keeps 12 hives in an apiary, and goes to considerable trouble to comply with some rather arbitrary rules to have his honey certified as "organic." The red paint is a traditional color for rural buildings in this area.
As it happens, the director of that film had stayed with me during his initial scouting visit to the U.S., and I was responsible for introducing him to my friend John Miller, who was unfortunately (and I'm sure unknowingly) to be cast in the role of the evil bee abuser, so I felt some responsibility to dispel those misconceptions to the concerned audience. And this brings me to my next subject...
Bees are currently enjoying a great deal of attention from a fearful public eager to do something, anything to help them. This could be a really good thing for the bees, for beekeepers, and for the environment as a whole if such public concern and activism could be guided into meaningful actions. I can't really blame the public for being confused, since the entertaining and sensational docu-dramas about the impending extinction of the honey bee resonate more emotionally than do the dry and qualified explanations by scientists as to the "multifactorial" causes of colony mortality.
As a result of all the misinformation and hysteria out there, an unsure and distrustful public puts pressure their representatives to pass this or that new regulation to "save the bees." This scares me. I feel that we should heed the sage advice of Thomas Jefferson:
People are inherently capable of making proper judgments when they are properly informed.
And therein lies the problem: due to the complexity of what's happening with bees these days from the biological, environmental, agricultural, and economic standpoints, it's danged hard to be "properly informed." My gosh, just look at me trying to do that "informing"--I first thought that the "Sick Bee" series was only going to be two or three articles long! So what to do?
Challenging One's Beliefs
One should be careful about embracing the popular stories about why "the bees are dying." Some of the myths resonate so emotionally that they win uncritical acceptance by the mainstream, despite the fact that they cannot be reconciled with obvious facts (e.g., that bees can indeed thrive surrounded by GMO corn and soy, or on neonic-treated canola). As the popular scientific author Stephen Jay Gould pointed out:
The most erroneous stories are those we think we know best - and therefore never scrutinize or question.
Anyone who knows me (or has had the misfortune of trying to promote an unsubstantiated argument in my presence) can tell you that I'm a challenging and provocative person by nature. I've found that the best way to get to the truth is to learn how to argue your opponent's side of a debate as well as you can argue your own. Therefore, I am more than willing to play Devil's Advocate any time that I see one side of a legitimate argument being ineffectually presented. And I'm ruthlessly skeptical of any claims that do not jibe with what I see with my own eyes.
As you can imagine, this has earned me my share of vitriol from those who "know the truth" (read [5] for an enlightening discussion). Luckily, my mailbox runs about a hundred to one with thank you letters from beekeepers who appreciate my evaluation of the issues. I take this responsibility seriously; in order to remain objective and unbiased, I go out of my way to constantly question every one of my opinions (I avoid making "conclusions"). I eschew holding any "beliefs," but rather adhere to the following principles:
That I should respect Nature and all forms of life (my ethical environmentalist side),
That I should thoroughly investigate all research and explanations of any subject, and avoid cherry picking data that suits my ideological convictions (my curious open mindedness and willingness to do my homework).
That I should base my opinions upon information and experimental results which stand up to scrutiny and questioning (my scientific side),
That I should then truth-check those opinions against on-the-ground evidence and observations (my practical side).
Unfortunately, many crusaders allow their commendable environmental consciousness (and innate fear of technology) to override the last three principles, which is understandable, since doing the homework is really hard, and our understanding of the biology involved is as yet incomplete. But I have some suggestions as to where to start...
A Homework Assignment
Allow me to first assign you some required reading. Put down this article and read Berndt Heinrich's fascinating book Bumblebee Economics [6]. Heinrich studied the minute details of exactly how bees make a living in their ecological niche, focusing upon the economics of energy utilization. His revelationary insights changed my understanding of bee life completely. Then for something entirely different read Ron Miksha's Bad Beekeeping [7] for a perspective on the economic trials and tribulations faced by professional beekeepers (his comments on p. 243 are especially relevant). I'll wait 'til you're done...
OK, I hope those books were as thought-provoking to you as they were to me! Now let's take a look at the health of bees and beekeeping from ecological and economic perspectives.
It's All About Economics
Again and again, I find that everything boils down to economics and finding the right niche. This applies to both honey bees and to the business of beekeeping--either thrives in its ideal niche, and either must either adapt or die if the parameters of the niche change. And boy howdy, how we have changed the parameters of both of our niches in recent years!
Practical application: In this real world, each species, and each business, strives to exploit a niche to which it is particularly well adapted. A change in any of the parameters that define a particular niche may affect the profitability and survival of that species or business. If that species or business is efficient and profitable in its particular niche, then it thrives; if not, if must either adapt or go extinct.
For the remainder of this article, I will view the situation of both bees and beekeepers through the lenses of ecology and economics, and the changes that have occurred in the parameters that define our niches.
Let's Define Some Terms
Pollinators are in decline over much of the world, and have been for some time [8]. We beekeepers are mainly concerned with our favorite pollinator, the European honey bee, Apis mellifera, native to Europe and Africa, but now introduced worldwide. Unless I specify otherwise, henceforth I will be referring to this species.
It occurs to me that if pollinators have long been in decline worldwide, then that would imply that something has changed in their ecological niches (and that it started before the introductions of cell phones, neonics, or GMO's). It also occurred to me that the niches occupied by beekeepers have changed substantially (mine sure has; indeed several times). I'll try not to burden you with too many new terms:
Habitat--where the bee species lives (or could live). The bees in the U.S. are mongrel hybrids of various European or African races [9], each originally adapted to specific microhabitats in their home countries.
Ecological niche--a description of the bees' "occupation" in its specific microhabitat, including all environmental parameters and interactions with other species.
Fundamental niche-- the potential full range of environmental conditions and resources that the honey bee as a species could possibly occupy and use, without the limitations of predation, competition, or other factors.
Realized niche--the less-than-optimal niche that each subspecies of bee actually occupies; constrained by weather, resources, parasites, etc. In its home range, various subspecies of honey bee adapted to narrow realized niches occurring in the warm Mediterranean, the cold Alps, the British heathland, the Egyptian desert, the African savannah, etc. In each of those niches, the bees adapted to the seasonality of local nectar flows, the local plant toxins, temperature, predators, and parasite pressure. Conditions may not have been optimal, but each subspecies was economically successful at "making a living" within those parameters.
So let's list the most important parameters of the fundamental niche of the European honey bee:
It is a colonial species, existing as a superorganism with generally a single reproductive queen, supported by multiple patrilines of sterile workers, each exhibiting slightly differing genetics, behaviors, and resistance to parasites, toxins, and diseases (this within-hive diversity is extremely important, but often ignored by beekeepers).
It is a generalist species, able to gather food resources from a wide variety of plants. As such, it is adapted to metabolizing a wide range of toxic plant alleleochemicals (and by extension, synthetic pesticides).
It is primarily a pollinator; its diet normally consists solely of nectar and pollen, although those raw foodstuffs are processed into other products (honey, beebread, and jelly) for the actual consumption by the majority of the members of the superorganism.
The bee cannot forage unless the ambient temperature is above roughly 55degF (12degC). This limiting factor constrains its range to those areas that have adequate bloom available when the temperature exceeds that value; any colony with hungry brood when daytime temperatures do not exceed 55degF will soon become stressed due to an inadequate supply of protein (this is a huge management tip).
Unlike other insects, the European honey bee stores vast quantities of processed food for later consumption when resources are scarce.
This allows the colony to do something that no other species of temperate insect can do--maintain an elevated body temperature, and rear brood, throughout the winter.
In order to maintain that colonial body temperature, the European honey bee requires a protective insulated cavity within which to nest (Fig. 2).
Somehow, the European honey bee evolved with remarkably few parasites--the only significant ones being Nosema apis, the bacteria causing the two foulbrood diseases, the fly Braula, rare infection by two opportunistic fungi in pollen (chalkbrood or stonebrood), and what were normally "economically unimportant" infections by any of several insect viruses.
Figure 2. These bees are at the top of the winter cluster at the interface between empty cells and sealed honey. Despite the air temperature being below freezing, the temperature of the bees beneath the surface was 67degF (19degC). This remarkable technique of using stored sugars from the previous summer as an energy source during winter allows the honey bee to overwinter as a populous colony, ready to exploit early spring pollen and nectar sources.
In summary, the honey bee requires a dry cavity, in which it maintains a tropical environment throughout the year, allowing it to exploit food sources any time that the temperature is above 55degF, it is adapted to metabolize a wide variety of plant toxins, it only requires a brief honeyflow to provide it with food stores for the remainder of the year, and it evolved under low parasite pressure.
Practical application: this last point is of huge import when we attempt to understand the biological changes that have occurred in European honey bee populations worldwide in the last decades. To wit, virus infections have become serious "emerging diseases" [10].
Add The Beekeeper
OK, now let's add one more term:
Facilitation--Optimal conditions in the fundamental niche occur infrequently, if ever. The job of the beekeeper is to optimize the conditions for his bees as best he can, such as by supplemental feeding, medicating for parasites, protecting from predators, providing a larger nest cavity, or providing water or winter insulation. Such "facilitation" may allow bees to survive outside of their fundamental niche.
Practical application: I recently enjoyed a lunchtime conversation with a couple of professional beekeepers who moved their hives from almonds, to the tallow bloom in Texas, to the Dakotas for summer, and then to a mild area in California for wintering (their problem is having too many bees each spring). What they are doing is facilitating the optimal fundamental niche for their bees for the entire year (there are many other ways of doing so).
Practical application flip side: If a beekeeper is keeping colonies alive outside of their fundamental niche, such as in densely-packed apiaries, in areas of crop monoculture or high exposure to toxic chemicals, in flowerless forest or dry grassland, or by the chemical suppression of parasites, should that beekeeper falter in his constant facilitation, his bees may not be able to continue to survive without such help.
Limiting Factors
The realized niche of the honey bee is constrained by limiting factors, which may change from season to season. Common limiting factors for populations of honey bees are:
Climate--bees have very wide "tolerance limits" for cold, heat, rain, and length of seasons. But at the edges of their tolerance limits, colonies will be stressed, and may not be able to deal with other limiting factors.
Competition for food--in some areas there is such an abundance of nectar during the main flow that there is little competition (an important point when speaking with native pollinator advocates). The main competition for food resources occurs at other times of the year; assume that there is serious competition happening if robbing behavior is evident.
Suitability of available food--not all plants produce honey-bee-friendly nectar or pollen, especially outside of the honey bees' native range. This is clearly evident in America and Australia, where some pollen sources are notably nutritionally inadequate for honey bees (think corn, blueberry, watermelon, pumpkin, some eucalypts). And in some areas or under dearth conditions, bees will unwittingly collect naturally toxic pollen or nectar. And of course, some human-applied pesticides make the available food unsuitable.
Competition for nest sites--without hollow trees or other natural cavities, honey bees cannot survive the winter in temperate climates (Fig. 3).
Figure 3. One of my colonies swarmed late this spring and built open-air combs in a nearby hawthorn tree. We noticed it when the leaves fell in early December, following a week of subfreezing temperatures and a foot of snow. You can't see it, but there is still a cluster of live bees (which I hope to rescue when I'm done writing this article). The population had obviously grown large enough to build and completely cover all the combs, and could easily have survived the winter had it only found an appropriate cavity in which to build its nest.
Predation--Such as birds, bears, wasps, and ants. The main predator of bees, of course, are humans, who often rob too much honey from the hive, resulting in winter starvation.
Parasitism--Again, natural populations of European honey bees appear to historically have been minimally affected by parasites under normal conditions. We will return to how this has changed.
Transmission of parasites--This is very density dependent--the more colonies within flight range, and the more competition for resources, the greater the transmission of parasites. The swapping of combs by beekeepers also changes this dynamic.
Toxins--Natural plant allelochemicals, soil metals, industrial pollution, agrochemicals, and recently, a huge influx of beekeeper-applied miticides.
Bees have a wide range of tolerance for some limiting factors, and more narrow ranges for others. Usually, several factors interact (sometimes synergistically) to limit bee populations.
Practical application: there is often a single limiting factor that is the determinant for colony survival. A concept used in ecology is "Liebig's law of the Minimum" (Fig. 4). A beekeeper can work hard all season long to do everything he can for his bees, but should he overlook any single critical limiting factor, Liebig's Law may come into play, and he may lose his colonies.
Figure 4. An illustration of Liebig's Law of the Minimum as it applies to the practice of beekeeping. Despite everything else that you do to fill the barrel, the most unfavorable limiting factor(s) (or some combination thereof) at any critical period of time will limit the bees' (and your) success. Adapted from [[i]].
[i] Barrel illustration after Dobenecks, taken from Wikipedia http://en.wikipedia.org/wiki/Liebig%27s_law_of_the_minimum
Practical application: Each race of honey bee in Europe specialized by adapting to certain combinations of limiting factors, and thus gained a fitness advantage in its particular habitat. Since the arrival of varroa, which wiped out much of the feral population, the overall genetics of the U.S. bee population have likely shifted toward those propagated by commercial queen producers [12].
These "all-purpose" bee stocks are typically bred for color, temperament, and honey production, and maintained with a high degree of facilitation by the queen producer (feeding, treatments). There is no reason to expect those stocks to be well adapted for survival without constant facilitation. This is why I strongly support regional queen breeding for locally-adapted stock.
What Are The Limiting Factors For Honey Bees Today?
It would have been so simple had CCD actually been caused by cell phones! We could have banned the danged things, and wouldn't have to listen to people walking around loudly and obliviously talking to themselves. But alas, it appears to be more complex than that.
So as a biologist, it occurs to me to go back before CCD, in fact, to go back even further in time, and ask the question, "Which factor(s) limited honey bee populations in Europe prior to modern management by humans"? And then we can work forward in time to see what's changed since then. To be continued...
Footnotes And Citations
1 Directed by Jeremy Simmons (2009), and recommended for those who didn't experience the horror of CCD personally. Unfortunately, I can't suggest anywhere to purchase a copy of this well-done and heart wrenching film.
2 Pollinator Research.-The Committee is aware that pollinators are responsible for the production of one-third of the Nation's food supply, but the number of managed honeybee colonies in the United States has dropped in half since 1940. Because of the importance of pollinators in the production of the Nation's food supply and their impact on the stability of our agricultural economy, the Committee encourages [the Agricultural Research Service] to continue to dedicate resources to protecting the health of both honeybees and other native bees, including continued research into colony collapse disorder. http://www.gpo.gov/fdsys/pkg/CRPT-112srpt73/html/CRPT-112srpt73.htm
3 Symptoms of CCD:
1) In collapsed colonies
a) The complete absence of adult bees in colonies, with no or little build up of dead bees in the colonies or in front of those colonies.
b) The presence of capped brood in colonies.
c) The presence of food stores, both honey and bee bread
i) which is not immediately robbed by other bees
ii) when attacked by hive pests such as wax moth and small hive beetle, the attack is noticeably delayed.
2) In cases where the colony appear to be actively collapsing
a) An insufficient workforce to maintain the brood that is present
b) The workforce seems to be made up of young adult bees
c) The queen is present
d) The cluster is reluctant to consume provided feed, such as sugar syrup and protein supplement
From vanEngelsdorp, D, et al (2006, revised Jan 5, 2007) Investigations into the causes of sudden and alarming colony losses experienced by beekeepers in the fall of 2006. Preliminary Report: First Revision.
4 Williams, GR, et al (2010) Colony Collapse Disorder in context. Bioessays 32(10): 845-846. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3034041/
5 Janabi, F (2013) From anti-GMO to pro-science: 'A Layman's Guide to GMOs'. http://www.geneticliteracyproject.org/2013/12/03/from-anti-gmo-to-pro-science-a-laymans-guide-to-gmos/#.UqkDXdJ_dyI
6 Heinrich, B (2004) Bumblebee Economics. Harvard University Press. I highly recommend all of Heinrich's books--he's a brilliant scientist and an engaging writer whose passion it is to understand the details of how organisms survive in their niches.
7 Miksha, R (2004) Bad Beekeeping. Trafford. For a more data-based analysis, see:
Laate, EA (2013) Economics of Beekeeping in Alberta 2011. http://www1.agric.gov.ab.ca/$Department/deptdocs.nsf/all/agdex14472/$FILE/821-62.pdf
8 CSPNA &NRC (2007) Status of Pollinators in North America. https://download.nap.edu/login.php?record_id=11761&page=%2Fdownload.php%3Frecord_id%3D11761
9 The evolutionary origin of the European honey bee is currently under debate by scientists. See the following:
Han, F, et al (2012) From where did the Western honeybee (Apis mellifera) originate? Ecol. Evol. 2(8): 1949-1957. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3433997/
Kotthoff, U, et al (2013), Greater past disparity and diversity hints at ancient migrations of European honey bee lineages into Africa and Asia. Journal of Biogeography 40: 1832-1838. http://onlinelibrary.wiley.com/doi/10.1111/jbi.12151/pdf
10 Genersch, E & M Aubert (2010) Emerging and re-emerging viruses of the honey bee (Apis mellifera L.). Vet Res. 41(6): 54. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2883145/
11 Barrel illustration after Dobenecks, taken from Wikipedia http://en.wikipedia.org/wiki/Liebig%27s_law_of_the_minimum
12 Delaney, DA, et al (2009) Genetic characterization of commercial honey bee (Hymenoptera: Apidae) populations in the United States by using mitochondrial and microsatellite markers. Ann. Entomol. Soc. Am. 102(4): 666-673.
Category: Colony Health - Diseases, Viruses, CCD
Tags: ccd, colony, health | health Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/health/ |
News and Blogs
In order to be notified by email of updates and additions to this website, please sign up at ScientificBeekeeping Updates (I will not share your personal info or email with anyone, nor clog your inbox; I update once every few months at best).
Extended-release oxalic acid
I get a lot of questions about my research into extended-release oxalic acid ("OAE"). This treatment is not yet approved for use in the U.S., but I suspect that it will be a game-changer for managing varroa. Researchers can find details on how I created the test sponges for my 2020 trials at the end of Mite Control While Honey is on the Hive: Part 4
For instructions for preparation and use of OAE under permit, see How to Use OAE.
I've created a very useful varroa control model for all to use-check it out here. It is designed to run in Excel, and can be used to run simulations for mite management in your own operation.
Nicole from Heritage Acres interviewed me about the state of bees, breeding for mite resistance, and extended-release oxalic acid, treatment-free beekeeping, mite drift, and my recent research. You can listen to it at this podcast
My assistant Brooke Molina shot a quick video of me demonstrating how to use my home-made plastic cups to perform a swirl-type mite wash-showing how it takes less than 4 minutes per hive. Randy's Mite Wash Video
Extended-release oxalic acid
There is a crying need for a safe and effective varroa treatment for use during hot weather, when there are honey supers on the hive. I am working with USDA-ARS to get this application method approved by EPA. My latest update is at: Extended-Release Oxalic Acid Progress Report
An objective assessment of the neonics
I was recently asked to write an assessment of the neonics targeted for the nursery trade group-the University of California Nursery and Floriculture Alliance. It's brief and simple.
You can read it here: link
My colony age distribution chart
I get a lot of requests for the colony age distribution chart that I created from Lloyd Harris' data from Manitoba hives. Thanks to beekeeper Kat Satnik for pointed out a typo in previous versions. You can download a copy here.
Mite control updates 25 January 2018
Many of you have noticed the recent discovery that lithium salts may be of use in varroa control. I've gotten some lithium citrate and will be testing this season. It is currently legal to feed colonies a lithium salt as a nutritional supplement, but I cannot recommend putting it into your hives prior to further formal testing.
Re oxalic acid in glycerin (oxalic shop towels), I've made big strides in developing protocols for incubator trials this winter to test various formulations for best efficacy against the mites, coupled with minimal adverse effects to the bees.
These cup cages in my home incubator allow me to place precise amounts of various oxalic acid solutions on a measured square of cellulose fabric (note the blue piece of towel in the left hand cage) sized to be proportional to the surface area of the combs in a hive (using a piece of beeswax-coated plastic foundation as proxy). The screens at the bottoms of the cups allow me to measure the percentage of mites killed by the treatment.
I've also recently perfected a protocol that allows me to quickly titrate the amount of oxalic acid that actually gets transferred to the bees' bodies (note the pink indicator solution in the cup with bees). I've only run one formal trial using this method so far, but it shows great promise for me to be able to quickly screen for the optimal application method for distributing oxalic acid within the hive.
I thank you all for your donations in support of this research. I will continue to publish and post updates.
The 2017 Eclipse
Thanks to Idaho beekeepers Steve Sweet and Kevin Duesman for inviting Stephanie and I to join the Treasure Valley Beekeepers Association in camping out and viewing the eclipse directly under the path of totality!
We also shared the experience with some other bee researchers-Annette Bruun Jensen (from Denmark), Dennis vanEngelsdorp, and Steve Sheppard.
Update 10 March 2017 to the OA shop towel link below
There has been huge interest in my article from the Jan ABJ on extended-release oxalic acid dissolved in glycerin, and applied on shop towels. Please go to this link for updates: https://scientificbeekeeping.com/oxalic-shop-towel-updates/
Updates: Jan 29, 2016
California almond season is upon us! We've had it easy the past few seasons in almonds, since the lack of rain during our drought kept the orchards relatively dry. Not so this year! The orchards are a mess, and many are impassable.
My sons Eric and Ian, and I spent the past week welding up our new boom loader (original design, on the truck to the far right, largely constructed while working under a tent during the rain). We got a 3-day break in the rain this week, and used the window of opportunity to start moving our hives into the most problematic orchards. I took the photo of Eric and Ian with our three trucks as we arrived in the morning for offloading. It was relatively dry upon arrival, but it started raining shortly thereafter, and was a sloppy mess by the time we had finished unloading two hours later (after having to replace one loader motor, and swap a battery between the trucks-the usual almond problems).
The drought made beekeeping really tough last season, and we had to feed a record amount of pollen sub and syrup to our colonies in late summer and fall. Varroa only added to our problems. But we poured TLC (and dollars) into our hives, with the result that our colonies are looking OK for almonds (knock on wood).
I've added several new articles to the website, continuing on Colony Buildup and Decline, as well as investigating the fermentation of beebread (see https://scientificbeekeeping.com/articles-by-publication-date/).
I also updated my ppt on oxalic acid.
Beekeeper Jeff Anderson (and coplaintiffs) have recently filed a lawsuit against EPA to remove the current loophole that allows growers to plant pesticide-treated seed without the normal restrictions regarding pesticide application. EPA interpreted existing law as such:
Treated seed (and any resulting dust-off from treated seed) may be exempted from registration under FIFRA as a treated article and as such its planting is not considered a "pesticide use."
The above loophole has allowed serious problems with planting dust to remain unresolved. The lawsuit explains that the current EPA guidance document:
states there will not be investigation or enforcement against any of their bee kills or other harm caused by neonicotinoid-coated seeds or resulting contaminated dust because the kills and other harm incidents are "not considered a 'pesticide use.'"
Although I am not of the anti-neonic camp, and feel that seed treatments are perhaps the best use of neonics, they are indeed potent insecticides, and anyone (including the guy pulling the seeder) should have training in pesticide application, and follow restrictions to reduce pesticide drift. Thus I feel that beekeepers should support Jeff in this important lawsuit. Read more at: (Broken Link!) http://pollinatorstewardship.org/?p=3903
On the subject of pesticides, Dr. May Berenbaum has recently published the most succinct summary of the history of insecticide use that I've had the pleasure to read. Read it at: (Broken Link!) Does the Honey Bee "Risk Cup" Runneth Over?
We're now pushing 30 years with varroa, and from the look of it, in many operations varroa is winning. Lately I've been giving presentations on "A New Era in Mite Management," which I plan to spin into a series of articles.
I've also got a backlog of research trials that we've done (funded by the donors to ScientificBeekeeping), but have not yet had time to publish. There just haven't been enough hours in my days, due to building our operation and my many speaking engagements.
The good news is that we've finally reached the point that my sons are getting ready to take over the reins of our business (now at around 1200 hives), which I hope will free up time for me to catch up on the home front and concentrate on beekeeping research (as well as to improve the website).
Updates: Jan 9, 2016
A recently-filed lawsuit by beekeeper Jeff Anderson deserves our support, in order to close a huge loophole in pesticide regulation. Currently, the EPA does not classify pesticides applied on treated seed as pesticide "applications," and are thus exempt from the restrictions and liability due to drift or misuse as are other pesticide applications. The registration of seed treatments as pesticide applications will allow better monitoring of the overall environmental impact and fate of seed-applied pesticides (not only the neonics). For more information, see: (Broken Link!) Pollinator Stewardship News.
Also, see my updates on oxalic acid at Varroa treatments
Updates: Nov 2
There have been a couple of excellent and objective reviews of our state of knowledge on the effects of neonicotinoids on bees. Both are open access. The lay reader may wish to simply read the summaries in the second link.
A restatement of the natural science evidence base concerning neonicotinoid insecticides and insect pollinators
A restatement of recent advances in the natural science evidence base concerning neonicotinoid insecticides and insect pollinators
I've updated my analysis of the recent paper Neonicotinoid pesticides severely affect honey bee queens.
I also suggest the reading of an excellent Master's Thesis by Julia Goss of the Swedish University of Agricultural Sciences: Neonicotinoids and Honeybee Health. Julia tracked varroa, nosema, and virus levels in 96 colonies, equally divided between 16 fields of oilseed rape, half seed treated with clothianidin, half as untreated controls. She measured parasite levels before (June) and after flowering of the crop (late July-early August). Results: despite the confirmed exposure of the Test colonies to clothianidin at much higher rates than we ever see in North America, there were no differences in any of the parasite levels following exposure to the insecticide.
Update: August 23: I was asked to comment on Harvard Medical School's Dr. Lu's recent paper on neonics in Massachusetts. This may be of interest to those re a general discussion of the issue of good science vs. poor science. Read it at A Review of Dr. Lu's Latest.
Update June 26: I added a post that I made to Bee-L on monitoring varroa at Monitoring Varroa.
Update May 9: I've updated First Year Beekeeping, an added Oxalic acid dribble tips.
April 29: I've been derelict in updating the website, and have about 12 articles to post. A number of ABJ readers have asked me to post the following graphic from one of my recent articles.
You can view a full-sized version at Colony Demography.
I occasionally comment on bee issues or the news, or link to interesting blogs by others on beekeeping, bee biology, or the environment.
The "Flow Hive"
In recent months there has been a great deal of buzz about the "Flow Hive," developed by a father/son team of Australian beekeepers. The device consists of an arrangement of molded plastic parts that act as foundation upon which the bees build honey combs, but which can then be shifted by the turn of a handle to break open the cells of ripe honey and allow it to drain out of the hive through tubes. Although innovative, it is similar to a patent from 1939 (http://www.freepatentsonline.com/2223561.pdf).
The Flow Hive is likely the most well-funded beekeeping device ever brought to market, due to its inventors incredible media-savvy marketing via crowd sourcing on the internet. By means of producing brilliant and compelling fundraising videos, they have raised enough money to bring their product to market. Kudos to them!
I suspect that much of their funding has come from non beekeepers, who have always been fascinated by the promise of hive from which liquid honey could be directly taken without the need for actually handling bees.
The question regarding the Flow Hive is whether it will turn out to be practical, especially with regard to cost and whether it will stand up to repeated use. Longtime beekeepers tend to be skeptical, since we've seen so many beekeeping inventions come and go over the years.
But who knows? I'm as eager as anyone to see whether the Flow Hive proves to be a revolution in beekeeping. We'll see once the completed hives get delivered to buyers. I wish the developers the best of luck. Only time will tell whether the device actually flies or flops.
Neonics in Ontario
A recent hotbed of anti-neonic activism is Ontario, Canada, in which an unlikely coalition of a few beekeepers and some media-savvy NGO's is pushing the government to ban these insecticides. Let me state very clearly that I myself support organic and sustainable farming, use of Integrated Pest Management, and greatly reduced use of pesticides. That said, I feel that any pesticide regulations, and agricultural recommendations, should be based upon sound science.
An exemplar of this philosophy is Dr. Terry Daynard, formerly a professor and Assistant Dean of the Ontario Agricultural College, and currently a farmer himself. Daynard recently received the "2014 Farm & Food Care Champion" award from Farm and Food Care.org, with the introduction that "Daynard is a champion of agriculture in many ways. He is respected as a farmer, scientist, innovator and agricultural advocate, speaking up and advocating sound science even in the presence of criticism by those that don't agree with him."
Dr. Daynard applies a sound and scientific assessment of how misinformation can taint well-intentioned environmental regulation in his blog "Critique of "A Proposal for Enhancing Pollinator Health.""
We all want to minimize agriculture's negative effects on the environment. This includes greatly reducing our reliance upon pesticides. But such reduction needs to evolve as we learn (or re learn) alternate and more sustainable strategies for growing food. This is best done by rational and sober scientific assessment of current and alternative practices. I commend Dr. Daynard pointing this out.
I'm also impressed by a recent blog by Dr. David Zaruk, who is a Risk Governance Analyst at Risk Perception Management and an Assistant Professor Adjunct in Communications at Vesalius College, VUB, and Facultes universitaires St-Louis in Brussels. He blogs under the name of the "Risk Monger." He recently posted about the real-life agricultural and ecological consequences of the politically- (as opposed to scientifically-) motivated suspension of neonic seed treatments in the EU. http://risk-monger.blogactiv.eu/2014/09/30/the-save-the-bees-ban-failed-crops-and-another-precautionary-fail-who-is-to-blame/
Read previous blogs here:
https://scientificbeekeeping.com/news-and-blogs-page/
Dec 2, 2013 If you have interest in the recent petitions to ban the neonics, I recommend reading a letter to the respected journal Nature by a British bee researcher, Lynn Dicks, in which she points out the problems with hurried setting of policy based upon political pressure rather than upon careful scientific evaluation of the evidence http://www.nature.com/news/bees-lies-and-evidence-based-policy-1.12443
Such a careful evaluation of all evidence is what I'm all about, even if that is unpopular with those who don't want to be confused by the facts. I currently feel that the problem with planting dust from corn seeding has finally reached the point where the manufacturers either have to take responsibility for compensating beekeepers who suffer losses due to the application of their products, or EPA and PMRA need to restrict the use of neonic seed treatments to only planters that pass dust emission certification. However, I feel that to date there is not enough evidence to call for a complete ban on the neonics-there are simply too many beekeepers successfully keeping healthy hives in areas of seed-treated crops. Clearly this is a hot issue, and the neonics, along with all pesticides need to be closely watched and regulated. It appears to me that our regulatory agencies are doing a good job at this, even if progress seems to be excruciatingly slow.
The most recent blog of interest is on the real people involved in biotechnology (GMO's). Steve Savage writes:
"As with any new technology, the development and commercialization of biotech crops is a story about people. Its a story about people with ideas and vision; people who did hard and creative work; people who took career or business risks, and people who integrated this new technology into the complex business of farming... Their story is important, but it tends to get lost in much of the conversation about biotech crops.
Many narratives about "GMOs" leave out the people side, presenting it instead as some faceless, monolithic phenomenon devoid of human inspiration, intention and influence. Thats not how it happened. Other narratives about "GMOs" demonize those who made biotech crops a reality. Such portrayals are neither fair or accurate. The real stories of these people matter, because trust in a technology is greatly influenced by what people believe about those behind it."
Read the rest at:
http://appliedmythology.blogspot.com/2013/10/the-people-side-of-gmo-crops-part-i.html | News and Blogs - Scientific Beekeeping | https://scientificbeekeeping.com/home/news-and-blogs/ |
Understanding Colony Buildup and Decline: Part 7a - The Swarming Impulse
First published in: American Bee Journal, August 2015
Understanding Colony Buildup and Decline - Part 7a
The Swarming Impulse
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in Aug 2015
CONTENTS
The Swarming Impulse
Terminology
Reproductive Swarming And Emergency Swarming
The Effect Of Swarming Upon The Colony
Predicting Swarming
Issuance Of The Swarm
Acknowledgements
References
One of the main challenges of keeping bees for honey production is to manage one's hives to reach maximum strength by the start of the main honey flow, yet to somehow keep from blowing it by allowing those strong colonies to swarm.
An unmanaged colony of bees, should it survive the winter and successfully build up its population, must focus upon reproduction. Biologically, that means getting some of its genes into the next generation. There are two ways of doing so--by producing thousands of drones, on the chance that some of them might "get lucky" and mate with virgin queens from other colonies, or by undertaking the risky venture of sending off the mother queen and half the workers as a swarm.
Given good conditions, most wild (or feral) honey bee colonies will swarm more than once a season (if one counts the afterswarms [1]). Nature applies strong selective pressure for this behavior, since those colonies that are best at repopulating an area after a decimation event (such as plague, drought, forest fire, or a severe winter) are those whose genes will dominate the next generations.
But to the beekeeper, swarming is less desirable. The downside of swarming is that if it occurs shortly before (or during) the main honey flow, then the population of the hive is temporarily reduced, and honey production will suffer accordingly. As a result, bee breeders tend to select against the swarming trait, and we beekeepers attempt to prevent swarming through our management practices.
The Swarming Impulse
Swarming is a biological imperative once a colony has reached a certain size and food resources are abundant. Tropical races of bees tend to swarm more frequently, since they are less concerned about stocking away winter stores (they are also much more likely to abscond if faced with a dearth). The European races are a bit more cautious (since they don't normally abscond)-unless they keep their populations large enough to put away enough honey reserves, neither the parent colony nor the swarm will survive the winter. Accordingly, in this article I'm going to focus upon our managed European stocks [2].
By better understanding the biology of the swarming impulse, the beekeeper can make informed decisions regarding management options to minimize the event (but from personal experience, I can assure you that you are no more likely to completely prevent swarming than you are to prevent teenagers from following their innate biological urges).
To the beekeeper, the first indication of the swarming impulse is usually that the colony starts to build queen cells on the bottom bars (Fig. 1).
Figure 1. Colonies typically build swarm cells in the space between the brood chambers. This is the best place to look, but be aware that there may also be cells where other irregularities occur between the brood combs
The presence of queen cells is an intermediate step of the swarm impulse, and may or may not culminate with the actual issuing of a swarm. More importantly, it's better for the beekeeper to be proactive, and avert the colony's impulse to swarm before they even think about building cells.
To me, the fascinating thing about swarming is trying to understand exactly how the colony "mind" determines when to initiate the behavior, and how it translates that decision to the individual workers who then construct the queen cells, and then feed them or tear them down. But before we get into that, let's first define some terms...
Terminology
Prime swarm: the first swarm to leave, containing the overwintered "old" queen. Prime swarms are typically the largest swarms, and may contain 10 pounds of bees (Fig. 2).
Figure 2. A typical California swarm. Just kidding--we watched a few swarms in a yard coalesce into a monster, and then move from tree to tree, dropping walnut-sized balls of bees (each surrounding a queen), which we picked up and used to start 6 new colonies, using the bees from the swarm). This is not trick photography--I've seen the weight of a large swarm snap a 1" hardwood tree trunk.
Afterswarm: a normally smaller swarm that issues following the prime swarm (typically 10-15 days later).
Late season swarms: swarms which issue after the main honey flow. As Winston observes: "This is a curious behavior, since it is highly unlikely that such swarms and the new colonies that they issue from [referring to colonies previously founded as swarms earlier in the season] will survive the winter."
Usurpation swarms: swarms which invade and usurp an established colony [3]. This is a plausible explanation for how the above behavior could be adaptive.
A note on terminology: should the swarm that leaves be called the "parent" or "daughter" colony? It is the parent queen that actually issues along with half the parent colony, leaving her daughters behind to fight it out. But most beekeepers refer to the original hive as the "parent hive." I will follow that terminology in order to avoid confusion.
Queen cup: a downward-facing base of a queen cell, prepared to receive an egg (Fig. 3).
Figure 3. Empty queen cups along the bottom bar of a brood comb. Colonies tend to build plenty of these during spring (or other times of the year) in initial preparation for swarming or supersedure, but may or may not actually use them. Only when they are "wet" with jelly and a larva (Fig. 4) is the colony seriously starting to commit to swarming.
Figure 4. Swarm cells "wet" with jelly and a larva. At this point, swarming is imminent, unless conditions change to cause the colony to decide to throw it into reverse and consume them.
Queen cell: Any downward-facing cell containing an immature queen (Fig. 5). Queen cells are built by the bees in response to three different scenarios.
Figure 5. Some exceptionally elongated queen cells. They are swarm cells, but in an unusual location.
Swarm (reproductive) cells: queen cells created in preparation for swarming (colony reproduction), typically initiated in dedicated cups on the lower edges of a brood comb (Fig. 6).
Figure 6. A row of swarm cells (in a more "normal" location) shortly after the issuing of the prime swarm (note that the 5th cell from the right has already emerged). Depending upon the strength of the colony, the remaining unemerged queens may be killed in their cells, or allowed to emerge and either form afterswarms or fight to become the new mother queen of the colony.
Supersedure cell: A queen cell raised by the colony with the intent of replacing a failing, injured, or otherwise undesirable queen (Fig. 7). Russian bees are noted for frequently building and tearing down supersedure cells--apparently keeping immature reserve queens on hand "just in case." Unless your queens are marked, you may not notice the degree of supersedure that naturally occurs.
Figure 7. Supersedure cells are typically single cells built on the face of the comb. Sick colonies will often supersede the queen, apparently in an attempt to bring "new blood" into the hive.
Of note is that there is no particular reason for a queen to fight with her supersedure daughter, since they share at least half their genes, and are not really in competition. This may be why we so often see a mother and daughter queen happily ignoring each other. On the other hand, sister queens fight aggressively in order to become the sole mother of a colony.
Emergency cell: A queen cell created in response to the loss or removal of a queen. These are typically built by modifying an existing cell containing a newly-emerged worker larva (Fig. 8).
Figure 8. Emergency queen cells are formed by floating an existing young larva to the top of her cell by adding jelly, then extending the cell in a downward direction. The bees start a number of emergency cells, and then later cull out many of them.
Reproductive Swarming And Emergency Swarming
Colonies producing emergency cells following the loss of their queen exhibit a number of behaviors similar to those in colonies preparing for afterswarming. The study of such similarities may help us to understand the cues that cause bees to initiate certain behaviors, and thus how the colony "thinks."
Punnett and Winston [4] speculated that:
One possible explanation is that workers are not able to perceive differences between queen loss due to death and queen loss due to swarming. Thus, colonies may behave as if they were in an afterswarming situation following queen loss.
Surprisingly, the researchers also found that when a colony is made queenless, some emergency cells are built in queen cups (rather than by extending worker cells), meaning that they were started after the disappearance of the queen. The researchers concluded that workers must move either eggs or newly-emerged larvae into preexisting queen cups [5]. What, you say, workers move larvae? Apparently so. The only other possible way for larvae to appear in the cells would be by workers laying fertile eggs [6], which does not appear to be the case, since a number of researchers have noted that no additional emergency cells are initiated after 4 days of queenlessness [7].
Of interest is that this behavior is exhibited to an even greater extent by Africanized bees, suggesting that it is an innate ancestral behavior. What intrigues me is that it raises the question as to what extent the queen is actually involved in the swarm impulse--she apparently is not even required to lay eggs in the prepared swarm cups (although this is the normal way it is done), since the workers are able to move them (or young larvae) there themselves.
Biological question: if swarm cell formation does not depend upon the queen voluntarily laying eggs in them, then the implication is that the colony, independently of its queen, can decide if and when to swarm. Although the queen generally does lay eggs in the cells, and inspects the development of her daughter queens, it appears that it is the workers who are largely running the show. It is they who build the cells and feed the daughter queens, restrict the queen's diet prior to swarming, and finally goad her into flight. It could well be that in the process of swarming, the superorganism may act largely independently of its mother/ovary (the queen), although they are certainly reading some of her pheromonal signals. The question to me is to what degree the queen is necessarily involved in the decision making regarding the swarm impulse and execution. A second question is whether the workers apply a pheromone into the queen cups to "tell" the queen when and where to place an egg.
The Effect Of Swarming Upon The Colony
Over 50% of the workers leave with the swarm, most of them being less than 10 days of age. The loss of this nurse force then results in elevated mortality of the remaining young brood (over 40% may perish). This is quite a hit to the colony population. There is less immediate impact of honey loss to the swarm; by my math perhaps a couple of pounds.
Biological question: I find it of interest that the workers engorge with nectar for about 10 days prior to the actual issuance of the swarm. This finding suggests that the colony population initiates other preparations (besides producing queen cells) well in advance of departure. How this memo is communicated to each individual bee remains an open question, but raises the additional question of whether there are other physiological changes that take place in pre-swarming bees.
But since the colony is full of sealed brood at the time of swarm issuance, its population usually recovers rapidly, should it not continue to issue afterswarms. Unfortunately, the more brood present, the greater the chance of afterswarming [8]. Up to four more afterswarms may leave over the next several days, each containing one or more virgins (I once recovered something like 18 queens from one exceptionally large combined swarm). A colony will normally issue afterswarms only to the extent that it continues to maintain an adequate population, but I do occasionally see a colony appear to "swarm itself to death."
Practical application: it is frustrating to watch your strongest colonies hit the trees just before the main flow. Rather than putting honey into your supers, those bees (should you not catch the swarm (Figs. 9-11)) are now in competition with your hived colonies.
Figure 9. A perfect low-hanging swarm, a hive ready to receive it positioned below and with the cover off, with an empty super placed on top to act as a funnel.
Figure 10. One quick shake to dislodge the bees...
Figure 11. Ah, I wish they were all that easy!
There will also be a brood break of from 15-25 days (until all afterswarms have issued, and a new queen finally gets mated and starts laying). This brood break has a delayed effect of further reducing the adult population (when recruitment of replacement workers is curtailed beginning three weeks later).
Remember from my previous article about weaker colonies "catching up" with stronger colonies during the linear buildup phase? A colony that reaches peak population in advance of the main flow may as well swarm and attempt to recover its population in time for the main flow. Weaker colonies, by not swarming, may then be able to surpass the formerly strong colonies in honey production.
Practical application: as out-of-state almond pollinators are well aware, having strong colonies early in March is not necessarily a good thing. We California beekeepers shift quickly from building up our colonies for almond pollination to trying to keep them in their boxes after the bloom is over. It's all about timing--there's no sense in building up colonies too early in the season, unless you want to make increase. Ideally, you'd time the buildup so that all your hives are just approaching maximum population when your main honey flow begins.
Let's not forget varroa: There's conflicting data on the effect of swarming on varroa. Obviously, some mites get carried off with the swarm, and the brood break further reduces the mite population. But let's do the math. At the time of swarming, the colony is chock full of sealed brood (lots of it drone brood), so perhaps 2/3rds of the mites will be in the brood, leaving only 1/3 on the adult bees. Say that half the adult bees leave with the swarm. That means that roughly 1/6 of the mites go with the swarm, leaving 5/6 in the parent hive. If you are lucky enough to hive the swarm, you now have two "new" colonies. But one now starts with 5x as many mites in it, and likely should be managed more aggressively for varroa.
Predicting Swarming
Most swarming in any area occurs during a period of only a few weeks, generally keyed to plant phenology (the timing of bloom). In my area, swarm season usually occurs from mid April to mid May (when our main flow typically starts). But this season, drought and poor flight weather resulted in two peaks in swarming, one early, and a second peak in mid June. This was apparently due to lack of forage during the "normal" swarm season, so colonies curtailed swarming until a decent nectar flow began.
Practical application: learn from experienced beekeepers when to "expect" swarming, but realize that the timing can vary greatly from year to year.
Colonies typically swarm shortly after the first queen cell is sealed, but may leave earlier or later, depending upon weather conditions. Colonies may tear down cells to delay swarming, or lose the swarm impulse altogether (this can be easily observed at the end of almond pollination, when colonies left in the now forage-deficient orchards will quickly tear down their cells). Colonies will also sometimes keep virgins imprisoned in their cells, and the beekeeper can easily hear them piping at one another.
Practical application: continually lift your upper brood chambers of your strongest colonies to check for "wet" queen cells on the bottom bars (don't worry about "dry" queen cups, which don't indicate that the colony is yet serious about swarming). The presence of swarm cells containing a larva and jelly is your best cue that that the swarm impulse is in full gear. The bees may well tear these cells down should conditions change, but they are a call to action for the observant beekeeper.
The question then is what one can do to either prevent or reverse the swarm impulse. I will cover that topic in the next installment.
Issuance Of The Swarm
In this series, I'm only going to discuss the biology of the swarm impulse, which may eventually lead to the actual issuing of a swarm. The behavior and decision making of the colony (and certain individual bees) leading up to swarm departure is equally, if not more so, fascinating. For further reading on that fascinating subject, I highly recommend the wonderful research and observations by Dr. Tom Seeley and his collaborators, beautifully elaborated in his book Honeybee Democracy [9].
Acknowledgements
As always, I could not research these articles without the help of my friend Peter Borst, and the support of the donors to ScientificBeekeeping. And a belated thanks to Dr. Mark Winston for his research towards understanding swarming behavior, from which I've drawn heavily for this article.
References
[1] Winston, ML (1980) Swarming, afterswarming, and reproductive rate of unmanaged honeybee colonies (Apis mellifera). Insectes Sociaux 27(4): 391-398.
[2] Dr. Mark Winston went to great lengths to investigate and summarize swarming behavior in both Africanized and European races of bees. I've taken a great deal of information from his papers and book
Winston, ML (1987) The Biology of the Honey Bee. Harvard University Press. This book should be on every serious beekeeper's bookshelf.
[3] See https://scientificbeekeeping.com/whats-happening-to-the-bees-part-2/
[4] Punnett, EN & ML Winston (1983) Events following queen removal in colonies of European-derived honey bee races (Apis mellifera). Insectes Sociaux 30(4): 376-383.
[5] I've wondered about this a number of times, when I've found queen cells being built above an excluder. Such queen cell production from larvae transferred by the bees would be analogous to the Doolittle method of "grafting," practiced by most queen producers (illustrated at https://scientificbeekeeping.com/queens-for-pennies/).
[6] This is called thelytoky, which is common in the Cape Bee, but rare in other races:
Oldroyd, BP, et al (2008) Thelytokous parthenogenesis in unmated queen honeybees (Apis mellifera capensis): Central fusion and high recombination rates. Genetics 180(1): 359-366.
There is apparently one specific recessive allele that allows the Cape bees to do this:
Lattorff, HMG, et al (2005) A single locus determines thelytokous parthenogenesis of laying honeybee workers (Apis mellifera capensis). Heredity 94: 533-537.
[7] After which time there would no longer be any newly-emerging larvae from the previous queen.
[8] Winston (1980) op. cit.
[9] Seeley, TD (2010) Honeybee Democracy. Princeton University Press.
Category: Bee Behavior and Biology
Tags: effects, emergency swarming, predicting swarming, reproductive swarming, swarming | emergency swarming Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/emergency-swarming/ |
Understanding Colony Buildup and Decline: Part 7a - The Swarming Impulse
First published in: American Bee Journal, August 2015
Understanding Colony Buildup and Decline - Part 7a
The Swarming Impulse
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in Aug 2015
CONTENTS
The Swarming Impulse
Terminology
Reproductive Swarming And Emergency Swarming
The Effect Of Swarming Upon The Colony
Predicting Swarming
Issuance Of The Swarm
Acknowledgements
References
One of the main challenges of keeping bees for honey production is to manage one's hives to reach maximum strength by the start of the main honey flow, yet to somehow keep from blowing it by allowing those strong colonies to swarm.
An unmanaged colony of bees, should it survive the winter and successfully build up its population, must focus upon reproduction. Biologically, that means getting some of its genes into the next generation. There are two ways of doing so--by producing thousands of drones, on the chance that some of them might "get lucky" and mate with virgin queens from other colonies, or by undertaking the risky venture of sending off the mother queen and half the workers as a swarm.
Given good conditions, most wild (or feral) honey bee colonies will swarm more than once a season (if one counts the afterswarms [1]). Nature applies strong selective pressure for this behavior, since those colonies that are best at repopulating an area after a decimation event (such as plague, drought, forest fire, or a severe winter) are those whose genes will dominate the next generations.
But to the beekeeper, swarming is less desirable. The downside of swarming is that if it occurs shortly before (or during) the main honey flow, then the population of the hive is temporarily reduced, and honey production will suffer accordingly. As a result, bee breeders tend to select against the swarming trait, and we beekeepers attempt to prevent swarming through our management practices.
The Swarming Impulse
Swarming is a biological imperative once a colony has reached a certain size and food resources are abundant. Tropical races of bees tend to swarm more frequently, since they are less concerned about stocking away winter stores (they are also much more likely to abscond if faced with a dearth). The European races are a bit more cautious (since they don't normally abscond)-unless they keep their populations large enough to put away enough honey reserves, neither the parent colony nor the swarm will survive the winter. Accordingly, in this article I'm going to focus upon our managed European stocks [2].
By better understanding the biology of the swarming impulse, the beekeeper can make informed decisions regarding management options to minimize the event (but from personal experience, I can assure you that you are no more likely to completely prevent swarming than you are to prevent teenagers from following their innate biological urges).
To the beekeeper, the first indication of the swarming impulse is usually that the colony starts to build queen cells on the bottom bars (Fig. 1).
Figure 1. Colonies typically build swarm cells in the space between the brood chambers. This is the best place to look, but be aware that there may also be cells where other irregularities occur between the brood combs
The presence of queen cells is an intermediate step of the swarm impulse, and may or may not culminate with the actual issuing of a swarm. More importantly, it's better for the beekeeper to be proactive, and avert the colony's impulse to swarm before they even think about building cells.
To me, the fascinating thing about swarming is trying to understand exactly how the colony "mind" determines when to initiate the behavior, and how it translates that decision to the individual workers who then construct the queen cells, and then feed them or tear them down. But before we get into that, let's first define some terms...
Terminology
Prime swarm: the first swarm to leave, containing the overwintered "old" queen. Prime swarms are typically the largest swarms, and may contain 10 pounds of bees (Fig. 2).
Figure 2. A typical California swarm. Just kidding--we watched a few swarms in a yard coalesce into a monster, and then move from tree to tree, dropping walnut-sized balls of bees (each surrounding a queen), which we picked up and used to start 6 new colonies, using the bees from the swarm). This is not trick photography--I've seen the weight of a large swarm snap a 1" hardwood tree trunk.
Afterswarm: a normally smaller swarm that issues following the prime swarm (typically 10-15 days later).
Late season swarms: swarms which issue after the main honey flow. As Winston observes: "This is a curious behavior, since it is highly unlikely that such swarms and the new colonies that they issue from [referring to colonies previously founded as swarms earlier in the season] will survive the winter."
Usurpation swarms: swarms which invade and usurp an established colony [3]. This is a plausible explanation for how the above behavior could be adaptive.
A note on terminology: should the swarm that leaves be called the "parent" or "daughter" colony? It is the parent queen that actually issues along with half the parent colony, leaving her daughters behind to fight it out. But most beekeepers refer to the original hive as the "parent hive." I will follow that terminology in order to avoid confusion.
Queen cup: a downward-facing base of a queen cell, prepared to receive an egg (Fig. 3).
Figure 3. Empty queen cups along the bottom bar of a brood comb. Colonies tend to build plenty of these during spring (or other times of the year) in initial preparation for swarming or supersedure, but may or may not actually use them. Only when they are "wet" with jelly and a larva (Fig. 4) is the colony seriously starting to commit to swarming.
Figure 4. Swarm cells "wet" with jelly and a larva. At this point, swarming is imminent, unless conditions change to cause the colony to decide to throw it into reverse and consume them.
Queen cell: Any downward-facing cell containing an immature queen (Fig. 5). Queen cells are built by the bees in response to three different scenarios.
Figure 5. Some exceptionally elongated queen cells. They are swarm cells, but in an unusual location.
Swarm (reproductive) cells: queen cells created in preparation for swarming (colony reproduction), typically initiated in dedicated cups on the lower edges of a brood comb (Fig. 6).
Figure 6. A row of swarm cells (in a more "normal" location) shortly after the issuing of the prime swarm (note that the 5th cell from the right has already emerged). Depending upon the strength of the colony, the remaining unemerged queens may be killed in their cells, or allowed to emerge and either form afterswarms or fight to become the new mother queen of the colony.
Supersedure cell: A queen cell raised by the colony with the intent of replacing a failing, injured, or otherwise undesirable queen (Fig. 7). Russian bees are noted for frequently building and tearing down supersedure cells--apparently keeping immature reserve queens on hand "just in case." Unless your queens are marked, you may not notice the degree of supersedure that naturally occurs.
Figure 7. Supersedure cells are typically single cells built on the face of the comb. Sick colonies will often supersede the queen, apparently in an attempt to bring "new blood" into the hive.
Of note is that there is no particular reason for a queen to fight with her supersedure daughter, since they share at least half their genes, and are not really in competition. This may be why we so often see a mother and daughter queen happily ignoring each other. On the other hand, sister queens fight aggressively in order to become the sole mother of a colony.
Emergency cell: A queen cell created in response to the loss or removal of a queen. These are typically built by modifying an existing cell containing a newly-emerged worker larva (Fig. 8).
Figure 8. Emergency queen cells are formed by floating an existing young larva to the top of her cell by adding jelly, then extending the cell in a downward direction. The bees start a number of emergency cells, and then later cull out many of them.
Reproductive Swarming And Emergency Swarming
Colonies producing emergency cells following the loss of their queen exhibit a number of behaviors similar to those in colonies preparing for afterswarming. The study of such similarities may help us to understand the cues that cause bees to initiate certain behaviors, and thus how the colony "thinks."
Punnett and Winston [4] speculated that:
One possible explanation is that workers are not able to perceive differences between queen loss due to death and queen loss due to swarming. Thus, colonies may behave as if they were in an afterswarming situation following queen loss.
Surprisingly, the researchers also found that when a colony is made queenless, some emergency cells are built in queen cups (rather than by extending worker cells), meaning that they were started after the disappearance of the queen. The researchers concluded that workers must move either eggs or newly-emerged larvae into preexisting queen cups [5]. What, you say, workers move larvae? Apparently so. The only other possible way for larvae to appear in the cells would be by workers laying fertile eggs [6], which does not appear to be the case, since a number of researchers have noted that no additional emergency cells are initiated after 4 days of queenlessness [7].
Of interest is that this behavior is exhibited to an even greater extent by Africanized bees, suggesting that it is an innate ancestral behavior. What intrigues me is that it raises the question as to what extent the queen is actually involved in the swarm impulse--she apparently is not even required to lay eggs in the prepared swarm cups (although this is the normal way it is done), since the workers are able to move them (or young larvae) there themselves.
Biological question: if swarm cell formation does not depend upon the queen voluntarily laying eggs in them, then the implication is that the colony, independently of its queen, can decide if and when to swarm. Although the queen generally does lay eggs in the cells, and inspects the development of her daughter queens, it appears that it is the workers who are largely running the show. It is they who build the cells and feed the daughter queens, restrict the queen's diet prior to swarming, and finally goad her into flight. It could well be that in the process of swarming, the superorganism may act largely independently of its mother/ovary (the queen), although they are certainly reading some of her pheromonal signals. The question to me is to what degree the queen is necessarily involved in the decision making regarding the swarm impulse and execution. A second question is whether the workers apply a pheromone into the queen cups to "tell" the queen when and where to place an egg.
The Effect Of Swarming Upon The Colony
Over 50% of the workers leave with the swarm, most of them being less than 10 days of age. The loss of this nurse force then results in elevated mortality of the remaining young brood (over 40% may perish). This is quite a hit to the colony population. There is less immediate impact of honey loss to the swarm; by my math perhaps a couple of pounds.
Biological question: I find it of interest that the workers engorge with nectar for about 10 days prior to the actual issuance of the swarm. This finding suggests that the colony population initiates other preparations (besides producing queen cells) well in advance of departure. How this memo is communicated to each individual bee remains an open question, but raises the additional question of whether there are other physiological changes that take place in pre-swarming bees.
But since the colony is full of sealed brood at the time of swarm issuance, its population usually recovers rapidly, should it not continue to issue afterswarms. Unfortunately, the more brood present, the greater the chance of afterswarming [8]. Up to four more afterswarms may leave over the next several days, each containing one or more virgins (I once recovered something like 18 queens from one exceptionally large combined swarm). A colony will normally issue afterswarms only to the extent that it continues to maintain an adequate population, but I do occasionally see a colony appear to "swarm itself to death."
Practical application: it is frustrating to watch your strongest colonies hit the trees just before the main flow. Rather than putting honey into your supers, those bees (should you not catch the swarm (Figs. 9-11)) are now in competition with your hived colonies.
Figure 9. A perfect low-hanging swarm, a hive ready to receive it positioned below and with the cover off, with an empty super placed on top to act as a funnel.
Figure 10. One quick shake to dislodge the bees...
Figure 11. Ah, I wish they were all that easy!
There will also be a brood break of from 15-25 days (until all afterswarms have issued, and a new queen finally gets mated and starts laying). This brood break has a delayed effect of further reducing the adult population (when recruitment of replacement workers is curtailed beginning three weeks later).
Remember from my previous article about weaker colonies "catching up" with stronger colonies during the linear buildup phase? A colony that reaches peak population in advance of the main flow may as well swarm and attempt to recover its population in time for the main flow. Weaker colonies, by not swarming, may then be able to surpass the formerly strong colonies in honey production.
Practical application: as out-of-state almond pollinators are well aware, having strong colonies early in March is not necessarily a good thing. We California beekeepers shift quickly from building up our colonies for almond pollination to trying to keep them in their boxes after the bloom is over. It's all about timing--there's no sense in building up colonies too early in the season, unless you want to make increase. Ideally, you'd time the buildup so that all your hives are just approaching maximum population when your main honey flow begins.
Let's not forget varroa: There's conflicting data on the effect of swarming on varroa. Obviously, some mites get carried off with the swarm, and the brood break further reduces the mite population. But let's do the math. At the time of swarming, the colony is chock full of sealed brood (lots of it drone brood), so perhaps 2/3rds of the mites will be in the brood, leaving only 1/3 on the adult bees. Say that half the adult bees leave with the swarm. That means that roughly 1/6 of the mites go with the swarm, leaving 5/6 in the parent hive. If you are lucky enough to hive the swarm, you now have two "new" colonies. But one now starts with 5x as many mites in it, and likely should be managed more aggressively for varroa.
Predicting Swarming
Most swarming in any area occurs during a period of only a few weeks, generally keyed to plant phenology (the timing of bloom). In my area, swarm season usually occurs from mid April to mid May (when our main flow typically starts). But this season, drought and poor flight weather resulted in two peaks in swarming, one early, and a second peak in mid June. This was apparently due to lack of forage during the "normal" swarm season, so colonies curtailed swarming until a decent nectar flow began.
Practical application: learn from experienced beekeepers when to "expect" swarming, but realize that the timing can vary greatly from year to year.
Colonies typically swarm shortly after the first queen cell is sealed, but may leave earlier or later, depending upon weather conditions. Colonies may tear down cells to delay swarming, or lose the swarm impulse altogether (this can be easily observed at the end of almond pollination, when colonies left in the now forage-deficient orchards will quickly tear down their cells). Colonies will also sometimes keep virgins imprisoned in their cells, and the beekeeper can easily hear them piping at one another.
Practical application: continually lift your upper brood chambers of your strongest colonies to check for "wet" queen cells on the bottom bars (don't worry about "dry" queen cups, which don't indicate that the colony is yet serious about swarming). The presence of swarm cells containing a larva and jelly is your best cue that that the swarm impulse is in full gear. The bees may well tear these cells down should conditions change, but they are a call to action for the observant beekeeper.
The question then is what one can do to either prevent or reverse the swarm impulse. I will cover that topic in the next installment.
Issuance Of The Swarm
In this series, I'm only going to discuss the biology of the swarm impulse, which may eventually lead to the actual issuing of a swarm. The behavior and decision making of the colony (and certain individual bees) leading up to swarm departure is equally, if not more so, fascinating. For further reading on that fascinating subject, I highly recommend the wonderful research and observations by Dr. Tom Seeley and his collaborators, beautifully elaborated in his book Honeybee Democracy [9].
Acknowledgements
As always, I could not research these articles without the help of my friend Peter Borst, and the support of the donors to ScientificBeekeeping. And a belated thanks to Dr. Mark Winston for his research towards understanding swarming behavior, from which I've drawn heavily for this article.
References
[1] Winston, ML (1980) Swarming, afterswarming, and reproductive rate of unmanaged honeybee colonies (Apis mellifera). Insectes Sociaux 27(4): 391-398.
[2] Dr. Mark Winston went to great lengths to investigate and summarize swarming behavior in both Africanized and European races of bees. I've taken a great deal of information from his papers and book
Winston, ML (1987) The Biology of the Honey Bee. Harvard University Press. This book should be on every serious beekeeper's bookshelf.
[3] See https://scientificbeekeeping.com/whats-happening-to-the-bees-part-2/
[4] Punnett, EN & ML Winston (1983) Events following queen removal in colonies of European-derived honey bee races (Apis mellifera). Insectes Sociaux 30(4): 376-383.
[5] I've wondered about this a number of times, when I've found queen cells being built above an excluder. Such queen cell production from larvae transferred by the bees would be analogous to the Doolittle method of "grafting," practiced by most queen producers (illustrated at https://scientificbeekeeping.com/queens-for-pennies/).
[6] This is called thelytoky, which is common in the Cape Bee, but rare in other races:
Oldroyd, BP, et al (2008) Thelytokous parthenogenesis in unmated queen honeybees (Apis mellifera capensis): Central fusion and high recombination rates. Genetics 180(1): 359-366.
There is apparently one specific recessive allele that allows the Cape bees to do this:
Lattorff, HMG, et al (2005) A single locus determines thelytokous parthenogenesis of laying honeybee workers (Apis mellifera capensis). Heredity 94: 533-537.
[7] After which time there would no longer be any newly-emerging larvae from the previous queen.
[8] Winston (1980) op. cit.
[9] Seeley, TD (2010) Honeybee Democracy. Princeton University Press.
Category: Bee Behavior and Biology
Tags: effects, emergency swarming, predicting swarming, reproductive swarming, swarming | effects Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/effects/ |
Overwintering of Honey Bee Colonies
Overwintering of honey bee colonies This subject has long generated endless debate among beekeepers. There are a few excellent resources by those who have collected hard data: Dr. Floyd Moeller was a USDA researcher who performed extensive field research to test various beekeeping management practices. This excellent publication covers practices to improve overwintering success, and [...]
Read More | Practical Beekeeping Management Archives - Scientific Beekeeping | https://scientificbeekeeping.com/practical-beekeeping-management/ |
Reevaluating Beebread: Part 2 - The Players
First published in: American Bee Journal, November 2015
Reevaluating Beebread: Part 2
The Players
Randy Oliver
ScientificBeekeeping.com
First published in ABJ Nov 2015
CONTENTS
Why Do Bees Go To Such Effort To Prepare Pollen In This Manner?
Which Microorganisms Are Involved?
Establishment Of Nest And Gut Microbiota
What About Antibiotics?
Next
Acknowledgements
References And Notes
In the last two decades, the widespread application of genetic and genomic approaches has revealed a bacterial world astonishing in its ubiquity and diversity [1]. It's become clear that the superorganism that we call the honey bee colony includes a number of symbiotic bacteria. Some appear to be involved in nutrition and immunocompetence, but we are only beginning to understand which players are involved, and what they do.
In the last installment, I introduced Dr. Kirk Anderson. When hired by the Tucson ARS lab (on the downside of the CCD epidemic) he really did his homework, and boned up on everything known about the honey bee microbiome, from which he summarized the then current state of knowledge thoroughly and succinctly in an open-access paper [2], from which I'll lift a few snips:
The hive of the honey bee may be best characterized as an extended organism that not only houses developing young and nutrient rich food stores, but also serves as a niche for symbiotic microbial communities that aid in nutrition and defend against pathogens. The niche requirements and maintenance of beneficial honey bee symbionts are largely unknown, as are the ways in which such communities contribute to honey bee nutrition, immunity, and overall health.
Kirk pointed out that ants, termites, aphids, and other insects cultivate beneficial bacterial and fungal symbionts, but that:
Given the depth of understanding in the aforementioned systems, it is alarming to consider that virtually nothing is known about the beneficial microbial symbionts of the honey bee, a social insect vital to the worlds food supply. Many thousands of different microbial strains have been cultured from honey bee colonies [he credits Dr. Martha Gilliam], yet we know virtually nothing of honey bee microbial ecology.
Kirk then laid out a vision of a lab devoted to furthering our understanding of how the naturally occurring microbiota of the honey bee colony contribute to bee health and nutrition. Let me be clear that the Anderson Lab is not the only group looking at the bee microbiome--in the U.S. alone, research in this nascent field is also being performed in the labs of Drs. Nancy Moran, Irene Newton, Jay Evans, Gene Robinson, and Quinn McFrederick [3], among others. This is spawning a new generation of bee researchers with proficiency in state-of-the-art technique and analysis.
It's abundantly clear that we have a great deal yet to learn about the importance (or lack thereof) of the microbiota associated with the honey bee. But for now, let's return to the subject of this article: the role of the microbes involved in the process of fermenting raw pollen into beebread. Such fermentation could be for either (or both) of two reasons--for simple preservation, or to enhance its nutritional quality. As Kirk explains [4]:
Nutrient conversion is readily distinguished from food preservation (storage). Although both processes have associated microbial communities, the primary function of food preservation is to prevent microbial degradation... preservation environments composed of plant material (e.g. silage) are typically dominated by Lactobacillus spp. and other acid tolerant microbes. Conversely, nutrient conversion involves an extended time component following the collection of plant matter, massive nutrient turnover prior to consumption and a vertically inherited mutualistic microbe or small community of microbes that emerges as the dominant force in the conversion of recalcitrant plant material.
The questions that arise are then:
Why do bees go to such effort to prepare pollen in this manner?
Which microorganisms are involved, and do the bees inoculate the beebread with specific symbiotic microbes?
What chemical and biological processes occur during the fermentation process?
What are the nurse bees' consumption preferences?
Is the fermentation necessary to release the nutrients of the pollen?
Is the pollen made more nutritious during the fermentation process?
In a relatively short period of intense investigation, Kirk and his associates were able to obtain (at least preliminary) answers to most of the above questions, published in an open access paper [5]. So let's cover each of the above questions in turn.
Why Do Bees Go To Such Effort To Prepare Pollen In This Manner?
Let's first consider the dynamics of pollen within the hive. Pollen is the predominant source of protein and other colony nutrition; a continual supply is thus critical if brood is to be reared. Unfortunately, that supply is completely dependent upon an ever changing bloom and capricious weather. When colonies are in their rapid growth phase, or during pollen dearths, there is often little pollen to be seen in the combs. But that doesn't mean that the colony doesn't have a reserve stored. So where is it?
In the previous installment I described how the pollen foragers place their loads into cells adjacent to the broodnest, after which mid-aged bees pack it into place for storage. But this then creates the problem of how to protect such a rich larder of stored food (at the warm temperature of the broodnest) from the slew of pollen-feeding insects, mites, fungi, and bacteria eager to consume or decompose it. So what to do?
As Kirk observes, "nutrition stored within the body of an individual is protected by anatomical barriers and active immune physiology." So nurse and mid-aged bees ravenously consume that freshly-stored pollen, thus protecting it within their bodies (Fig. 1).
Figure 1. Forager bees (sampled from the entrance) tend to have very little pollen in their guts, but "house bees" (nurses and mid-aged bees) tell a different story. I took this sample of 50 bees from an outside frame of the upper hive body in early November (after 2 days of confinement by rain), froze them to kill them, and then crushed them with a roller to squash out their gut contents. Note that the gut of every single bee was full of pollen. In other samples taken during the summer pollen dearth, a small proportion of bees from similar combs lacked pollen in their guts.
A question: The pollen in the above photo was mostly in the hindguts of the bees (post normal digestion). I wonder why they retain the remnants of digested pollen grains for so long, rather than defecating immediately. Could it be that additional nutrients are released or generated by the bacteria that thrive in the rectum?
Nurse and mid-age bees digest that consumed pollen and glandularly convert it into jelly (analogous to mammal milk)--which can be considered as the in-hive "currency" of protein, to be equally shared according to need. Any excess is converted to vitellogenin and stored in the fat bodies of all but the foragers. The colony is thus able to distribute protein reserves throughout the colony population as a whole.
In good times though, foragers bring in more pollen than the nurses can consume, so the colony must preserve it in some additional manner. They do so by fermenting it into beebread, using a process similar to that used for the creation of silage or sauerkraut--by allowing lactic acid bacteria to produce their preservative namesake, thus creating an environment hostile to other microorganisms, allowing for the relatively long term storage of pollen for later consumption.
The question then, is exactly...
Which Microorganisms Are Involved?
First, current day genomic research into the hive microbiome is not something that you do with a microscope. The literature is incredibly jargon-heavy, tedious to read, and consists of monster spreadsheets of numbers meaningless to all but those well versed in this arcane field (I'm definitely not one of them). But there is some common terminology and methodology that I need to briefly explain.
Until recently, scientists' ability to study the microorganisms in the bee gut was largely limited to culturing them in petri dishes, ala Martha Gilliam's meticulous research. The problem with that methodology is that many gut bacteria are difficult to culture. It was only with the development of PCR (polymerase chain reaction) to amplify scraps of DNA that we could start to identify organisms by parts of their genome alone. This technology was quickly followed by "metagenomics," which allowed the identification of unknown and unculturable microorganisms from a sample of biological material. By convention, researchers compare differences in the "spelling" of the 16S ribosomal DNA genes present [6] in order to estimate how many different "species" of bacteria are present. From this analysis, they can then create phylogenetic "trees" of relationships. To their amazement, scientists found that we had missed about 99% of species of bacteria in various environments.
Only recently (2003 [7]) did researchers note that there appeared to be a distinctive gut microbiome in the honey bee, furthered by Diana Cox-Foster's metagenomic analysis of colonies suffering from CCD [8]. We now know that honey bees tend to harbor a fairly consistent community of symbiotic bacteria [9,10], consisting of what appears to be around eight different "phylotypes" (the separation of bacteria into species is not as clear cut as it is for higher organisms [11]; bacteria identified only by DNA analysis are separated into OTUs (Operational Taxonomic Units, each having a group name such as "Firm 5"). In any phylotype, there may be several clades of OTUs (each OTU presumably being a closely-related species or strain, likely adapted to a slightly different niche, with a different biochemical profile, and thus possibly involved in a different symbiotic relationship, or performing different functions) [12]. As researchers refine their methods, they will surely further split these OTUs into additional named species. Each type of bacteria typically occupies a specific niche in the bee (or hive). Based largely upon an excellent recent review by Dr. Nancy Moran [13] and communication with Kirk Anderson, I created the graphic below to show where they are typically found (Fig. 2).
Figure 2. An adult honey bee may harbor a billion bacteria, with roughly 95% residing in the waste material in the hindgut; few survive in the microbe-hostile crop. Foragers bring environmental bacteria from flowers back to the hive-notably Lactobacillus kunkeei, which then thrives in the fructose-rich nest environment (especially in beebread). Other bacteria are nest symbionts, such as the Alpha 2.2 group found in jelly. And then there are the "core" gut bacteria, exhibiting strict niche fidelity within the bee gut.
Establishment Of Nest And Gut Microbiota
Let me first make clear that the research community is at a very preliminary stage at understanding the establishment and functions of the honey bee microbial community. Bacteria and fungi (as well as pathogens [14]) are brought into the hive with the nectar and pollen. Due to colony hygiene and the unfavorable environments of jelly, beebread, and honey, many species do not survive for long. But some find niches to their liking. And then there are other symbiotic bacteria which may be unique to the hive environment or bee gut--apparently transferred from one generation of bees to the next. And although there are "core" and "typical" communities of bacteria in the bees and the hive, they may vary substantially from colony to colony, race to race, and location to location [15].
Of interest is that Kirk recently found that the newly-emerged bees do not need to be exposed to older bees in order to acquire their inoculum of core bacteria--they apparently ingest it from the combs during their first few hours after emergence [16].
Kirk's associate Lana Vojvodic tracked the establishment of bacteria in the larval gut [17], and Kirk recently found [18] that the worker gut microbial community structure is quickly established in young bees, with the core bacteria showing up within hours. Then over the next few days a process of succession occurs, with pioneer species establishing first, followed by a climax community that persists for the rest of the bee's life (despite the huge change in diet as bees progress from nursing to foraging). Another group of researchers [19] recently found that the queen bee microbial community follows a similar course of development-with a huge difference-the queens, which are fed only jelly, develop a different climax community than that of the workers who feed them, consisting predominately (and not surprisingly) of the Alpha 2.1 and Alpha 2.2 bacteria associated with jelly.
The Alpha 1 and 2 phylotypes are as yet poorly understood. Researchers have now figured out how to culture some of these bacteria in the lab, so we may soon learn more about them. It's likely that the bee and the bacteria have coevolved mutually-beneficial symbioses, presumably with natural selection tweaking the bee hindgut epithelial cells to favor colonization by favored bacteria, which may help with the digestion of honey and pollen, produce important molecules not already present in the food, modulate immunity to pathogens, or aid in the metabolism of plant (or agricultural) toxins.
Biology is always a dynamic work in progress, and there is continual evolutionary adjustment of any system. This appears to be occurring (on the evolutionary time scale) with bees and their symbionts. Symbiotic relationships typically begin as parasitic invasion or opportunistic exploitation of a food source (as in undigested gut contents), which may then evolve into commensalism, and eventually mutualism (see box).
Types of Symbiotic Relationships
A parasitic relationship is one in which one member of the association benefits while the other is harmed.
Commensalism describes a relationship between two living organisms where one benefits and the other is not significantly harmed or helped.
Mutualism or interspecies reciprocal altruism is a relationship between individuals of different species where both individuals benefit. In the case of bees and bacteria, the bees provide a habitat and food source, and in turn the bacteria likely aid in digestion, immunity to pathogens, creation of essential nutrients, and detoxification of plant chemicals or pesticides.
Definitions from Wikipedia
In the case of the evolution of the honey bee microbiome, certain bacteria invaded the bee gut and fought to establish a niche. Of course, the bee would try to flush out harmful invaders, but some figured out how to adhere to the gut cells and establish a biofilm [20]. The bee and each species of bacteria then evolutionarily worked out some sort of agreement, presumably in which both species benefitted (mutualism).
The least refined relationships appear to be with the Alpha 2.2 Acetobacteraceae and Lactobacillus kunkeei, which are facultative symbionts--meaning that they can exist in other niches (such as in plant nectar), but some strains also thrive when bees create a hospitable habitat either within their guts or elsewhere in the hive (as in the jelly or beebread). Then there is Frischella perrara, an early invader of the guts of young bees, which causes formation of a scab (see the great photomicrographs at [21]). This bacterium may be transitioning from a parasitic to perhaps a commensal relationship. Finally, there are the highly refined and apparently mutualistic relationships with Snodgrassella and Gilliamella (and of the two species with one another). These species are perhaps only found only in the bee gut, where they form biofilms in the nutrient-rich ileum (where the bee absorbs the digestion products of pollen from the midgut). We do not yet know to what extent the bees depend upon them for health or survival.
One might ask why there are so few groups of bacteria in bees compared to the thousands associated with humans. One researcher suggests that it may be because mammals have a more developed adaptive immune system than do insects (by creating antibodies), which allows for the regulation of more complex relationships [22], or perhaps the abundance of real estate in the mammalian gut simply provides a greater number of distinct neighborhoods for bacterial colonization.
We are only beginning to grasp the complexity of the system; this is where Kirk's lab is focusing its attention--to try to understand where bacteria and fungi fit into the hive environment as a whole. What I really appreciate about Kirk is that he's scientifically skeptical (as am I) of nearly everything claimed about honey bees until he's seen it tested and confirmed. So his lab has gone back to the beginning, assuming nothing, and confirming or refuting several previous "findings" regarding the hive microbiome.
For example, Kirk's associate Vanessa Corby-Harris continued Vojvodic's research, and recently named a species of Alpha 2.2 bacteria (Parasaccharibacter apium) which she found in the jelly produced by the hypopharyngeal glands of nurse bees [23]. Of interest is that jelly is clearly strongly antibacterial, yet she found bacteria that not only thrive in jelly, but confer mutualistic benefit to the larvae. Her research suggests that the source of inoculum of symbiotic bacteria to larvae may be the jelly, rather than the contents of the crop.
Practical application (probiotics): to date, there is only suggestive research that the gut symbionts confer appreciable benefit to the bee (this will surely become a hot topic of research). Nevertheless, there are plenty of sellers eager to market "probiotics" to beekeepers. The two predominant bacterial phylotypes in the bee gut are unnamed Lactobacilli, in the same group of bacteria that ferment yogurt, sauerkraut, and pickles. But don't think that feeding yogurt, pickles, or any off-the-shelf probiotic will help your bees, since each of the many types of Lactobacillus is very specific to a certain niche. There will likely eventually be proven products on the market, but I don't know of any as of yet.
What About Antibiotics?
Similar as to in your gut, the community of bee gut microbiota are in a constant competitive battle for real estate. If you enjoy street tacos in Mexico as I do, you likely have experienced what happens when a new player enters the neighborhood in your gut. Similarly, the application of antibiotics to your gut (or a hive) can shift the balance by (temporarily) knocking out some susceptible species. As suggested by Dr. Nancy Moran:
It would seem prudent to avoid overuse of antibiotics, as this could have detrimental consequences for colony health, just as chronic use of antibiotics might affect human health by continually perturbing resident gut communities.
But the gut bacteria don't give up easily, and eventually incorporate genes for resistance to regularly-used antibiotics. This has happened with the U.S. managed bee population, following decades of exposure to oxytetracycline [24].
Does this hurt the bees? Perhaps at first, but I remember that back before varroa, when many of us treated twice a year with oxytet, we sure had healthy hives. A recent experiment by Drs. Eric Mussen and Brian Johnson didn't find any negative effect on the growth of colonies after feeding a blast of antibiotics [25].
Practical application (antibiotics): there are two extreme views--(1) bees should never be fed antibiotics, and (2) antibiotics should be given prophylactically twice a year to prevent disease. Those promoting View 1 have apparently never had a sick kid whose life was saved by a course of antibiotics; the others are likely wasting money on risk management, chancing contaminating their honey with residues, and breeding antibiotic-resistant bacteria (keep in mind that only when some beekeepers created constant exposure to the antibiotic by using extender patties did we finally see AFB bacteria develop resistance to the treatment).
I suspect that much of the money spent on fumagillin, oxytet, and tylosin is not cost effective, and would better be spent on better nutrition and mite management. On the other hand, when actual monitoring indicates that the presence of a pathogen exceeds a threshold value, treatment can be of great benefit. This was the case in my operation in January, when EFB showed signs of going rampant. We treated all our hives prophylactically for the first time in over a decade, and were pleased with the results. But I have no intention of doing so next season unless clearly called for. The reasons? It's expensive and time consuming to treat, and I want the antibiotic to still be effective the next time I need it.
Next
In the next installment we'll delve into the details of what occurs during the fermentation of pollen into beebread.
Acknowledgements
I thank Pete Borst for his generous assistance in literature search, and Dr. Kirk Anderson for the great deal of time spent in discussion and explanation of this research.
References And Notes
[1] McFall-Ngaia, M, et al (2013) Animals in a bacterial world, a new imperative for the life sciences. PNAS 110(9): 3229-3236. http://web.stanford.edu/~fukamit/mcfall-ngai-et-al-2013.pdf This excellent review covers our current state of knowledge of symbiotic bacteria in general (not just for bees).
[2] Anderson, KE, et al (2011) An emerging paradigm of colony health: microbial balance of the honey bee and hive (Apis mellifera). Insect. Soc. 58: 431-444. http://naldc.nal.usda.gov/download/57606/PDF. This is the best open access paper to read for a deeper understanding of the subject, including details of honey bee digestion, state-of-the-art genetic sequencing technology (and discrepancies in analysis), descriptions of the eight "core" bacterial groups, and the microbial niches present in the hive environment. Note that this is a very hot topic these days, with new research coming out monthly.
[3] These researchers communicate informally, as well as by reviewing each others' work, as explained in a recent blog by Quinn McFredrick: https://melittology.wordpress.com/2012/04/03/bee-microbiome-initiative/
[4] Snipped and paraphrased from Anderson, KE, et al (2014) Hive-stored pollen of honey bees: many lines of evidence are consistent with pollen preservation, not nutrient conversion. Molecular Ecology 23: 5904-5917.
[5] Anderson, KE, et al (2014) ibid.
[6] For you techies: for phylogenetic classification, the 16S ribosomal RNA gene is commonly used because of its ubiquitous presence in all living organisms, its small size, and its alternating structure of highly conserved (slowly evolving) and hypervariable regions. Researchers can analyze either the DNA or the RNA, which can then suggest the functions of each species (metabolism of certain sugars, creation of vitamins, digestion of cellulose, detoxification of plant chemicals, etc.).
[7] Jeyaprakash A, et al (2003) Bacterial diversity in worker adults of Apis mellifera capensis and Apis mellifera scutellata (Insecta: Hymenoptera) assessed using 16S rRNA sequences. J Invertebr Pathol 84:96-103.
[8] Cox-Foster (2007) cited in previous installment of this series.
[9] Martinson VG, et al. (2011) A simple and distinctive microbiota associated with honey bees and bumble bees. Mol Ecol 20:619-628.
[10] Moran NA, et al (2012) Distinctive gut microbiota of honey bees assessed using deep sampling from individual worker bees. PLoS ONE 7(4): e36393. doi:10.1371/journal.pone.0036393
[11] Newton, I (2012) The utility of bacterial nomenclature. http://microdiv.blogspot.com/2012/08/the-utility-of-bacterial-nomenclature.html
[12] Engel, PE, et al (2012) Functional diversity within the simple gut microbiota of the honey bee. PNAS 109(27): 11002-11007.
[13] The best current review of this is by Nancy Moran (2015) Genomics of the honey bee microbiome. Current Opinion in Insect Science 10: 22-28.
[14] Graystock, P, et al (2015) Parasites in bloom: flowers aid dispersal and transmission of pollinator parasites within and between bee species. Proc. R. Soc. B 282 http://dx.doi.org/10.1098/rspb.2015.1371 This exemplary experiment demonstrated how quickly and easily pathogens are transmitted between colonies via flowers.
[15] Disayathanoowat, T, et al (2012) T-RFLP analysis of bacterial communities in the midguts of Apis mellifera and Apis cerana honey bees in Thailand. Journal of Apicultural Research 51(4): 312-319.
Vojvodic S, SM Rehan, KE Anderson (2013) Microbial gut diversity of Africanized and European honey bee larval instars. PLoS ONE 8(8): e72106.
[16] The timing suggests that the inoculum may come from the meconium ingested during cell cleaning (which would imply that those bacteria remain viable over the 12 days post pupation), or from the nectar or honey consumed for the bee's first meal, since newly-emerged workers typically do not begin consuming beebread until their second day.
[17] Vojvodic (2013) Ibid.
[18] Anderson, K, et al (in press) Ecological succession in the honey bee gut: Colonization by core bacteria during early adult development.
[19] Tarpy, David, Heather Mattila, Irene Newton (2015) Development of the honey bee gut microbiome throughout the queen-rearing process. Appl Environ Microbiol 81:3182-3191.
[20] Stones, DH & A-M Krachler (2015) Fatal attraction: how bacterial adhesins affect host signaling and what we can learn from them. Int J Mol Sci 16(2): 2626-2640 (open access).
[21] Engel, P, et al (2015) The bacterium Frischella perrara causes scab formation in the gut of its honeybee host. MBio doi: 10.1128/mBio.00193-15
[22] McFall-Ngai M (2007) Adaptive immunity: Care for the community. Nature 445(7124):153.
[23] Corby-Harris, V, et al (2014) Origin and effect of Alpha 2.2 Acetobacteraceae in honey bee larvae and description of Parasaccharibacter apium gen. nov., sp. nov. Appl. Environ. Microbiol. 80(24):7460.
[24] Tian, B, et al (Moran lab) (2012) Long-term exposure to antibiotics has caused accumulation of resistance determinants in the gut microbiota of honeybees. http://mbio.asm.org/content/3/6/e00377-12.full
[25] Johnson, BR, W Synka, WC Jasper & E Mussen (2014) Effects of high fructose corn syrup and probiotics on growth rates of newly founded honey bee colonies. Journal of Apicultural Research Volume 53, Issue 1: 165-170.
Category: Bee Nutrition
Tags: antibiotics, beebread, Dr. Anderson, microbiota, microorganisms | antibiotics Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/antibiotics/ |
Reevaluating Beebread: Part 2 - The Players
First published in: American Bee Journal, November 2015
Reevaluating Beebread: Part 2
The Players
Randy Oliver
ScientificBeekeeping.com
First published in ABJ Nov 2015
CONTENTS
Why Do Bees Go To Such Effort To Prepare Pollen In This Manner?
Which Microorganisms Are Involved?
Establishment Of Nest And Gut Microbiota
What About Antibiotics?
Next
Acknowledgements
References And Notes
In the last two decades, the widespread application of genetic and genomic approaches has revealed a bacterial world astonishing in its ubiquity and diversity [1]. It's become clear that the superorganism that we call the honey bee colony includes a number of symbiotic bacteria. Some appear to be involved in nutrition and immunocompetence, but we are only beginning to understand which players are involved, and what they do.
In the last installment, I introduced Dr. Kirk Anderson. When hired by the Tucson ARS lab (on the downside of the CCD epidemic) he really did his homework, and boned up on everything known about the honey bee microbiome, from which he summarized the then current state of knowledge thoroughly and succinctly in an open-access paper [2], from which I'll lift a few snips:
The hive of the honey bee may be best characterized as an extended organism that not only houses developing young and nutrient rich food stores, but also serves as a niche for symbiotic microbial communities that aid in nutrition and defend against pathogens. The niche requirements and maintenance of beneficial honey bee symbionts are largely unknown, as are the ways in which such communities contribute to honey bee nutrition, immunity, and overall health.
Kirk pointed out that ants, termites, aphids, and other insects cultivate beneficial bacterial and fungal symbionts, but that:
Given the depth of understanding in the aforementioned systems, it is alarming to consider that virtually nothing is known about the beneficial microbial symbionts of the honey bee, a social insect vital to the worlds food supply. Many thousands of different microbial strains have been cultured from honey bee colonies [he credits Dr. Martha Gilliam], yet we know virtually nothing of honey bee microbial ecology.
Kirk then laid out a vision of a lab devoted to furthering our understanding of how the naturally occurring microbiota of the honey bee colony contribute to bee health and nutrition. Let me be clear that the Anderson Lab is not the only group looking at the bee microbiome--in the U.S. alone, research in this nascent field is also being performed in the labs of Drs. Nancy Moran, Irene Newton, Jay Evans, Gene Robinson, and Quinn McFrederick [3], among others. This is spawning a new generation of bee researchers with proficiency in state-of-the-art technique and analysis.
It's abundantly clear that we have a great deal yet to learn about the importance (or lack thereof) of the microbiota associated with the honey bee. But for now, let's return to the subject of this article: the role of the microbes involved in the process of fermenting raw pollen into beebread. Such fermentation could be for either (or both) of two reasons--for simple preservation, or to enhance its nutritional quality. As Kirk explains [4]:
Nutrient conversion is readily distinguished from food preservation (storage). Although both processes have associated microbial communities, the primary function of food preservation is to prevent microbial degradation... preservation environments composed of plant material (e.g. silage) are typically dominated by Lactobacillus spp. and other acid tolerant microbes. Conversely, nutrient conversion involves an extended time component following the collection of plant matter, massive nutrient turnover prior to consumption and a vertically inherited mutualistic microbe or small community of microbes that emerges as the dominant force in the conversion of recalcitrant plant material.
The questions that arise are then:
Why do bees go to such effort to prepare pollen in this manner?
Which microorganisms are involved, and do the bees inoculate the beebread with specific symbiotic microbes?
What chemical and biological processes occur during the fermentation process?
What are the nurse bees' consumption preferences?
Is the fermentation necessary to release the nutrients of the pollen?
Is the pollen made more nutritious during the fermentation process?
In a relatively short period of intense investigation, Kirk and his associates were able to obtain (at least preliminary) answers to most of the above questions, published in an open access paper [5]. So let's cover each of the above questions in turn.
Why Do Bees Go To Such Effort To Prepare Pollen In This Manner?
Let's first consider the dynamics of pollen within the hive. Pollen is the predominant source of protein and other colony nutrition; a continual supply is thus critical if brood is to be reared. Unfortunately, that supply is completely dependent upon an ever changing bloom and capricious weather. When colonies are in their rapid growth phase, or during pollen dearths, there is often little pollen to be seen in the combs. But that doesn't mean that the colony doesn't have a reserve stored. So where is it?
In the previous installment I described how the pollen foragers place their loads into cells adjacent to the broodnest, after which mid-aged bees pack it into place for storage. But this then creates the problem of how to protect such a rich larder of stored food (at the warm temperature of the broodnest) from the slew of pollen-feeding insects, mites, fungi, and bacteria eager to consume or decompose it. So what to do?
As Kirk observes, "nutrition stored within the body of an individual is protected by anatomical barriers and active immune physiology." So nurse and mid-aged bees ravenously consume that freshly-stored pollen, thus protecting it within their bodies (Fig. 1).
Figure 1. Forager bees (sampled from the entrance) tend to have very little pollen in their guts, but "house bees" (nurses and mid-aged bees) tell a different story. I took this sample of 50 bees from an outside frame of the upper hive body in early November (after 2 days of confinement by rain), froze them to kill them, and then crushed them with a roller to squash out their gut contents. Note that the gut of every single bee was full of pollen. In other samples taken during the summer pollen dearth, a small proportion of bees from similar combs lacked pollen in their guts.
A question: The pollen in the above photo was mostly in the hindguts of the bees (post normal digestion). I wonder why they retain the remnants of digested pollen grains for so long, rather than defecating immediately. Could it be that additional nutrients are released or generated by the bacteria that thrive in the rectum?
Nurse and mid-age bees digest that consumed pollen and glandularly convert it into jelly (analogous to mammal milk)--which can be considered as the in-hive "currency" of protein, to be equally shared according to need. Any excess is converted to vitellogenin and stored in the fat bodies of all but the foragers. The colony is thus able to distribute protein reserves throughout the colony population as a whole.
In good times though, foragers bring in more pollen than the nurses can consume, so the colony must preserve it in some additional manner. They do so by fermenting it into beebread, using a process similar to that used for the creation of silage or sauerkraut--by allowing lactic acid bacteria to produce their preservative namesake, thus creating an environment hostile to other microorganisms, allowing for the relatively long term storage of pollen for later consumption.
The question then, is exactly...
Which Microorganisms Are Involved?
First, current day genomic research into the hive microbiome is not something that you do with a microscope. The literature is incredibly jargon-heavy, tedious to read, and consists of monster spreadsheets of numbers meaningless to all but those well versed in this arcane field (I'm definitely not one of them). But there is some common terminology and methodology that I need to briefly explain.
Until recently, scientists' ability to study the microorganisms in the bee gut was largely limited to culturing them in petri dishes, ala Martha Gilliam's meticulous research. The problem with that methodology is that many gut bacteria are difficult to culture. It was only with the development of PCR (polymerase chain reaction) to amplify scraps of DNA that we could start to identify organisms by parts of their genome alone. This technology was quickly followed by "metagenomics," which allowed the identification of unknown and unculturable microorganisms from a sample of biological material. By convention, researchers compare differences in the "spelling" of the 16S ribosomal DNA genes present [6] in order to estimate how many different "species" of bacteria are present. From this analysis, they can then create phylogenetic "trees" of relationships. To their amazement, scientists found that we had missed about 99% of species of bacteria in various environments.
Only recently (2003 [7]) did researchers note that there appeared to be a distinctive gut microbiome in the honey bee, furthered by Diana Cox-Foster's metagenomic analysis of colonies suffering from CCD [8]. We now know that honey bees tend to harbor a fairly consistent community of symbiotic bacteria [9,10], consisting of what appears to be around eight different "phylotypes" (the separation of bacteria into species is not as clear cut as it is for higher organisms [11]; bacteria identified only by DNA analysis are separated into OTUs (Operational Taxonomic Units, each having a group name such as "Firm 5"). In any phylotype, there may be several clades of OTUs (each OTU presumably being a closely-related species or strain, likely adapted to a slightly different niche, with a different biochemical profile, and thus possibly involved in a different symbiotic relationship, or performing different functions) [12]. As researchers refine their methods, they will surely further split these OTUs into additional named species. Each type of bacteria typically occupies a specific niche in the bee (or hive). Based largely upon an excellent recent review by Dr. Nancy Moran [13] and communication with Kirk Anderson, I created the graphic below to show where they are typically found (Fig. 2).
Figure 2. An adult honey bee may harbor a billion bacteria, with roughly 95% residing in the waste material in the hindgut; few survive in the microbe-hostile crop. Foragers bring environmental bacteria from flowers back to the hive-notably Lactobacillus kunkeei, which then thrives in the fructose-rich nest environment (especially in beebread). Other bacteria are nest symbionts, such as the Alpha 2.2 group found in jelly. And then there are the "core" gut bacteria, exhibiting strict niche fidelity within the bee gut.
Establishment Of Nest And Gut Microbiota
Let me first make clear that the research community is at a very preliminary stage at understanding the establishment and functions of the honey bee microbial community. Bacteria and fungi (as well as pathogens [14]) are brought into the hive with the nectar and pollen. Due to colony hygiene and the unfavorable environments of jelly, beebread, and honey, many species do not survive for long. But some find niches to their liking. And then there are other symbiotic bacteria which may be unique to the hive environment or bee gut--apparently transferred from one generation of bees to the next. And although there are "core" and "typical" communities of bacteria in the bees and the hive, they may vary substantially from colony to colony, race to race, and location to location [15].
Of interest is that Kirk recently found that the newly-emerged bees do not need to be exposed to older bees in order to acquire their inoculum of core bacteria--they apparently ingest it from the combs during their first few hours after emergence [16].
Kirk's associate Lana Vojvodic tracked the establishment of bacteria in the larval gut [17], and Kirk recently found [18] that the worker gut microbial community structure is quickly established in young bees, with the core bacteria showing up within hours. Then over the next few days a process of succession occurs, with pioneer species establishing first, followed by a climax community that persists for the rest of the bee's life (despite the huge change in diet as bees progress from nursing to foraging). Another group of researchers [19] recently found that the queen bee microbial community follows a similar course of development-with a huge difference-the queens, which are fed only jelly, develop a different climax community than that of the workers who feed them, consisting predominately (and not surprisingly) of the Alpha 2.1 and Alpha 2.2 bacteria associated with jelly.
The Alpha 1 and 2 phylotypes are as yet poorly understood. Researchers have now figured out how to culture some of these bacteria in the lab, so we may soon learn more about them. It's likely that the bee and the bacteria have coevolved mutually-beneficial symbioses, presumably with natural selection tweaking the bee hindgut epithelial cells to favor colonization by favored bacteria, which may help with the digestion of honey and pollen, produce important molecules not already present in the food, modulate immunity to pathogens, or aid in the metabolism of plant (or agricultural) toxins.
Biology is always a dynamic work in progress, and there is continual evolutionary adjustment of any system. This appears to be occurring (on the evolutionary time scale) with bees and their symbionts. Symbiotic relationships typically begin as parasitic invasion or opportunistic exploitation of a food source (as in undigested gut contents), which may then evolve into commensalism, and eventually mutualism (see box).
Types of Symbiotic Relationships
A parasitic relationship is one in which one member of the association benefits while the other is harmed.
Commensalism describes a relationship between two living organisms where one benefits and the other is not significantly harmed or helped.
Mutualism or interspecies reciprocal altruism is a relationship between individuals of different species where both individuals benefit. In the case of bees and bacteria, the bees provide a habitat and food source, and in turn the bacteria likely aid in digestion, immunity to pathogens, creation of essential nutrients, and detoxification of plant chemicals or pesticides.
Definitions from Wikipedia
In the case of the evolution of the honey bee microbiome, certain bacteria invaded the bee gut and fought to establish a niche. Of course, the bee would try to flush out harmful invaders, but some figured out how to adhere to the gut cells and establish a biofilm [20]. The bee and each species of bacteria then evolutionarily worked out some sort of agreement, presumably in which both species benefitted (mutualism).
The least refined relationships appear to be with the Alpha 2.2 Acetobacteraceae and Lactobacillus kunkeei, which are facultative symbionts--meaning that they can exist in other niches (such as in plant nectar), but some strains also thrive when bees create a hospitable habitat either within their guts or elsewhere in the hive (as in the jelly or beebread). Then there is Frischella perrara, an early invader of the guts of young bees, which causes formation of a scab (see the great photomicrographs at [21]). This bacterium may be transitioning from a parasitic to perhaps a commensal relationship. Finally, there are the highly refined and apparently mutualistic relationships with Snodgrassella and Gilliamella (and of the two species with one another). These species are perhaps only found only in the bee gut, where they form biofilms in the nutrient-rich ileum (where the bee absorbs the digestion products of pollen from the midgut). We do not yet know to what extent the bees depend upon them for health or survival.
One might ask why there are so few groups of bacteria in bees compared to the thousands associated with humans. One researcher suggests that it may be because mammals have a more developed adaptive immune system than do insects (by creating antibodies), which allows for the regulation of more complex relationships [22], or perhaps the abundance of real estate in the mammalian gut simply provides a greater number of distinct neighborhoods for bacterial colonization.
We are only beginning to grasp the complexity of the system; this is where Kirk's lab is focusing its attention--to try to understand where bacteria and fungi fit into the hive environment as a whole. What I really appreciate about Kirk is that he's scientifically skeptical (as am I) of nearly everything claimed about honey bees until he's seen it tested and confirmed. So his lab has gone back to the beginning, assuming nothing, and confirming or refuting several previous "findings" regarding the hive microbiome.
For example, Kirk's associate Vanessa Corby-Harris continued Vojvodic's research, and recently named a species of Alpha 2.2 bacteria (Parasaccharibacter apium) which she found in the jelly produced by the hypopharyngeal glands of nurse bees [23]. Of interest is that jelly is clearly strongly antibacterial, yet she found bacteria that not only thrive in jelly, but confer mutualistic benefit to the larvae. Her research suggests that the source of inoculum of symbiotic bacteria to larvae may be the jelly, rather than the contents of the crop.
Practical application (probiotics): to date, there is only suggestive research that the gut symbionts confer appreciable benefit to the bee (this will surely become a hot topic of research). Nevertheless, there are plenty of sellers eager to market "probiotics" to beekeepers. The two predominant bacterial phylotypes in the bee gut are unnamed Lactobacilli, in the same group of bacteria that ferment yogurt, sauerkraut, and pickles. But don't think that feeding yogurt, pickles, or any off-the-shelf probiotic will help your bees, since each of the many types of Lactobacillus is very specific to a certain niche. There will likely eventually be proven products on the market, but I don't know of any as of yet.
What About Antibiotics?
Similar as to in your gut, the community of bee gut microbiota are in a constant competitive battle for real estate. If you enjoy street tacos in Mexico as I do, you likely have experienced what happens when a new player enters the neighborhood in your gut. Similarly, the application of antibiotics to your gut (or a hive) can shift the balance by (temporarily) knocking out some susceptible species. As suggested by Dr. Nancy Moran:
It would seem prudent to avoid overuse of antibiotics, as this could have detrimental consequences for colony health, just as chronic use of antibiotics might affect human health by continually perturbing resident gut communities.
But the gut bacteria don't give up easily, and eventually incorporate genes for resistance to regularly-used antibiotics. This has happened with the U.S. managed bee population, following decades of exposure to oxytetracycline [24].
Does this hurt the bees? Perhaps at first, but I remember that back before varroa, when many of us treated twice a year with oxytet, we sure had healthy hives. A recent experiment by Drs. Eric Mussen and Brian Johnson didn't find any negative effect on the growth of colonies after feeding a blast of antibiotics [25].
Practical application (antibiotics): there are two extreme views--(1) bees should never be fed antibiotics, and (2) antibiotics should be given prophylactically twice a year to prevent disease. Those promoting View 1 have apparently never had a sick kid whose life was saved by a course of antibiotics; the others are likely wasting money on risk management, chancing contaminating their honey with residues, and breeding antibiotic-resistant bacteria (keep in mind that only when some beekeepers created constant exposure to the antibiotic by using extender patties did we finally see AFB bacteria develop resistance to the treatment).
I suspect that much of the money spent on fumagillin, oxytet, and tylosin is not cost effective, and would better be spent on better nutrition and mite management. On the other hand, when actual monitoring indicates that the presence of a pathogen exceeds a threshold value, treatment can be of great benefit. This was the case in my operation in January, when EFB showed signs of going rampant. We treated all our hives prophylactically for the first time in over a decade, and were pleased with the results. But I have no intention of doing so next season unless clearly called for. The reasons? It's expensive and time consuming to treat, and I want the antibiotic to still be effective the next time I need it.
Next
In the next installment we'll delve into the details of what occurs during the fermentation of pollen into beebread.
Acknowledgements
I thank Pete Borst for his generous assistance in literature search, and Dr. Kirk Anderson for the great deal of time spent in discussion and explanation of this research.
References And Notes
[1] McFall-Ngaia, M, et al (2013) Animals in a bacterial world, a new imperative for the life sciences. PNAS 110(9): 3229-3236. http://web.stanford.edu/~fukamit/mcfall-ngai-et-al-2013.pdf This excellent review covers our current state of knowledge of symbiotic bacteria in general (not just for bees).
[2] Anderson, KE, et al (2011) An emerging paradigm of colony health: microbial balance of the honey bee and hive (Apis mellifera). Insect. Soc. 58: 431-444. http://naldc.nal.usda.gov/download/57606/PDF. This is the best open access paper to read for a deeper understanding of the subject, including details of honey bee digestion, state-of-the-art genetic sequencing technology (and discrepancies in analysis), descriptions of the eight "core" bacterial groups, and the microbial niches present in the hive environment. Note that this is a very hot topic these days, with new research coming out monthly.
[3] These researchers communicate informally, as well as by reviewing each others' work, as explained in a recent blog by Quinn McFredrick: https://melittology.wordpress.com/2012/04/03/bee-microbiome-initiative/
[4] Snipped and paraphrased from Anderson, KE, et al (2014) Hive-stored pollen of honey bees: many lines of evidence are consistent with pollen preservation, not nutrient conversion. Molecular Ecology 23: 5904-5917.
[5] Anderson, KE, et al (2014) ibid.
[6] For you techies: for phylogenetic classification, the 16S ribosomal RNA gene is commonly used because of its ubiquitous presence in all living organisms, its small size, and its alternating structure of highly conserved (slowly evolving) and hypervariable regions. Researchers can analyze either the DNA or the RNA, which can then suggest the functions of each species (metabolism of certain sugars, creation of vitamins, digestion of cellulose, detoxification of plant chemicals, etc.).
[7] Jeyaprakash A, et al (2003) Bacterial diversity in worker adults of Apis mellifera capensis and Apis mellifera scutellata (Insecta: Hymenoptera) assessed using 16S rRNA sequences. J Invertebr Pathol 84:96-103.
[8] Cox-Foster (2007) cited in previous installment of this series.
[9] Martinson VG, et al. (2011) A simple and distinctive microbiota associated with honey bees and bumble bees. Mol Ecol 20:619-628.
[10] Moran NA, et al (2012) Distinctive gut microbiota of honey bees assessed using deep sampling from individual worker bees. PLoS ONE 7(4): e36393. doi:10.1371/journal.pone.0036393
[11] Newton, I (2012) The utility of bacterial nomenclature. http://microdiv.blogspot.com/2012/08/the-utility-of-bacterial-nomenclature.html
[12] Engel, PE, et al (2012) Functional diversity within the simple gut microbiota of the honey bee. PNAS 109(27): 11002-11007.
[13] The best current review of this is by Nancy Moran (2015) Genomics of the honey bee microbiome. Current Opinion in Insect Science 10: 22-28.
[14] Graystock, P, et al (2015) Parasites in bloom: flowers aid dispersal and transmission of pollinator parasites within and between bee species. Proc. R. Soc. B 282 http://dx.doi.org/10.1098/rspb.2015.1371 This exemplary experiment demonstrated how quickly and easily pathogens are transmitted between colonies via flowers.
[15] Disayathanoowat, T, et al (2012) T-RFLP analysis of bacterial communities in the midguts of Apis mellifera and Apis cerana honey bees in Thailand. Journal of Apicultural Research 51(4): 312-319.
Vojvodic S, SM Rehan, KE Anderson (2013) Microbial gut diversity of Africanized and European honey bee larval instars. PLoS ONE 8(8): e72106.
[16] The timing suggests that the inoculum may come from the meconium ingested during cell cleaning (which would imply that those bacteria remain viable over the 12 days post pupation), or from the nectar or honey consumed for the bee's first meal, since newly-emerged workers typically do not begin consuming beebread until their second day.
[17] Vojvodic (2013) Ibid.
[18] Anderson, K, et al (in press) Ecological succession in the honey bee gut: Colonization by core bacteria during early adult development.
[19] Tarpy, David, Heather Mattila, Irene Newton (2015) Development of the honey bee gut microbiome throughout the queen-rearing process. Appl Environ Microbiol 81:3182-3191.
[20] Stones, DH & A-M Krachler (2015) Fatal attraction: how bacterial adhesins affect host signaling and what we can learn from them. Int J Mol Sci 16(2): 2626-2640 (open access).
[21] Engel, P, et al (2015) The bacterium Frischella perrara causes scab formation in the gut of its honeybee host. MBio doi: 10.1128/mBio.00193-15
[22] McFall-Ngai M (2007) Adaptive immunity: Care for the community. Nature 445(7124):153.
[23] Corby-Harris, V, et al (2014) Origin and effect of Alpha 2.2 Acetobacteraceae in honey bee larvae and description of Parasaccharibacter apium gen. nov., sp. nov. Appl. Environ. Microbiol. 80(24):7460.
[24] Tian, B, et al (Moran lab) (2012) Long-term exposure to antibiotics has caused accumulation of resistance determinants in the gut microbiota of honeybees. http://mbio.asm.org/content/3/6/e00377-12.full
[25] Johnson, BR, W Synka, WC Jasper & E Mussen (2014) Effects of high fructose corn syrup and probiotics on growth rates of newly founded honey bee colonies. Journal of Apicultural Research Volume 53, Issue 1: 165-170.
Category: Bee Nutrition
Tags: antibiotics, beebread, Dr. Anderson, microbiota, microorganisms | microbiota Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/microbiota/ |
Understanding Colony Buildup and Decline: Part 6 - Hiccups in Colony Linear Buildup
First published in: American Bee Journal, July 2015
Understanding Colony Buildup and Decline - Part 6
Hiccups In Colony Linear Buildup
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in July 2015
CONTENTS
Return To Playing Catch Up
Real World Hiccups
The Effect Of Cold Weather
The Effect Of Rainy Weather
Spring Starvation
From Too Little To Too Much
Brood Survivorship
Adult Survivorship
Take Home Message
Acknowledgements
Citations and Footnotes
Under ideal conditions, colonies grow in a linear manner once the broodnest is well established. But ideal conditions don't always occur in the real world. By being aware of factors that may reduce the rate of colony buildup, the beekeeper may be able to intervene and get the colony back on track.
Return To Playing Catch Up
Creating a mathematical model for colony buildup and decline is not a mere academic exercise-it has great practical application. When you attempt to create a mathematical model, you quickly find out which critical elements you don't fully understand.
Practical application: in my own case, my newfound understanding of exactly why weak colonies are able to catch up in size with stronger colonies helps me to better grasp why springtime splits have the potential to grow as large as established colonies. Ideally, I want to split my colonies small enough to keep them from swarming, but large enough that they can build to optimal honey-producing strength.
But when I was faced with my sons' questions as to what is the ideal amount of brood and adult bees to put into each split, I realized that I couldn't honestly answer with certainty. So I spent considerable time in creating a spreadsheet to calculate the growth of nucs dependent upon those variables (as well as temperature and quality of the queen). I'm currently testing that model by carefully tracking the individual buildup of nucs in a test group specifically created with different measured amounts of brood and bees. I'll let you know when I get the results.
Real World Hiccups
I find the modeling of colony growth under ideal conditions to be mathematically elegant. But of course in the real world, conditions are often less than ideal. Any number of transient phenomena can handicap colony growth, or thwart it altogether. So let's take another look at the hiccups in growth exhibited by Harris' colonies in my colorful chart of colony demographics (Fig. 1):
Figure 1. Note the three instances (in mid May, early and late July) in which broodrearing was curtailed, leading to hiccups in the expected linear growth of the colonies [[i]]. I've indicated on this graph the timing of a spring cold snap, as well as the main honeyflow.
[i] These hiccups in egglaying are broken out by individual queen in Fig. 1 of my previous article
So what caused those sudden reductions in egglaying?
The Effect Of Cold Weather
I searched the weather history for Manitoba during the period of time during which Harris collected his data. It appears that the first dip in egglaying occurred during a cold snap in early May, right during the critical "spring turnover." The cold weather would have precluded foraging for pollen, and the freezing nighttime temperatures (15degF) would have forced the tiny clusters (averaging only about 7000 adult bees--less than 4 frame's worth) to contract tightly--thus limiting the amount of comb suitable for broodrearing.
Practical application: cold nighttime temperatures are a major limiting factor for the buildup of small colonies, since they must go into tight cluster, which severely limits both the size of the broodnest, as well as the number of bees available for nursing duties (since the majority must be engaged in forming a heat-generating "insulating shell").
The Effect Of Rainy Weather
April showers may bring May flowers, but even a single day of rainy weather may have a profound effect upon a growing colony. In a meticulous and intriguing study from the lab of Austrian bee researcher Karl Crailsheim [2], a rain machine was used to prevent the bees in an observation hive from foraging for only a single day at time, while keeping the inside temperature constant. What they found was that:
During rainy periods nurses spent less than half as much time nursing brood as they did during sunny periods. Our experiment suggests that the activity of the nurses is linked to the influx of food and its passage from bee to bee. Nurses receive food more often and over a longer period on days with good weather conditions than on days with bad weather conditions... It seems that the flow of nectar diminishes after only one night and causes the decline in nursing activity even on the first day with bad weather conditions and the following night.
Wow, even a single day of rain cuts nursing visits to brood by half! The researches didn't make observations on what happened during longer storms, but I have. After about three days of rainy weather, a rapidly-growing colony will have completely depleted its pollen stores, and begins to go into protein deficit, forcing the nurses to start using their body reserves (in their fat bodies). And then it may get worse...
During prolonged rainy weather, a colony may shift from rapid growth to cannibalism of the brood within a matter of days. Such an unexpected disaster hit us hard a few years ago. In the photo below, we were adding second brood chambers to strong singles on a nice nectar and pollen flow in mid May, right at the beginning of our main honey flow (Figs. 2-5).
Figure 2. In mid May 2011, our colonies were rapidly building during our spring flow, and we had recently added the second brood chambers for them to move into, with the expectation that they'd be quickly filled with brood and honey. This was beekeeping at its best!
Figure 3. We were running an experiment at the time, and I happened to take a photo of a typical brood frame. Note the reserves of honey and beebread present on May 10th. A few days later the colonies were shaking nectar and whitening wax.
Figure 4. We live in the mountains, where the weather is rapidly changeable. We got hit by a surprise snowstorm on April 25. All photos were taken in the same yard.
Figure 5. Within four days, the hungry colonies had consumed all honey reserves and all pollen reserves. They then desperately started cannibalizing the brood-first the eggs, then young larvae, then older larvae. They don't normally cannibalize sealed brood, since it no longer needs to be fed, and those pupae may be the colony's only chance for survival.
We donned our cold weather gear and madly fed syrup. We were able to avert major brood cannibalism in most of our colonies, which quickly recovered when the weather turned back to warm. But those colonies that were forced to cannibalize their brood got set back so hard that they were unable to even put on winter stores during the main flow, and needed to be fed later in the season.
Practical application: someone incredulously asked me, do you really go out and feed bees during miserable weather? I answered, Well, duh, 'cuz during good weather they're able to feed themselves-that's why we are called bee keepers.
Such brood cannibalism [3], albeit less dramatic, frequently occurs in my area during the two week pollen and nectar dearth that we typically experience between the end of apple bloom and the beginning of the late spring flow. I often observe plenty of freshly-laid eggs each day, but the nurses apparently eat them up rather than trying to feed larvae when there is not enough protein coming in.
Practical application: the main determinant of the development of a busting colony for honey production is having a steady supply of pollen and nectar coming in during the period beginning 6-8 weeks before the start of the main flow. It is during this time that the feeding of pollen sub can be of great benefit during periods of inclement weather or pollen dearth (as occurs in my area immediately after the end of fruit bloom).
Spring Starvation
In my area, other than during storms or the two-week post fruit bloom dearth, there is usually plenty of nectar and pollen coming in during springtime, and we rarely need to feed our splits. But from time to time, we must perform emergency feeding of the ravenous growing colonies. In the case of the colonies in the experiment shown in the photos above, I could not get approval to break protocol and feed the hives during the storm (despite my daily entreaties). The result was that a number starved on the fourth night (Figs. 6 & 7).
Figure 6. It breaks my heart to see a vigorous young colony starve to death, as indicated by the heads buried in the cells.
Fig. 7. After 4 days of bad weather, many of the colonies in the experimental yard succumbed to starvation. It was heartbreaking and ugly-this is a view of a typical bottom board. This disaster could have been easily averted by the feeding of a few dollars worth of sugar in any form.
I've also seen similar starvation of my strongest colonies during almond bloom if the weather turns foul. Many's the time that I've dumped granulated sugar over the combs (if I didn't have syrup with me) in order to save a colony. One time, all it took was a can of soda pop poured over the immobile bees to give them enough energy to move onto some swapped frames of honey.
During intermittent nectar dearths, colonies lacking adequate honey reserves can suffer minor starvation events. Unless you are closely monitoring the yards, all that you may see is a handful of dead bees in front of the hive, and if there has been a resumption of the nectar flow since the brief dearth, you may not be able to figure out what caused the kill (Fig. 8).
Figure 8. A "minor" starvation event occurred in this outyard in late June during a brief break in nectar availability. No colonies died, but similar to this one, most had a small pile of dead bees in front (this occurred in an area far from any pesticide applications). Only by checking the age structure of the remaining brood was I able to figure out what had gone wrong, since by the time I took this photo the colonies had replenished their nectar stores.
Practical application: during these recent drought years in California, we can no longer count on our normal nectar flows. This spring has been scary--our colonies have repeatedly been on the edge of starvation, since we kept expecting the "normal" nectar flows to kick in. As I type these words, I'm starting to resign myself to the possibility that the main flow is simply not gonna happen, and that I am going to be forced to spend a fortune on sugar in order to keep my colonies alive.
It's clear that a shortage of nectar/pollen (even due to a few days of rain) can bring recruitment to a temporary halt; conversely, a surfeit can also do the same...
From Too Little To Too Much
A nice nectar and pollen flow is extremely stimulating to broodrearing. But on the other hand, too much nectar or pollen can result in the bees plugging the broodnest, filling comb that the queen would normally fill with eggs (Fig. 9).
Figure 9. A brood comb following favorable weather in almond bloom. The past few years we've had great foraging weather during almond bloom, sometimes resulting in the broodnests getting plugged out with pollen and nectar. Since the queen can't find a place in which to lay eggs, there will little recruitment of emerging workers three weeks later, and colony populations may temporarily dwindle, much to the dismay of those beekeepers needing to shake packages or make splits.
Practical application: during spring buildup, it may be necessary to either reverse the brood chambers, or to add drawn comb to the broodnest to give the queen additional room in which to lay.
Tip for beginners: excessive feeding of syrup to colonies can also cause plugging out of the broodnest, leading to swarming in the spring, or poor wintering in the fall (due to lack of broodrearing at the end of the season).
Brood Survivorship
Keep in mind that colony buildup is all about the difference between the rates of recruitment of new workers and the rate of attrition of older workers. Pathogens that affect the brood reduce the rate of recruitment. When I began beekeeping, AFB was the only brood disease that we worried about--chalkbrood had yet to reach our shores, and EFB would go away on its own once a good nectar flow resumed. Nowadays, I rarely see AFB. What I do see in spring is persistent EFB (Fig. 10), and sometimes other unidentifiable brood diseases [4].
Figure 10. European Foulbrood can bring colony buildup to a screeching halt by decreasing the rate of larval survival. The larvae in this photo are clearly symptomatic, but in many cases are difficult to detect. Unlike the EFB of yore, today's EFB may not clear up without treatment.
Although I don't see much chalkbrood any more, a few years ago I visited apiaries on the East Coast in which chalkbrood was running rampant, preventing colonies from building up. And it is not just pathogen-caused brood disease that may cause a problem. Toxic pollen (such as that of California Buckeye), nutritionally inadequate pollen, smokestack pollution, chilling of the brood due to anything that causes high adult mortality (virus, nosema, pesticides), or pesticide/miticide residues can all affect the colony similarly, in that they may reduce larval survivability.
Practical application: any factor that reduces larval survivability (such as chilling, poor nutrition, toxins, or disease) will decrease the rate of recruitment, and have a profound effect upon not only the rate of colony buildup, but unless the problem is resolved, also upon its ultimate population size.
Adult Survivorship
The rate of colony buildup is also determined by the rate of attrition of the adult bees. Ideally, springtime workers can be expected to live for an average of about 35 days. During spring buildup, adult survivorship is critical to colony success. I find that infection by either viruses or nosema can prevent a successful spring turnover due to their decreasing adult survivorship [5].
It doesn't take much of a reduction in adult survivorship to exhibit a profound effect (Fig. 11):
Figure 11. In order to create this graph, I shifted Harris' survivorship curves either longer or shorter by 5 days (roughly a 14% increase or decrease in average survivorship). Note how even a few days increase or reduction in average worker longevity has a profound effect upon colony buildup and eventual maximum population.
Practical application: any factor that negatively affects either larval or adult worker survivorship can make a huge difference in eventual colony size and honey production.
Take Home Message
Once a broodnest is established and the population has grown to the extent that the queen can hit her stride in egglaying (which takes a cluster covering at least 7 frames), the honey bee colony has the potential to grow at a linear rate of increase of nearly 2 frames of bees per week. But things don't always go well for growing colonies. As beekeepers, we can provide husbandry to minimize any breaks in the momentum of colony buildup, as well put by Jeffrey in 1959 [6]:
...in Britain colonies are ordinarily increasing in size for only about three months out of the twelve, and in late summer and throughout the long autumn, winter and early spring, numbers are steadily declining This would apparently point to two important principles in commercially successful bee-keeping: first, that the bee-keeper ought to guard carefully against any break in that swift and steady upward surge in the number of bees during April, May and June--for a break at this time cannot be fully retrieved later--and in particular it is suggested that queenless intervals should be most carefully avoided; and secondly, steps should be taken to reduce to a minimum the rate of decline during those other nine long months.
Next month: I'll continue with the swarming impulse
Acknowledgements
As always, my thanks to Lloyd Harris and Peter Borst.
Citations And Footnotes
[1] These hiccups in egglaying are broken out by individual queen in Fig. 1 of my previous article
[2] Riessberger U, & K Crailsheim (1887) Short-term effect of different weather conditions upon the behaviour of forager and nurse honey bees (Apis mellifera carnica Pollmann). Apidologie 28: 411-426. Open access.
[3] Schmickl T & K Crailsheim (2001) Cannibalism and early capping: strategy of honeybee colonies in times of experimental pollen shortages. J Comp Physiol A 187(7):541-547.
[4] For symptoms of some of the "new" brood diseases, see https://scientificbeekeeping.com/sick-bees-part-18a-colony-collaspse-revisited/
[5] See Figure 11 in Part 3 of this series.
[6] Jeffree, EP (1959) Op cit.
See also Jeffree, EP (1955) Observations on the growth and decline of honey bee colonies. Journal of Economic Entomology. 48: 732-726.
Category: Bee Behavior and Biology
Tags: adult survivorship, brood survivorship, cold weather, rainy weather, spring, starvation | starvation Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/starvation/ |
Understanding Colony Buildup and Decline: Part 6 - Hiccups in Colony Linear Buildup
First published in: American Bee Journal, July 2015
Understanding Colony Buildup and Decline - Part 6
Hiccups In Colony Linear Buildup
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in July 2015
CONTENTS
Return To Playing Catch Up
Real World Hiccups
The Effect Of Cold Weather
The Effect Of Rainy Weather
Spring Starvation
From Too Little To Too Much
Brood Survivorship
Adult Survivorship
Take Home Message
Acknowledgements
Citations and Footnotes
Under ideal conditions, colonies grow in a linear manner once the broodnest is well established. But ideal conditions don't always occur in the real world. By being aware of factors that may reduce the rate of colony buildup, the beekeeper may be able to intervene and get the colony back on track.
Return To Playing Catch Up
Creating a mathematical model for colony buildup and decline is not a mere academic exercise-it has great practical application. When you attempt to create a mathematical model, you quickly find out which critical elements you don't fully understand.
Practical application: in my own case, my newfound understanding of exactly why weak colonies are able to catch up in size with stronger colonies helps me to better grasp why springtime splits have the potential to grow as large as established colonies. Ideally, I want to split my colonies small enough to keep them from swarming, but large enough that they can build to optimal honey-producing strength.
But when I was faced with my sons' questions as to what is the ideal amount of brood and adult bees to put into each split, I realized that I couldn't honestly answer with certainty. So I spent considerable time in creating a spreadsheet to calculate the growth of nucs dependent upon those variables (as well as temperature and quality of the queen). I'm currently testing that model by carefully tracking the individual buildup of nucs in a test group specifically created with different measured amounts of brood and bees. I'll let you know when I get the results.
Real World Hiccups
I find the modeling of colony growth under ideal conditions to be mathematically elegant. But of course in the real world, conditions are often less than ideal. Any number of transient phenomena can handicap colony growth, or thwart it altogether. So let's take another look at the hiccups in growth exhibited by Harris' colonies in my colorful chart of colony demographics (Fig. 1):
Figure 1. Note the three instances (in mid May, early and late July) in which broodrearing was curtailed, leading to hiccups in the expected linear growth of the colonies [[i]]. I've indicated on this graph the timing of a spring cold snap, as well as the main honeyflow.
[i] These hiccups in egglaying are broken out by individual queen in Fig. 1 of my previous article
So what caused those sudden reductions in egglaying?
The Effect Of Cold Weather
I searched the weather history for Manitoba during the period of time during which Harris collected his data. It appears that the first dip in egglaying occurred during a cold snap in early May, right during the critical "spring turnover." The cold weather would have precluded foraging for pollen, and the freezing nighttime temperatures (15degF) would have forced the tiny clusters (averaging only about 7000 adult bees--less than 4 frame's worth) to contract tightly--thus limiting the amount of comb suitable for broodrearing.
Practical application: cold nighttime temperatures are a major limiting factor for the buildup of small colonies, since they must go into tight cluster, which severely limits both the size of the broodnest, as well as the number of bees available for nursing duties (since the majority must be engaged in forming a heat-generating "insulating shell").
The Effect Of Rainy Weather
April showers may bring May flowers, but even a single day of rainy weather may have a profound effect upon a growing colony. In a meticulous and intriguing study from the lab of Austrian bee researcher Karl Crailsheim [2], a rain machine was used to prevent the bees in an observation hive from foraging for only a single day at time, while keeping the inside temperature constant. What they found was that:
During rainy periods nurses spent less than half as much time nursing brood as they did during sunny periods. Our experiment suggests that the activity of the nurses is linked to the influx of food and its passage from bee to bee. Nurses receive food more often and over a longer period on days with good weather conditions than on days with bad weather conditions... It seems that the flow of nectar diminishes after only one night and causes the decline in nursing activity even on the first day with bad weather conditions and the following night.
Wow, even a single day of rain cuts nursing visits to brood by half! The researches didn't make observations on what happened during longer storms, but I have. After about three days of rainy weather, a rapidly-growing colony will have completely depleted its pollen stores, and begins to go into protein deficit, forcing the nurses to start using their body reserves (in their fat bodies). And then it may get worse...
During prolonged rainy weather, a colony may shift from rapid growth to cannibalism of the brood within a matter of days. Such an unexpected disaster hit us hard a few years ago. In the photo below, we were adding second brood chambers to strong singles on a nice nectar and pollen flow in mid May, right at the beginning of our main honey flow (Figs. 2-5).
Figure 2. In mid May 2011, our colonies were rapidly building during our spring flow, and we had recently added the second brood chambers for them to move into, with the expectation that they'd be quickly filled with brood and honey. This was beekeeping at its best!
Figure 3. We were running an experiment at the time, and I happened to take a photo of a typical brood frame. Note the reserves of honey and beebread present on May 10th. A few days later the colonies were shaking nectar and whitening wax.
Figure 4. We live in the mountains, where the weather is rapidly changeable. We got hit by a surprise snowstorm on April 25. All photos were taken in the same yard.
Figure 5. Within four days, the hungry colonies had consumed all honey reserves and all pollen reserves. They then desperately started cannibalizing the brood-first the eggs, then young larvae, then older larvae. They don't normally cannibalize sealed brood, since it no longer needs to be fed, and those pupae may be the colony's only chance for survival.
We donned our cold weather gear and madly fed syrup. We were able to avert major brood cannibalism in most of our colonies, which quickly recovered when the weather turned back to warm. But those colonies that were forced to cannibalize their brood got set back so hard that they were unable to even put on winter stores during the main flow, and needed to be fed later in the season.
Practical application: someone incredulously asked me, do you really go out and feed bees during miserable weather? I answered, Well, duh, 'cuz during good weather they're able to feed themselves-that's why we are called bee keepers.
Such brood cannibalism [3], albeit less dramatic, frequently occurs in my area during the two week pollen and nectar dearth that we typically experience between the end of apple bloom and the beginning of the late spring flow. I often observe plenty of freshly-laid eggs each day, but the nurses apparently eat them up rather than trying to feed larvae when there is not enough protein coming in.
Practical application: the main determinant of the development of a busting colony for honey production is having a steady supply of pollen and nectar coming in during the period beginning 6-8 weeks before the start of the main flow. It is during this time that the feeding of pollen sub can be of great benefit during periods of inclement weather or pollen dearth (as occurs in my area immediately after the end of fruit bloom).
Spring Starvation
In my area, other than during storms or the two-week post fruit bloom dearth, there is usually plenty of nectar and pollen coming in during springtime, and we rarely need to feed our splits. But from time to time, we must perform emergency feeding of the ravenous growing colonies. In the case of the colonies in the experiment shown in the photos above, I could not get approval to break protocol and feed the hives during the storm (despite my daily entreaties). The result was that a number starved on the fourth night (Figs. 6 & 7).
Figure 6. It breaks my heart to see a vigorous young colony starve to death, as indicated by the heads buried in the cells.
Fig. 7. After 4 days of bad weather, many of the colonies in the experimental yard succumbed to starvation. It was heartbreaking and ugly-this is a view of a typical bottom board. This disaster could have been easily averted by the feeding of a few dollars worth of sugar in any form.
I've also seen similar starvation of my strongest colonies during almond bloom if the weather turns foul. Many's the time that I've dumped granulated sugar over the combs (if I didn't have syrup with me) in order to save a colony. One time, all it took was a can of soda pop poured over the immobile bees to give them enough energy to move onto some swapped frames of honey.
During intermittent nectar dearths, colonies lacking adequate honey reserves can suffer minor starvation events. Unless you are closely monitoring the yards, all that you may see is a handful of dead bees in front of the hive, and if there has been a resumption of the nectar flow since the brief dearth, you may not be able to figure out what caused the kill (Fig. 8).
Figure 8. A "minor" starvation event occurred in this outyard in late June during a brief break in nectar availability. No colonies died, but similar to this one, most had a small pile of dead bees in front (this occurred in an area far from any pesticide applications). Only by checking the age structure of the remaining brood was I able to figure out what had gone wrong, since by the time I took this photo the colonies had replenished their nectar stores.
Practical application: during these recent drought years in California, we can no longer count on our normal nectar flows. This spring has been scary--our colonies have repeatedly been on the edge of starvation, since we kept expecting the "normal" nectar flows to kick in. As I type these words, I'm starting to resign myself to the possibility that the main flow is simply not gonna happen, and that I am going to be forced to spend a fortune on sugar in order to keep my colonies alive.
It's clear that a shortage of nectar/pollen (even due to a few days of rain) can bring recruitment to a temporary halt; conversely, a surfeit can also do the same...
From Too Little To Too Much
A nice nectar and pollen flow is extremely stimulating to broodrearing. But on the other hand, too much nectar or pollen can result in the bees plugging the broodnest, filling comb that the queen would normally fill with eggs (Fig. 9).
Figure 9. A brood comb following favorable weather in almond bloom. The past few years we've had great foraging weather during almond bloom, sometimes resulting in the broodnests getting plugged out with pollen and nectar. Since the queen can't find a place in which to lay eggs, there will little recruitment of emerging workers three weeks later, and colony populations may temporarily dwindle, much to the dismay of those beekeepers needing to shake packages or make splits.
Practical application: during spring buildup, it may be necessary to either reverse the brood chambers, or to add drawn comb to the broodnest to give the queen additional room in which to lay.
Tip for beginners: excessive feeding of syrup to colonies can also cause plugging out of the broodnest, leading to swarming in the spring, or poor wintering in the fall (due to lack of broodrearing at the end of the season).
Brood Survivorship
Keep in mind that colony buildup is all about the difference between the rates of recruitment of new workers and the rate of attrition of older workers. Pathogens that affect the brood reduce the rate of recruitment. When I began beekeeping, AFB was the only brood disease that we worried about--chalkbrood had yet to reach our shores, and EFB would go away on its own once a good nectar flow resumed. Nowadays, I rarely see AFB. What I do see in spring is persistent EFB (Fig. 10), and sometimes other unidentifiable brood diseases [4].
Figure 10. European Foulbrood can bring colony buildup to a screeching halt by decreasing the rate of larval survival. The larvae in this photo are clearly symptomatic, but in many cases are difficult to detect. Unlike the EFB of yore, today's EFB may not clear up without treatment.
Although I don't see much chalkbrood any more, a few years ago I visited apiaries on the East Coast in which chalkbrood was running rampant, preventing colonies from building up. And it is not just pathogen-caused brood disease that may cause a problem. Toxic pollen (such as that of California Buckeye), nutritionally inadequate pollen, smokestack pollution, chilling of the brood due to anything that causes high adult mortality (virus, nosema, pesticides), or pesticide/miticide residues can all affect the colony similarly, in that they may reduce larval survivability.
Practical application: any factor that reduces larval survivability (such as chilling, poor nutrition, toxins, or disease) will decrease the rate of recruitment, and have a profound effect upon not only the rate of colony buildup, but unless the problem is resolved, also upon its ultimate population size.
Adult Survivorship
The rate of colony buildup is also determined by the rate of attrition of the adult bees. Ideally, springtime workers can be expected to live for an average of about 35 days. During spring buildup, adult survivorship is critical to colony success. I find that infection by either viruses or nosema can prevent a successful spring turnover due to their decreasing adult survivorship [5].
It doesn't take much of a reduction in adult survivorship to exhibit a profound effect (Fig. 11):
Figure 11. In order to create this graph, I shifted Harris' survivorship curves either longer or shorter by 5 days (roughly a 14% increase or decrease in average survivorship). Note how even a few days increase or reduction in average worker longevity has a profound effect upon colony buildup and eventual maximum population.
Practical application: any factor that negatively affects either larval or adult worker survivorship can make a huge difference in eventual colony size and honey production.
Take Home Message
Once a broodnest is established and the population has grown to the extent that the queen can hit her stride in egglaying (which takes a cluster covering at least 7 frames), the honey bee colony has the potential to grow at a linear rate of increase of nearly 2 frames of bees per week. But things don't always go well for growing colonies. As beekeepers, we can provide husbandry to minimize any breaks in the momentum of colony buildup, as well put by Jeffrey in 1959 [6]:
...in Britain colonies are ordinarily increasing in size for only about three months out of the twelve, and in late summer and throughout the long autumn, winter and early spring, numbers are steadily declining This would apparently point to two important principles in commercially successful bee-keeping: first, that the bee-keeper ought to guard carefully against any break in that swift and steady upward surge in the number of bees during April, May and June--for a break at this time cannot be fully retrieved later--and in particular it is suggested that queenless intervals should be most carefully avoided; and secondly, steps should be taken to reduce to a minimum the rate of decline during those other nine long months.
Next month: I'll continue with the swarming impulse
Acknowledgements
As always, my thanks to Lloyd Harris and Peter Borst.
Citations And Footnotes
[1] These hiccups in egglaying are broken out by individual queen in Fig. 1 of my previous article
[2] Riessberger U, & K Crailsheim (1887) Short-term effect of different weather conditions upon the behaviour of forager and nurse honey bees (Apis mellifera carnica Pollmann). Apidologie 28: 411-426. Open access.
[3] Schmickl T & K Crailsheim (2001) Cannibalism and early capping: strategy of honeybee colonies in times of experimental pollen shortages. J Comp Physiol A 187(7):541-547.
[4] For symptoms of some of the "new" brood diseases, see https://scientificbeekeeping.com/sick-bees-part-18a-colony-collaspse-revisited/
[5] See Figure 11 in Part 3 of this series.
[6] Jeffree, EP (1959) Op cit.
See also Jeffree, EP (1955) Observations on the growth and decline of honey bee colonies. Journal of Economic Entomology. 48: 732-726.
Category: Bee Behavior and Biology
Tags: adult survivorship, brood survivorship, cold weather, rainy weather, spring, starvation | spring Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/spring/ |
Understanding Colony Buildup and Decline: Part 6 - Hiccups in Colony Linear Buildup
First published in: American Bee Journal, July 2015
Understanding Colony Buildup and Decline - Part 6
Hiccups In Colony Linear Buildup
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in July 2015
CONTENTS
Return To Playing Catch Up
Real World Hiccups
The Effect Of Cold Weather
The Effect Of Rainy Weather
Spring Starvation
From Too Little To Too Much
Brood Survivorship
Adult Survivorship
Take Home Message
Acknowledgements
Citations and Footnotes
Under ideal conditions, colonies grow in a linear manner once the broodnest is well established. But ideal conditions don't always occur in the real world. By being aware of factors that may reduce the rate of colony buildup, the beekeeper may be able to intervene and get the colony back on track.
Return To Playing Catch Up
Creating a mathematical model for colony buildup and decline is not a mere academic exercise-it has great practical application. When you attempt to create a mathematical model, you quickly find out which critical elements you don't fully understand.
Practical application: in my own case, my newfound understanding of exactly why weak colonies are able to catch up in size with stronger colonies helps me to better grasp why springtime splits have the potential to grow as large as established colonies. Ideally, I want to split my colonies small enough to keep them from swarming, but large enough that they can build to optimal honey-producing strength.
But when I was faced with my sons' questions as to what is the ideal amount of brood and adult bees to put into each split, I realized that I couldn't honestly answer with certainty. So I spent considerable time in creating a spreadsheet to calculate the growth of nucs dependent upon those variables (as well as temperature and quality of the queen). I'm currently testing that model by carefully tracking the individual buildup of nucs in a test group specifically created with different measured amounts of brood and bees. I'll let you know when I get the results.
Real World Hiccups
I find the modeling of colony growth under ideal conditions to be mathematically elegant. But of course in the real world, conditions are often less than ideal. Any number of transient phenomena can handicap colony growth, or thwart it altogether. So let's take another look at the hiccups in growth exhibited by Harris' colonies in my colorful chart of colony demographics (Fig. 1):
Figure 1. Note the three instances (in mid May, early and late July) in which broodrearing was curtailed, leading to hiccups in the expected linear growth of the colonies [[i]]. I've indicated on this graph the timing of a spring cold snap, as well as the main honeyflow.
[i] These hiccups in egglaying are broken out by individual queen in Fig. 1 of my previous article
So what caused those sudden reductions in egglaying?
The Effect Of Cold Weather
I searched the weather history for Manitoba during the period of time during which Harris collected his data. It appears that the first dip in egglaying occurred during a cold snap in early May, right during the critical "spring turnover." The cold weather would have precluded foraging for pollen, and the freezing nighttime temperatures (15degF) would have forced the tiny clusters (averaging only about 7000 adult bees--less than 4 frame's worth) to contract tightly--thus limiting the amount of comb suitable for broodrearing.
Practical application: cold nighttime temperatures are a major limiting factor for the buildup of small colonies, since they must go into tight cluster, which severely limits both the size of the broodnest, as well as the number of bees available for nursing duties (since the majority must be engaged in forming a heat-generating "insulating shell").
The Effect Of Rainy Weather
April showers may bring May flowers, but even a single day of rainy weather may have a profound effect upon a growing colony. In a meticulous and intriguing study from the lab of Austrian bee researcher Karl Crailsheim [2], a rain machine was used to prevent the bees in an observation hive from foraging for only a single day at time, while keeping the inside temperature constant. What they found was that:
During rainy periods nurses spent less than half as much time nursing brood as they did during sunny periods. Our experiment suggests that the activity of the nurses is linked to the influx of food and its passage from bee to bee. Nurses receive food more often and over a longer period on days with good weather conditions than on days with bad weather conditions... It seems that the flow of nectar diminishes after only one night and causes the decline in nursing activity even on the first day with bad weather conditions and the following night.
Wow, even a single day of rain cuts nursing visits to brood by half! The researches didn't make observations on what happened during longer storms, but I have. After about three days of rainy weather, a rapidly-growing colony will have completely depleted its pollen stores, and begins to go into protein deficit, forcing the nurses to start using their body reserves (in their fat bodies). And then it may get worse...
During prolonged rainy weather, a colony may shift from rapid growth to cannibalism of the brood within a matter of days. Such an unexpected disaster hit us hard a few years ago. In the photo below, we were adding second brood chambers to strong singles on a nice nectar and pollen flow in mid May, right at the beginning of our main honey flow (Figs. 2-5).
Figure 2. In mid May 2011, our colonies were rapidly building during our spring flow, and we had recently added the second brood chambers for them to move into, with the expectation that they'd be quickly filled with brood and honey. This was beekeeping at its best!
Figure 3. We were running an experiment at the time, and I happened to take a photo of a typical brood frame. Note the reserves of honey and beebread present on May 10th. A few days later the colonies were shaking nectar and whitening wax.
Figure 4. We live in the mountains, where the weather is rapidly changeable. We got hit by a surprise snowstorm on April 25. All photos were taken in the same yard.
Figure 5. Within four days, the hungry colonies had consumed all honey reserves and all pollen reserves. They then desperately started cannibalizing the brood-first the eggs, then young larvae, then older larvae. They don't normally cannibalize sealed brood, since it no longer needs to be fed, and those pupae may be the colony's only chance for survival.
We donned our cold weather gear and madly fed syrup. We were able to avert major brood cannibalism in most of our colonies, which quickly recovered when the weather turned back to warm. But those colonies that were forced to cannibalize their brood got set back so hard that they were unable to even put on winter stores during the main flow, and needed to be fed later in the season.
Practical application: someone incredulously asked me, do you really go out and feed bees during miserable weather? I answered, Well, duh, 'cuz during good weather they're able to feed themselves-that's why we are called bee keepers.
Such brood cannibalism [3], albeit less dramatic, frequently occurs in my area during the two week pollen and nectar dearth that we typically experience between the end of apple bloom and the beginning of the late spring flow. I often observe plenty of freshly-laid eggs each day, but the nurses apparently eat them up rather than trying to feed larvae when there is not enough protein coming in.
Practical application: the main determinant of the development of a busting colony for honey production is having a steady supply of pollen and nectar coming in during the period beginning 6-8 weeks before the start of the main flow. It is during this time that the feeding of pollen sub can be of great benefit during periods of inclement weather or pollen dearth (as occurs in my area immediately after the end of fruit bloom).
Spring Starvation
In my area, other than during storms or the two-week post fruit bloom dearth, there is usually plenty of nectar and pollen coming in during springtime, and we rarely need to feed our splits. But from time to time, we must perform emergency feeding of the ravenous growing colonies. In the case of the colonies in the experiment shown in the photos above, I could not get approval to break protocol and feed the hives during the storm (despite my daily entreaties). The result was that a number starved on the fourth night (Figs. 6 & 7).
Figure 6. It breaks my heart to see a vigorous young colony starve to death, as indicated by the heads buried in the cells.
Fig. 7. After 4 days of bad weather, many of the colonies in the experimental yard succumbed to starvation. It was heartbreaking and ugly-this is a view of a typical bottom board. This disaster could have been easily averted by the feeding of a few dollars worth of sugar in any form.
I've also seen similar starvation of my strongest colonies during almond bloom if the weather turns foul. Many's the time that I've dumped granulated sugar over the combs (if I didn't have syrup with me) in order to save a colony. One time, all it took was a can of soda pop poured over the immobile bees to give them enough energy to move onto some swapped frames of honey.
During intermittent nectar dearths, colonies lacking adequate honey reserves can suffer minor starvation events. Unless you are closely monitoring the yards, all that you may see is a handful of dead bees in front of the hive, and if there has been a resumption of the nectar flow since the brief dearth, you may not be able to figure out what caused the kill (Fig. 8).
Figure 8. A "minor" starvation event occurred in this outyard in late June during a brief break in nectar availability. No colonies died, but similar to this one, most had a small pile of dead bees in front (this occurred in an area far from any pesticide applications). Only by checking the age structure of the remaining brood was I able to figure out what had gone wrong, since by the time I took this photo the colonies had replenished their nectar stores.
Practical application: during these recent drought years in California, we can no longer count on our normal nectar flows. This spring has been scary--our colonies have repeatedly been on the edge of starvation, since we kept expecting the "normal" nectar flows to kick in. As I type these words, I'm starting to resign myself to the possibility that the main flow is simply not gonna happen, and that I am going to be forced to spend a fortune on sugar in order to keep my colonies alive.
It's clear that a shortage of nectar/pollen (even due to a few days of rain) can bring recruitment to a temporary halt; conversely, a surfeit can also do the same...
From Too Little To Too Much
A nice nectar and pollen flow is extremely stimulating to broodrearing. But on the other hand, too much nectar or pollen can result in the bees plugging the broodnest, filling comb that the queen would normally fill with eggs (Fig. 9).
Figure 9. A brood comb following favorable weather in almond bloom. The past few years we've had great foraging weather during almond bloom, sometimes resulting in the broodnests getting plugged out with pollen and nectar. Since the queen can't find a place in which to lay eggs, there will little recruitment of emerging workers three weeks later, and colony populations may temporarily dwindle, much to the dismay of those beekeepers needing to shake packages or make splits.
Practical application: during spring buildup, it may be necessary to either reverse the brood chambers, or to add drawn comb to the broodnest to give the queen additional room in which to lay.
Tip for beginners: excessive feeding of syrup to colonies can also cause plugging out of the broodnest, leading to swarming in the spring, or poor wintering in the fall (due to lack of broodrearing at the end of the season).
Brood Survivorship
Keep in mind that colony buildup is all about the difference between the rates of recruitment of new workers and the rate of attrition of older workers. Pathogens that affect the brood reduce the rate of recruitment. When I began beekeeping, AFB was the only brood disease that we worried about--chalkbrood had yet to reach our shores, and EFB would go away on its own once a good nectar flow resumed. Nowadays, I rarely see AFB. What I do see in spring is persistent EFB (Fig. 10), and sometimes other unidentifiable brood diseases [4].
Figure 10. European Foulbrood can bring colony buildup to a screeching halt by decreasing the rate of larval survival. The larvae in this photo are clearly symptomatic, but in many cases are difficult to detect. Unlike the EFB of yore, today's EFB may not clear up without treatment.
Although I don't see much chalkbrood any more, a few years ago I visited apiaries on the East Coast in which chalkbrood was running rampant, preventing colonies from building up. And it is not just pathogen-caused brood disease that may cause a problem. Toxic pollen (such as that of California Buckeye), nutritionally inadequate pollen, smokestack pollution, chilling of the brood due to anything that causes high adult mortality (virus, nosema, pesticides), or pesticide/miticide residues can all affect the colony similarly, in that they may reduce larval survivability.
Practical application: any factor that reduces larval survivability (such as chilling, poor nutrition, toxins, or disease) will decrease the rate of recruitment, and have a profound effect upon not only the rate of colony buildup, but unless the problem is resolved, also upon its ultimate population size.
Adult Survivorship
The rate of colony buildup is also determined by the rate of attrition of the adult bees. Ideally, springtime workers can be expected to live for an average of about 35 days. During spring buildup, adult survivorship is critical to colony success. I find that infection by either viruses or nosema can prevent a successful spring turnover due to their decreasing adult survivorship [5].
It doesn't take much of a reduction in adult survivorship to exhibit a profound effect (Fig. 11):
Figure 11. In order to create this graph, I shifted Harris' survivorship curves either longer or shorter by 5 days (roughly a 14% increase or decrease in average survivorship). Note how even a few days increase or reduction in average worker longevity has a profound effect upon colony buildup and eventual maximum population.
Practical application: any factor that negatively affects either larval or adult worker survivorship can make a huge difference in eventual colony size and honey production.
Take Home Message
Once a broodnest is established and the population has grown to the extent that the queen can hit her stride in egglaying (which takes a cluster covering at least 7 frames), the honey bee colony has the potential to grow at a linear rate of increase of nearly 2 frames of bees per week. But things don't always go well for growing colonies. As beekeepers, we can provide husbandry to minimize any breaks in the momentum of colony buildup, as well put by Jeffrey in 1959 [6]:
...in Britain colonies are ordinarily increasing in size for only about three months out of the twelve, and in late summer and throughout the long autumn, winter and early spring, numbers are steadily declining This would apparently point to two important principles in commercially successful bee-keeping: first, that the bee-keeper ought to guard carefully against any break in that swift and steady upward surge in the number of bees during April, May and June--for a break at this time cannot be fully retrieved later--and in particular it is suggested that queenless intervals should be most carefully avoided; and secondly, steps should be taken to reduce to a minimum the rate of decline during those other nine long months.
Next month: I'll continue with the swarming impulse
Acknowledgements
As always, my thanks to Lloyd Harris and Peter Borst.
Citations And Footnotes
[1] These hiccups in egglaying are broken out by individual queen in Fig. 1 of my previous article
[2] Riessberger U, & K Crailsheim (1887) Short-term effect of different weather conditions upon the behaviour of forager and nurse honey bees (Apis mellifera carnica Pollmann). Apidologie 28: 411-426. Open access.
[3] Schmickl T & K Crailsheim (2001) Cannibalism and early capping: strategy of honeybee colonies in times of experimental pollen shortages. J Comp Physiol A 187(7):541-547.
[4] For symptoms of some of the "new" brood diseases, see https://scientificbeekeeping.com/sick-bees-part-18a-colony-collaspse-revisited/
[5] See Figure 11 in Part 3 of this series.
[6] Jeffree, EP (1959) Op cit.
See also Jeffree, EP (1955) Observations on the growth and decline of honey bee colonies. Journal of Economic Entomology. 48: 732-726.
Category: Bee Behavior and Biology
Tags: adult survivorship, brood survivorship, cold weather, rainy weather, spring, starvation | rainy weather Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/rainy-weather/ |
The "Nosema Twins" - Part 1
©️ Randy Oliver
It appears that a new bully has moved into town, and we didn't even realize it! Maybe now we can explain some of the nasty things that have been going on.
As of a few months ago, I knew diddly squat about nosema. Sure, I bought Fumidil-B some twenty years ago when I was shipping queens, but never even used up the bottle! In California bees, nosema is usually not a problem. That is, until some beekeepers started noticing changes in their bees a few years ago. Was something new afoot?
The European honey bee has a longtime association with the familiar midgut parasite Nosema apis. N. apis is a relatively benign parasite in warmer climes where bees can fly freely for cleansing flights during winter, and generally only becomes a problem where bees are restricted from such flights by long, cold winters.
Nosema spores spread by being ingested by foragers at water sources contaminated by bee droppings. Such older bees are short lived anyway, so the occasional infection is no big deal. Infected bees also tend to altruistically prevent spreading the infection by flying away and not returning to the hive. Kralj (2006) refers to this behavior as "suicidal pathogen removal".
Nosema becomes a problem, however, when newly-emerged bees ingest spores. When this happens, the infection messes up their ability to digest pollen, and thus keeps them from ever developing their hypopharyngeal glands. So how does a "house bee" get infected? This happens when extended cold or rainy weather prevents cleansing flights. But when a bee's got dysentery from nosema she just can't hold it. The house bees then say "OhMyGod, somebody's pooped in the hive!" The insidious thing is that cleanup is a job delegated to newly emerged bees, who then ingest the spores in the process, and the infection thus moves from older bees to the very youngest. When this happens, nosema can go epidemic in the hive, with dire results. Infected queens can be superceded, and unless the newly-reared virgin replacement can fly, the colony will go queenless.
Life cycle of Nosema apis. The spore injects its contents into a gut epithelial cell, multiplies, and eventually causes the cell to burst and release the new spores back into the gut. Nosema can also reproduce "vegetatively" cell to cell. ©️ Springer Life Sciences
Even more importantly, the life spans of infected young bees can be reduced by up to 78%, plus they are unable to feed brood! At this point the death rate of the bees exceeds the birth rate, and the colony collapses. "In a typical case of a colony being depleted because of a Nosema [apis] infection, the queen can be observed surrounded by a few bees, confusedly attending to brood that is already sealed" (Anon 2004). (Does this sound familiar to anyone? Note that the remaining newly-emerged bees may not test positive for nosema yet--allowing the culprit to go undetected).
We've been discussing bee nutrition. Here's an important point from Dr. Ingemar Fries: "Under conditions where old infected bees must rejuvenate the production capacity of their hypopharyngeal glands - nosema disease may be devastating." This means that if you want a colony to brood up after a dearth, or after winter, and the population consists of older bees infected with nosema, they aren't going to be able to do it, no matter how well they are fed!
The frustrating thing about nosema is that "the majority of Nosema-infected colonies will appear normal, with no obvious signs of disease even when the disease is sufficient to cause significant losses in honey production and pollination efficiency" (Hornitzky 2005). In general, Nosema apis has historically been a serious problem only in areas with cold winters, and then was most noticeable in early spring. However, in the last several years, we've started seeing unusual nosema problems during summer...
Nosema ceranae--the "new" kid on the block
Nosema ceranae grabbed headlines in the U.S. in April of this year (Raven 2007) when Drs. Joe DeRisi and Don Ganem of U.C. San Francisco were given samples of CCD bees by the Army virologists working with Dr. Jerry Bromenshenk. DeRisi, who had helped solve the SARS disease mystery, analyzed the bees, and was surprised to find that they contained considerable DNA from N. ceranae--a parasite previously unreported in North America.
At that point, the USARS CCD team announced they had already been preparing a paper to formally announce that ceranae had been in the U.S. since at least 1995 (based upon analysis of stored samples of bees) (Chen 2007). This new bug had only been first named in 1996 by Dr. Ingemar Fries, but wasn't detected in Apis mellifera until 2004 in Vietnam, then in Taiwan, and by 2006 was reported to be widespread in Europe, Asia, Israel, the Caribbean, and North and South America (Paxton 2007, Klee, et al. 2007). Amazingly, in a few short years N. ceranae appears to have supplanted N. apis throughout much of North America and the world! In many areas, it is now difficult to find the previously common N. apis!
So ceranae snuck in under our noses, spread widely, and now researchers worldwide are scrambling feverishly to find out answers about this new, and apparently different acting, species. Once again, just as with varroa, our poor bees are being forced to evolve yet another new host/parasite relationship (not to mention Israeli Acute Paralysis Virus). How did ceranae get here? Cox-Foster (2007) found it in imported Chinese royal jelly used by queen producers, but Williams's (2007) genetic sequencing indicates that the likely origin was from Europe.
Is N. ceranae going to be (or is it already) a problem? I've spoken or corresponded with scientists and beekeepers worldwide, and the answer is: we don't know enough, and not all agree. There are currently several camps, based upon their favorite suspects for colony collapses. One camp (led by Spanish researchers) believes that ceranae is more virulent than apis, and is trashing bees throughout Europe. Other researchers are more conservative, and suggest that ceranae may be relatively benign unless unfavorable weather conditions prevail, especially when they cause nutritional stress. Others suggest that ceranae might be an opportunistic pathogen that thrives once the bees' immune systems are impaired by pesticide, viral, or other unknown stresses.
The $64,000 question is: "Is N. ceranae the cause of CCD?" The very short answer is that the Cox-Foster team found it in 100% of their CCD samples, yet have additional evidence to suggest that it may only be a player, not the underlying cause. I do not want to enter into the CCD debate here (and I greatly respect the work of the CCD scientists), but there is considerable evidence from the rest of the world that N. ceranae is likely responsible for a substantial proportion of the colony collapses in those countries in which it is found. Indeed, Martin-Hernandez (2007) states: "The relative risk of bee depopulation observed in colonies with either both species or only N. ceranae (almost six times greater than those with negative PCR results), indicates a significant causative association between the presence of N. ceranae and the development of hive depopulation." How's that for conservative "science-speak"?
The authors have a stunning graph that shows how nosema infections in Spain have changed over the course of seven years. Up through 1999, infections peaked in December and March, and were quite low the rest of the year. However, the lows filled in progressively each year, until by 2005 nosema infection level was nearly constant through the entire year! The bees no longer get a break.
Percent Nosema-positive samples, by month, in Spain for the years 1999-2005. Based upon samples received in the Bee Pathology Laboratory (after Martin-Hernandez, et al. 2007).
"Good old" N. apis requires the bees to spread it by defecation during winter, and does not do well in hot weather (Manning 2007), so it is usually a rather benign parasite, when bees are kept in their normal climatic range. The level of infected bees peaks in early spring, then drops close to zero by June, and stays low until next winter. The yearly drop in infection generally allows the colonies to recover. However, N. ceranae is a very different animal! It appears to peak in summer. As best I can tell, beekeepers in every country where ceranae has been identified have been reporting that they now have nosema problems during summer.
I can't help but to share with you with this scary tidbit: Delaguila (2006), in developing methods to culture N. ceranae in vitro, found that "as mammal cells were infected at 37degC [human body temperature], this opens up the possibility of [it] being a source of human microsporidiosis." Yet another reason to keep our fingers out of our mouths when in the beeyard!
Symptoms and consequences of N. ceranae infection
One European researcher feels that we have been so distracted by varroa, that we have simply overlooked the poor buildup, queen failures, poor honey crops, and colony collapse due to N. ceranae. Other scapegoats have been fingered. French beekeepers, who have been experiencing major colony losses in recent years, blamed the neonicitonoid pesticides, and got them banned in their country. However, at the last meeting of the "Bee Losses Group" held at Wageningen (Holland) last March, the French research group stated that the pesticide hypothesis had finally been discarded because none of the research could establish a relationship between colony deaths and the crops treated with imidacloprid or fipronil. N. ceranae has now been found to be well established in France (Chauzat 2007), and is currently a major suspect, as it is in Spain. The similarity between the French die offs and the effects of N. ceranae are striking.
Side note: I'm not in any way trying to denigrate the effects of pesticides on our bees, and fully support further research on the subject--especially with regard to the neonicitinoids.
So are we having the same problems in the U.S. as they are in Europe? One consideration is that the haplotype of N. ceranae found in Minnesota and Canada is different than that found in Spain, Germany, or China, and may differ in virulence (Williams 2007). The American bee research establishment appears to have been caught as much by surprise by ceranae as everyone else, and is just now gearing up to try to find answers to our questions.
Researchers have found ceranae spore counts to explode in a matter of days. Higes (2007) saw 100% mortality of inoculated bees within 8 days in the lab! Yet, on the other hand, ceranae has been in the U.S. since at least 1995, and there are still plenty of colonies of bees still alive! Clearly, ceranae is not invincible, as far as our bees are concerned. It's been noted that various races of bees vary in their natural resistance to N. apis--perhaps the same will hold true for ceranae. In its original host, Apis cerana, N. ceranae is often isolated to islands of single infected epithelial cells. In Apis mellifera, however, ceranae runs amok from cell to cell and quickly spreads. Perhaps some of our bees have developed similar resistance.
Nosema spores, species unknown, with bee setae (brushy hairs) for scale. Photomicrograph of a wet mount of a macerated bee abdomen at 400x. The spores are the oblong capsules that appear to glow in the center (three are off the tip of the pointer). This bee is sick. Photo by the author.
Unfortunately, there is yet another reason that ceranae could affect our bees more than apis did. Otteni (2004) found the gut epithelium to be an effective barrier against a virus. Remember earlier when I described that bees digest food by shedding the epithelial cells of their guts? This normal shedding mitigates the effect of N. apis infection, since infected cells may well have been eventually shed anyway. Glinski & Jarosz (2001, a good read) also describe how the resulting scar tissue is more resistant to further infection (but may eventually give way to bacteria). They also make clear that a damaged gut is the prime route of entry for viruses. Problem is, Higes (2007) found that N. ceranae destroys not only the epithelial cells, but also the basal cells of the gut. To me, it brings up the question, "does a nonfatal ceranae infection make the gut barrier permeable to other infections, including viruses?"
Let's play detective. Carreck (1997) states that "three viruses almost invariably multiply only in those individual bees which are also infected with Nosema apis" (Black Queen Cell Virus is especially noted for this association). Inactive viruses in a bee can be initiated to begin reproducing if triggered by another pathogen entering the bee's hemolymph (Yang & Cox-Foster 2005). Could ceranae be doing just that, or opening the door for gut bacteria and/or fungi to enter the body cavity? Bauer (1998) found that "viral infectivity [in gypsy moths] increased 10-fold when larvae were preinfected with Nosema sp." Oh, how complex this all gets, especially with our old "friend" varroa shutting down the bees' immune systems and vectoring viruses.
Martin-Hernandez (2007) states that "pathological data from Spanish apiaries affected by N. ceranae do not show a fast acting, short duration syndrome. On the contrary, only nonspecific symptoms, such as a gradual depopulation, higher autumn/winter colony death or low honey production are associated with the presence of this parasite. None of the dysentery or crawling bee behaviour usually related with Nosema apis infection has been reported. A similar syndrome has recently been reported from France and called 'dry nosemosis'."
So if there is no dysentery, how does ceranae spread from bee to bee? Higes (2007) found that infected foragers contaminate the pollen they collect with spores, apparently when they moisten the pellets with nectar from their crops. This contaminated pollen is then delivered to the brood nest, where it is consumed by young bees. This important discovery could explain why ceranae can be so prevalent during summer. The oldest, most spore-infested bees transmit spores to the food that the youngest bees are about to eat. As if this weren't enough, stored beebread pollen has been found to have virus particles in the various layers (Cox-Foster 2005), so the young bees could simultaneously ingest both N. ceranae spores plus virions. The young bees might be doomed from their first meal!
Are these bees eating pollen that is contaminated with Nosema ceranae and virions?
Are you putting the pieces together? Note the positive feedback--nutritionally-stressed bees can't fight nosema, then fill full of spores, and contaminate the bee bread of the colony. The young bees that eat that bee bread are immediately infected and are soon unable to digest their food, and thus are even more nutritionally stressed. Then these poor short-lived bees are unable to provide jelly to the queen, foragers, and especially the brood. The poorly-fed brood then emerges already nutritionally stressed, and may not even live long enough to become productive foragers. Without foragers, the colony is toast!
However, there are also surprising, and seemingly contrary, observations from Spain. Infected colonies may actually increase the number of frames of brood, even when the climatic conditions are not the optimum for broodrearing! Also, ceranae infection does not disappear during good foraging periods, when plenty of pollen and nectar is being collected. In Spain, nutritional stress (at least at colony level) does not appear to be a prerequisite for N. ceranae problems--however, I wonder whether the disease itself creates enough nutritional stress to start a feedback loop. (The astute reader may have noted the similarity of the above observations to CCD symptoms).
On the subject of CCD, we've had recurrent bouts of colony collapses for as far back as anyone can remember. One would do well to read Andy Nachbauer's (1996) column, written about beekeeping prior to varroa, N. ceranae, imidacloprid, or IAPV, in which he describes "Stress Accelerated Decline" (seems that there's very little new under the sun, as far as beekeeping is concerned). Even if CCD proves to be due to something novel, beekeepers will still have to deal with recurrent weather-modulated nutritional stress events. When bees are stressed, nosema and viruses thrive, and colonies collapse. We can't do much about the weather or viruses, but we can sure help our bees with nutrition, and by keeping an eye on nosema, whether it be apis or ceranae.
I have great faith in the bee researchers to eventually figure out how we can deal with Nosema ceranae. Currently, there are many unanswered questions (heck, we don't even know some of the questions to ask!) about this critter, its interactions with nutrition, varroa, and other pathogens, or how it fits into the CCD picture. I'm in no way trying to second guess the CCD researchers, but one can't help but notice how the symptoms of ceranae fit closely to many of the problems that beekeepers have reported, and appear to coincide with its invasion of the continent. Independent of CCD, though, yet another added burden has clearly been placed upon our poor bees, and beekeepers need to be aware of it. However, I'm always the optimist, and have no doubt that we and our bees will pull through once again.
Upcoming: In subsequent articles I will describe management techniques and treatments for nosema, including alternatives to fumigillin. Then I will cover sampling methods and considerations, with a photo essay on simplified techniques for taking spore counts yourself.
References and Resources
A wonderful drawing of Nosema life cycle:(Broken Link!) http://parasitology.informatik.uni-wuerzburg.de/login/b/me14229.png.php
For great photomicrographs of nosema, see the ppt presentation by Dr. Ingemar Fries:
(Broken Link!)
http://www.dipucordoba.es/medioambiente/pdf/XJornadasApiPonencia01.pdf
A great review on N. apis from a California perspective: Mussen, Eric (2002) Diagnosing and Treating Nosema Disease. (Broken Link! http://entomology.ucdavis.edu/faculty/Mussen/beebriefs/Nosema_Disease.pdf
An excellent review on N. ceranae: Flottum, K. (2007) Know about Nosema ceranae. Bee Culture 135(5): 12-14.
A good Australian summary on N. apis (Broken Link!) http://www.rirdc.gov.au/reports/HBE/05-055.pdf
Anon (2004) Nosemosis of Bees in Manual of Diagnostic Tests and Vaccines for Terrestrial Animals, 5th Ed. World Organisation for Animal Health (Broken Link!) http://www.oie.int/eng/Normes/mmanual/A_00123.htm
Bauer, Leah S.; Miller, Deborah L.; Maddox, Joseph V.; McManus, Michael L. (1998) Interaction between a Nosema sp. (Microspora: Nosematidae) and Nuclear Polyhedrosis Virus Infecting the Gypsy Moth, Lymantria dispar (Lepidoptera: Lymantriidae). Journal of Invertebrate Pathology. Vol. 74 no.1.:p. 147-153.
Carreck, N. (1997) The IACR-Rothamsted Varroa Project. http://www.ibiblio.org/pub/academic/agriculture/entomology/beekeeping/general/biology/varroa_virus.txt
Chauzat M-P, Mariano Higes, Raquel Martin-Hernandez, Aranzazu Meana, Nicolas Cougoule and Jean-Paul Faucon (2007) Presence of Nosema ceranae in French honey bee colonies. Journal of Apicultural Research 46(2): 127-128
Chen, Yanping , (Broken Link!) Jay D Evans , I Bart Smith , Jeffery S Pettis (2007) Nosema ceranae is a long-present and wide-spread microsporidian infection of the European honey bee (Apis mellifera) in the United States. J Invertebr Pathol. 2007 Aug 6; : 17880997
Cox-Foster (2005) Colony Collapse Disorder--Determining the causes. http://www.ucs.iastate.edu/mnet/_repository/2005/plantbee/pdf/prese ntations/coxfoster.pdf
Cox-Foster, and others too numerous to mention (2007) A metagenomic survey of microbes in honey bee colony collapse disorder. Science 318(5848): 283-287.
Delaguila C , F. Izquierdo, P.G. Palencia, R. Martin , M. Higes, S. Fenoy (2006) First Steps Towards The In vitro Cultivation of Nosema ceranae. Proceedings of the Second European Conference of Apidology EurBee
Fries I, R Martin,A Meana, P Garcia-Palencia,M Higes (2006) Natural infections of Nosema ceranae in European honey bees. Journal of Apicultural Research 45(3): 230-233 (2006)
Flottum, K (2007) Know about Nosema ceranae. Bee Culture 135(5): 12-13.
Glinski, Z & J. Jarosz (2001) Infection and immunity in the honey bee Apis mellifera. Apiacta 36(1), 12 - 24.
Higes M, Garcia-Palencia P, Martin-Hernandez R and Meana A. (2007) Experimental infection of Apis mellifera honeybees with Nosema ceranae (Microsporidia). J Invertebr Pathol. 94(3):211-7
Higes, Mariano , Raquel Martin-Hernandez , Encarna Garrido-Bailon , Pilar Garcia-Palencia , Aranzazu Meana (2007) Detection of infective Nosema ceranae (Microsporidia) spores in corbicular pollen of forager honeybees. J Invertebr Pathol. 2007 Jun 20; : 17651750
Higes M, Martin R, Meana A., J (2006) Nosema ceranae, a new microsporidian parasite in honeybees in Europe, Invertebr Pathol. 92(2):93-5.
Hornitzky (2005) Nosema Disease in Honeybees. (Broken Link!) http://www.rirdc.gov.au/reports/HBE/05-055.pdf
Klee, J., et al. (2007) Widespread dispersal of the microsporidian Nosema ceranae, an emergent pathogen of the western honey bee, Apis mellifera. J. Invertebr. Pathol.. doi:10.1016/
Kralj J, S. Fuchs, J. Tautz (2006) Disease removal by altered flight behavior of forager honey bees (Apis mellifera) infested with Nosema apis. Proceedings of the Second European Conference of Apidology EurBee
Manning R,, Kate Lancaster, April Rutkay and Linda Eaton (2007) Survey of feral honey bee (Apis mellifera) colonies for Nosema apis in Western Australia. Australian Journal of Experimental Agriculture (47): 883-886. www.publish.csiro.au/journals/ajea
Martin-Hernandez, Raquel, Aranzazu Meana, Lourdes Prieto, Amparo Martinez Salvador, Encarna Garrido-Bailon, and Mariano Higes (2007) The outcome of the colonization of Apis mellifera by Nosema ceranae. Applied and Environmental Microbiology http://aem.asm.org/cgi/content/abstract/AEM.00270-07v1
Nachbauer, Andy (1996) SAD & BAD Bees (Broken Link!) http://www.beesource.com/pov/andy/sad_bad.htm
Otteni, M & W. Ritter (2004) Effects of the acute paralysis virus on honey bees (Apis mellifera l.) infested by Nosema apis Z. Apiacta 39: 91-97.
Paxton, RJ (2007) Nosema ceranae - a new threat to Apis mellifera honey bees. Bees for Development Journal 81.
Raven, W. (2007) Bee deviled: Why are our honeybees vanishing? UCSF Sleuths Identify Suspects in Mystery of Vanishing Honeybees. UCFS Today (Broken Link!) http://pub.ucsf.edu/today/cache/feature/200704251.html
Rice, RN (2001) Nosema in honeybees, Genetic variation and control. Pub 01/46 Rural Industries Research and Development Corp, Australia
(Broken Link!) http://www.rirdc.gov.au/reports/HBE/01-046.pdf Nosema Disease in Honeybees
Sanford, MT (2007) A new nosema. Bee Culture 135(2): 18-20.
Williams, G.R. et al., (2007) First detection of Nosema ceranae, a microsporidian parasite of European honey bees (Apis mellifera), in Canada and central USA., J. Invertebr. Pathol. (2007), doi:10.1016/j.jip.2007.08.005
Yang X, Cox-Foster DL (2005) Impact of an ectoparasite on the immunity and pathology of an invertebrate: evidence for host immunosuppression and viral amplification. Proc Natl Acad Sci U S A 2005, 102:7470-7475.
Category: Nosema ceranae | The "Nosema Twins" - Part 1 - Scientific Beekeeping | https://scientificbeekeeping.com/the-nosema-twins-part-1/ |
Understanding Colony Buildup and Decline: Part 6 - Hiccups in Colony Linear Buildup
First published in: American Bee Journal, July 2015
Understanding Colony Buildup and Decline - Part 6
Hiccups In Colony Linear Buildup
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in July 2015
CONTENTS
Return To Playing Catch Up
Real World Hiccups
The Effect Of Cold Weather
The Effect Of Rainy Weather
Spring Starvation
From Too Little To Too Much
Brood Survivorship
Adult Survivorship
Take Home Message
Acknowledgements
Citations and Footnotes
Under ideal conditions, colonies grow in a linear manner once the broodnest is well established. But ideal conditions don't always occur in the real world. By being aware of factors that may reduce the rate of colony buildup, the beekeeper may be able to intervene and get the colony back on track.
Return To Playing Catch Up
Creating a mathematical model for colony buildup and decline is not a mere academic exercise-it has great practical application. When you attempt to create a mathematical model, you quickly find out which critical elements you don't fully understand.
Practical application: in my own case, my newfound understanding of exactly why weak colonies are able to catch up in size with stronger colonies helps me to better grasp why springtime splits have the potential to grow as large as established colonies. Ideally, I want to split my colonies small enough to keep them from swarming, but large enough that they can build to optimal honey-producing strength.
But when I was faced with my sons' questions as to what is the ideal amount of brood and adult bees to put into each split, I realized that I couldn't honestly answer with certainty. So I spent considerable time in creating a spreadsheet to calculate the growth of nucs dependent upon those variables (as well as temperature and quality of the queen). I'm currently testing that model by carefully tracking the individual buildup of nucs in a test group specifically created with different measured amounts of brood and bees. I'll let you know when I get the results.
Real World Hiccups
I find the modeling of colony growth under ideal conditions to be mathematically elegant. But of course in the real world, conditions are often less than ideal. Any number of transient phenomena can handicap colony growth, or thwart it altogether. So let's take another look at the hiccups in growth exhibited by Harris' colonies in my colorful chart of colony demographics (Fig. 1):
Figure 1. Note the three instances (in mid May, early and late July) in which broodrearing was curtailed, leading to hiccups in the expected linear growth of the colonies [[i]]. I've indicated on this graph the timing of a spring cold snap, as well as the main honeyflow.
[i] These hiccups in egglaying are broken out by individual queen in Fig. 1 of my previous article
So what caused those sudden reductions in egglaying?
The Effect Of Cold Weather
I searched the weather history for Manitoba during the period of time during which Harris collected his data. It appears that the first dip in egglaying occurred during a cold snap in early May, right during the critical "spring turnover." The cold weather would have precluded foraging for pollen, and the freezing nighttime temperatures (15degF) would have forced the tiny clusters (averaging only about 7000 adult bees--less than 4 frame's worth) to contract tightly--thus limiting the amount of comb suitable for broodrearing.
Practical application: cold nighttime temperatures are a major limiting factor for the buildup of small colonies, since they must go into tight cluster, which severely limits both the size of the broodnest, as well as the number of bees available for nursing duties (since the majority must be engaged in forming a heat-generating "insulating shell").
The Effect Of Rainy Weather
April showers may bring May flowers, but even a single day of rainy weather may have a profound effect upon a growing colony. In a meticulous and intriguing study from the lab of Austrian bee researcher Karl Crailsheim [2], a rain machine was used to prevent the bees in an observation hive from foraging for only a single day at time, while keeping the inside temperature constant. What they found was that:
During rainy periods nurses spent less than half as much time nursing brood as they did during sunny periods. Our experiment suggests that the activity of the nurses is linked to the influx of food and its passage from bee to bee. Nurses receive food more often and over a longer period on days with good weather conditions than on days with bad weather conditions... It seems that the flow of nectar diminishes after only one night and causes the decline in nursing activity even on the first day with bad weather conditions and the following night.
Wow, even a single day of rain cuts nursing visits to brood by half! The researches didn't make observations on what happened during longer storms, but I have. After about three days of rainy weather, a rapidly-growing colony will have completely depleted its pollen stores, and begins to go into protein deficit, forcing the nurses to start using their body reserves (in their fat bodies). And then it may get worse...
During prolonged rainy weather, a colony may shift from rapid growth to cannibalism of the brood within a matter of days. Such an unexpected disaster hit us hard a few years ago. In the photo below, we were adding second brood chambers to strong singles on a nice nectar and pollen flow in mid May, right at the beginning of our main honey flow (Figs. 2-5).
Figure 2. In mid May 2011, our colonies were rapidly building during our spring flow, and we had recently added the second brood chambers for them to move into, with the expectation that they'd be quickly filled with brood and honey. This was beekeeping at its best!
Figure 3. We were running an experiment at the time, and I happened to take a photo of a typical brood frame. Note the reserves of honey and beebread present on May 10th. A few days later the colonies were shaking nectar and whitening wax.
Figure 4. We live in the mountains, where the weather is rapidly changeable. We got hit by a surprise snowstorm on April 25. All photos were taken in the same yard.
Figure 5. Within four days, the hungry colonies had consumed all honey reserves and all pollen reserves. They then desperately started cannibalizing the brood-first the eggs, then young larvae, then older larvae. They don't normally cannibalize sealed brood, since it no longer needs to be fed, and those pupae may be the colony's only chance for survival.
We donned our cold weather gear and madly fed syrup. We were able to avert major brood cannibalism in most of our colonies, which quickly recovered when the weather turned back to warm. But those colonies that were forced to cannibalize their brood got set back so hard that they were unable to even put on winter stores during the main flow, and needed to be fed later in the season.
Practical application: someone incredulously asked me, do you really go out and feed bees during miserable weather? I answered, Well, duh, 'cuz during good weather they're able to feed themselves-that's why we are called bee keepers.
Such brood cannibalism [3], albeit less dramatic, frequently occurs in my area during the two week pollen and nectar dearth that we typically experience between the end of apple bloom and the beginning of the late spring flow. I often observe plenty of freshly-laid eggs each day, but the nurses apparently eat them up rather than trying to feed larvae when there is not enough protein coming in.
Practical application: the main determinant of the development of a busting colony for honey production is having a steady supply of pollen and nectar coming in during the period beginning 6-8 weeks before the start of the main flow. It is during this time that the feeding of pollen sub can be of great benefit during periods of inclement weather or pollen dearth (as occurs in my area immediately after the end of fruit bloom).
Spring Starvation
In my area, other than during storms or the two-week post fruit bloom dearth, there is usually plenty of nectar and pollen coming in during springtime, and we rarely need to feed our splits. But from time to time, we must perform emergency feeding of the ravenous growing colonies. In the case of the colonies in the experiment shown in the photos above, I could not get approval to break protocol and feed the hives during the storm (despite my daily entreaties). The result was that a number starved on the fourth night (Figs. 6 & 7).
Figure 6. It breaks my heart to see a vigorous young colony starve to death, as indicated by the heads buried in the cells.
Fig. 7. After 4 days of bad weather, many of the colonies in the experimental yard succumbed to starvation. It was heartbreaking and ugly-this is a view of a typical bottom board. This disaster could have been easily averted by the feeding of a few dollars worth of sugar in any form.
I've also seen similar starvation of my strongest colonies during almond bloom if the weather turns foul. Many's the time that I've dumped granulated sugar over the combs (if I didn't have syrup with me) in order to save a colony. One time, all it took was a can of soda pop poured over the immobile bees to give them enough energy to move onto some swapped frames of honey.
During intermittent nectar dearths, colonies lacking adequate honey reserves can suffer minor starvation events. Unless you are closely monitoring the yards, all that you may see is a handful of dead bees in front of the hive, and if there has been a resumption of the nectar flow since the brief dearth, you may not be able to figure out what caused the kill (Fig. 8).
Figure 8. A "minor" starvation event occurred in this outyard in late June during a brief break in nectar availability. No colonies died, but similar to this one, most had a small pile of dead bees in front (this occurred in an area far from any pesticide applications). Only by checking the age structure of the remaining brood was I able to figure out what had gone wrong, since by the time I took this photo the colonies had replenished their nectar stores.
Practical application: during these recent drought years in California, we can no longer count on our normal nectar flows. This spring has been scary--our colonies have repeatedly been on the edge of starvation, since we kept expecting the "normal" nectar flows to kick in. As I type these words, I'm starting to resign myself to the possibility that the main flow is simply not gonna happen, and that I am going to be forced to spend a fortune on sugar in order to keep my colonies alive.
It's clear that a shortage of nectar/pollen (even due to a few days of rain) can bring recruitment to a temporary halt; conversely, a surfeit can also do the same...
From Too Little To Too Much
A nice nectar and pollen flow is extremely stimulating to broodrearing. But on the other hand, too much nectar or pollen can result in the bees plugging the broodnest, filling comb that the queen would normally fill with eggs (Fig. 9).
Figure 9. A brood comb following favorable weather in almond bloom. The past few years we've had great foraging weather during almond bloom, sometimes resulting in the broodnests getting plugged out with pollen and nectar. Since the queen can't find a place in which to lay eggs, there will little recruitment of emerging workers three weeks later, and colony populations may temporarily dwindle, much to the dismay of those beekeepers needing to shake packages or make splits.
Practical application: during spring buildup, it may be necessary to either reverse the brood chambers, or to add drawn comb to the broodnest to give the queen additional room in which to lay.
Tip for beginners: excessive feeding of syrup to colonies can also cause plugging out of the broodnest, leading to swarming in the spring, or poor wintering in the fall (due to lack of broodrearing at the end of the season).
Brood Survivorship
Keep in mind that colony buildup is all about the difference between the rates of recruitment of new workers and the rate of attrition of older workers. Pathogens that affect the brood reduce the rate of recruitment. When I began beekeeping, AFB was the only brood disease that we worried about--chalkbrood had yet to reach our shores, and EFB would go away on its own once a good nectar flow resumed. Nowadays, I rarely see AFB. What I do see in spring is persistent EFB (Fig. 10), and sometimes other unidentifiable brood diseases [4].
Figure 10. European Foulbrood can bring colony buildup to a screeching halt by decreasing the rate of larval survival. The larvae in this photo are clearly symptomatic, but in many cases are difficult to detect. Unlike the EFB of yore, today's EFB may not clear up without treatment.
Although I don't see much chalkbrood any more, a few years ago I visited apiaries on the East Coast in which chalkbrood was running rampant, preventing colonies from building up. And it is not just pathogen-caused brood disease that may cause a problem. Toxic pollen (such as that of California Buckeye), nutritionally inadequate pollen, smokestack pollution, chilling of the brood due to anything that causes high adult mortality (virus, nosema, pesticides), or pesticide/miticide residues can all affect the colony similarly, in that they may reduce larval survivability.
Practical application: any factor that reduces larval survivability (such as chilling, poor nutrition, toxins, or disease) will decrease the rate of recruitment, and have a profound effect upon not only the rate of colony buildup, but unless the problem is resolved, also upon its ultimate population size.
Adult Survivorship
The rate of colony buildup is also determined by the rate of attrition of the adult bees. Ideally, springtime workers can be expected to live for an average of about 35 days. During spring buildup, adult survivorship is critical to colony success. I find that infection by either viruses or nosema can prevent a successful spring turnover due to their decreasing adult survivorship [5].
It doesn't take much of a reduction in adult survivorship to exhibit a profound effect (Fig. 11):
Figure 11. In order to create this graph, I shifted Harris' survivorship curves either longer or shorter by 5 days (roughly a 14% increase or decrease in average survivorship). Note how even a few days increase or reduction in average worker longevity has a profound effect upon colony buildup and eventual maximum population.
Practical application: any factor that negatively affects either larval or adult worker survivorship can make a huge difference in eventual colony size and honey production.
Take Home Message
Once a broodnest is established and the population has grown to the extent that the queen can hit her stride in egglaying (which takes a cluster covering at least 7 frames), the honey bee colony has the potential to grow at a linear rate of increase of nearly 2 frames of bees per week. But things don't always go well for growing colonies. As beekeepers, we can provide husbandry to minimize any breaks in the momentum of colony buildup, as well put by Jeffrey in 1959 [6]:
...in Britain colonies are ordinarily increasing in size for only about three months out of the twelve, and in late summer and throughout the long autumn, winter and early spring, numbers are steadily declining This would apparently point to two important principles in commercially successful bee-keeping: first, that the bee-keeper ought to guard carefully against any break in that swift and steady upward surge in the number of bees during April, May and June--for a break at this time cannot be fully retrieved later--and in particular it is suggested that queenless intervals should be most carefully avoided; and secondly, steps should be taken to reduce to a minimum the rate of decline during those other nine long months.
Next month: I'll continue with the swarming impulse
Acknowledgements
As always, my thanks to Lloyd Harris and Peter Borst.
Citations And Footnotes
[1] These hiccups in egglaying are broken out by individual queen in Fig. 1 of my previous article
[2] Riessberger U, & K Crailsheim (1887) Short-term effect of different weather conditions upon the behaviour of forager and nurse honey bees (Apis mellifera carnica Pollmann). Apidologie 28: 411-426. Open access.
[3] Schmickl T & K Crailsheim (2001) Cannibalism and early capping: strategy of honeybee colonies in times of experimental pollen shortages. J Comp Physiol A 187(7):541-547.
[4] For symptoms of some of the "new" brood diseases, see https://scientificbeekeeping.com/sick-bees-part-18a-colony-collaspse-revisited/
[5] See Figure 11 in Part 3 of this series.
[6] Jeffree, EP (1959) Op cit.
See also Jeffree, EP (1955) Observations on the growth and decline of honey bee colonies. Journal of Economic Entomology. 48: 732-726.
Category: Bee Behavior and Biology
Tags: adult survivorship, brood survivorship, cold weather, rainy weather, spring, starvation | cold weather Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/cold-weather/ |
Understanding Colony Buildup and Decline: Part 6 - Hiccups in Colony Linear Buildup
First published in: American Bee Journal, July 2015
Understanding Colony Buildup and Decline - Part 6
Hiccups In Colony Linear Buildup
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in July 2015
CONTENTS
Return To Playing Catch Up
Real World Hiccups
The Effect Of Cold Weather
The Effect Of Rainy Weather
Spring Starvation
From Too Little To Too Much
Brood Survivorship
Adult Survivorship
Take Home Message
Acknowledgements
Citations and Footnotes
Under ideal conditions, colonies grow in a linear manner once the broodnest is well established. But ideal conditions don't always occur in the real world. By being aware of factors that may reduce the rate of colony buildup, the beekeeper may be able to intervene and get the colony back on track.
Return To Playing Catch Up
Creating a mathematical model for colony buildup and decline is not a mere academic exercise-it has great practical application. When you attempt to create a mathematical model, you quickly find out which critical elements you don't fully understand.
Practical application: in my own case, my newfound understanding of exactly why weak colonies are able to catch up in size with stronger colonies helps me to better grasp why springtime splits have the potential to grow as large as established colonies. Ideally, I want to split my colonies small enough to keep them from swarming, but large enough that they can build to optimal honey-producing strength.
But when I was faced with my sons' questions as to what is the ideal amount of brood and adult bees to put into each split, I realized that I couldn't honestly answer with certainty. So I spent considerable time in creating a spreadsheet to calculate the growth of nucs dependent upon those variables (as well as temperature and quality of the queen). I'm currently testing that model by carefully tracking the individual buildup of nucs in a test group specifically created with different measured amounts of brood and bees. I'll let you know when I get the results.
Real World Hiccups
I find the modeling of colony growth under ideal conditions to be mathematically elegant. But of course in the real world, conditions are often less than ideal. Any number of transient phenomena can handicap colony growth, or thwart it altogether. So let's take another look at the hiccups in growth exhibited by Harris' colonies in my colorful chart of colony demographics (Fig. 1):
Figure 1. Note the three instances (in mid May, early and late July) in which broodrearing was curtailed, leading to hiccups in the expected linear growth of the colonies [[i]]. I've indicated on this graph the timing of a spring cold snap, as well as the main honeyflow.
[i] These hiccups in egglaying are broken out by individual queen in Fig. 1 of my previous article
So what caused those sudden reductions in egglaying?
The Effect Of Cold Weather
I searched the weather history for Manitoba during the period of time during which Harris collected his data. It appears that the first dip in egglaying occurred during a cold snap in early May, right during the critical "spring turnover." The cold weather would have precluded foraging for pollen, and the freezing nighttime temperatures (15degF) would have forced the tiny clusters (averaging only about 7000 adult bees--less than 4 frame's worth) to contract tightly--thus limiting the amount of comb suitable for broodrearing.
Practical application: cold nighttime temperatures are a major limiting factor for the buildup of small colonies, since they must go into tight cluster, which severely limits both the size of the broodnest, as well as the number of bees available for nursing duties (since the majority must be engaged in forming a heat-generating "insulating shell").
The Effect Of Rainy Weather
April showers may bring May flowers, but even a single day of rainy weather may have a profound effect upon a growing colony. In a meticulous and intriguing study from the lab of Austrian bee researcher Karl Crailsheim [2], a rain machine was used to prevent the bees in an observation hive from foraging for only a single day at time, while keeping the inside temperature constant. What they found was that:
During rainy periods nurses spent less than half as much time nursing brood as they did during sunny periods. Our experiment suggests that the activity of the nurses is linked to the influx of food and its passage from bee to bee. Nurses receive food more often and over a longer period on days with good weather conditions than on days with bad weather conditions... It seems that the flow of nectar diminishes after only one night and causes the decline in nursing activity even on the first day with bad weather conditions and the following night.
Wow, even a single day of rain cuts nursing visits to brood by half! The researches didn't make observations on what happened during longer storms, but I have. After about three days of rainy weather, a rapidly-growing colony will have completely depleted its pollen stores, and begins to go into protein deficit, forcing the nurses to start using their body reserves (in their fat bodies). And then it may get worse...
During prolonged rainy weather, a colony may shift from rapid growth to cannibalism of the brood within a matter of days. Such an unexpected disaster hit us hard a few years ago. In the photo below, we were adding second brood chambers to strong singles on a nice nectar and pollen flow in mid May, right at the beginning of our main honey flow (Figs. 2-5).
Figure 2. In mid May 2011, our colonies were rapidly building during our spring flow, and we had recently added the second brood chambers for them to move into, with the expectation that they'd be quickly filled with brood and honey. This was beekeeping at its best!
Figure 3. We were running an experiment at the time, and I happened to take a photo of a typical brood frame. Note the reserves of honey and beebread present on May 10th. A few days later the colonies were shaking nectar and whitening wax.
Figure 4. We live in the mountains, where the weather is rapidly changeable. We got hit by a surprise snowstorm on April 25. All photos were taken in the same yard.
Figure 5. Within four days, the hungry colonies had consumed all honey reserves and all pollen reserves. They then desperately started cannibalizing the brood-first the eggs, then young larvae, then older larvae. They don't normally cannibalize sealed brood, since it no longer needs to be fed, and those pupae may be the colony's only chance for survival.
We donned our cold weather gear and madly fed syrup. We were able to avert major brood cannibalism in most of our colonies, which quickly recovered when the weather turned back to warm. But those colonies that were forced to cannibalize their brood got set back so hard that they were unable to even put on winter stores during the main flow, and needed to be fed later in the season.
Practical application: someone incredulously asked me, do you really go out and feed bees during miserable weather? I answered, Well, duh, 'cuz during good weather they're able to feed themselves-that's why we are called bee keepers.
Such brood cannibalism [3], albeit less dramatic, frequently occurs in my area during the two week pollen and nectar dearth that we typically experience between the end of apple bloom and the beginning of the late spring flow. I often observe plenty of freshly-laid eggs each day, but the nurses apparently eat them up rather than trying to feed larvae when there is not enough protein coming in.
Practical application: the main determinant of the development of a busting colony for honey production is having a steady supply of pollen and nectar coming in during the period beginning 6-8 weeks before the start of the main flow. It is during this time that the feeding of pollen sub can be of great benefit during periods of inclement weather or pollen dearth (as occurs in my area immediately after the end of fruit bloom).
Spring Starvation
In my area, other than during storms or the two-week post fruit bloom dearth, there is usually plenty of nectar and pollen coming in during springtime, and we rarely need to feed our splits. But from time to time, we must perform emergency feeding of the ravenous growing colonies. In the case of the colonies in the experiment shown in the photos above, I could not get approval to break protocol and feed the hives during the storm (despite my daily entreaties). The result was that a number starved on the fourth night (Figs. 6 & 7).
Figure 6. It breaks my heart to see a vigorous young colony starve to death, as indicated by the heads buried in the cells.
Fig. 7. After 4 days of bad weather, many of the colonies in the experimental yard succumbed to starvation. It was heartbreaking and ugly-this is a view of a typical bottom board. This disaster could have been easily averted by the feeding of a few dollars worth of sugar in any form.
I've also seen similar starvation of my strongest colonies during almond bloom if the weather turns foul. Many's the time that I've dumped granulated sugar over the combs (if I didn't have syrup with me) in order to save a colony. One time, all it took was a can of soda pop poured over the immobile bees to give them enough energy to move onto some swapped frames of honey.
During intermittent nectar dearths, colonies lacking adequate honey reserves can suffer minor starvation events. Unless you are closely monitoring the yards, all that you may see is a handful of dead bees in front of the hive, and if there has been a resumption of the nectar flow since the brief dearth, you may not be able to figure out what caused the kill (Fig. 8).
Figure 8. A "minor" starvation event occurred in this outyard in late June during a brief break in nectar availability. No colonies died, but similar to this one, most had a small pile of dead bees in front (this occurred in an area far from any pesticide applications). Only by checking the age structure of the remaining brood was I able to figure out what had gone wrong, since by the time I took this photo the colonies had replenished their nectar stores.
Practical application: during these recent drought years in California, we can no longer count on our normal nectar flows. This spring has been scary--our colonies have repeatedly been on the edge of starvation, since we kept expecting the "normal" nectar flows to kick in. As I type these words, I'm starting to resign myself to the possibility that the main flow is simply not gonna happen, and that I am going to be forced to spend a fortune on sugar in order to keep my colonies alive.
It's clear that a shortage of nectar/pollen (even due to a few days of rain) can bring recruitment to a temporary halt; conversely, a surfeit can also do the same...
From Too Little To Too Much
A nice nectar and pollen flow is extremely stimulating to broodrearing. But on the other hand, too much nectar or pollen can result in the bees plugging the broodnest, filling comb that the queen would normally fill with eggs (Fig. 9).
Figure 9. A brood comb following favorable weather in almond bloom. The past few years we've had great foraging weather during almond bloom, sometimes resulting in the broodnests getting plugged out with pollen and nectar. Since the queen can't find a place in which to lay eggs, there will little recruitment of emerging workers three weeks later, and colony populations may temporarily dwindle, much to the dismay of those beekeepers needing to shake packages or make splits.
Practical application: during spring buildup, it may be necessary to either reverse the brood chambers, or to add drawn comb to the broodnest to give the queen additional room in which to lay.
Tip for beginners: excessive feeding of syrup to colonies can also cause plugging out of the broodnest, leading to swarming in the spring, or poor wintering in the fall (due to lack of broodrearing at the end of the season).
Brood Survivorship
Keep in mind that colony buildup is all about the difference between the rates of recruitment of new workers and the rate of attrition of older workers. Pathogens that affect the brood reduce the rate of recruitment. When I began beekeeping, AFB was the only brood disease that we worried about--chalkbrood had yet to reach our shores, and EFB would go away on its own once a good nectar flow resumed. Nowadays, I rarely see AFB. What I do see in spring is persistent EFB (Fig. 10), and sometimes other unidentifiable brood diseases [4].
Figure 10. European Foulbrood can bring colony buildup to a screeching halt by decreasing the rate of larval survival. The larvae in this photo are clearly symptomatic, but in many cases are difficult to detect. Unlike the EFB of yore, today's EFB may not clear up without treatment.
Although I don't see much chalkbrood any more, a few years ago I visited apiaries on the East Coast in which chalkbrood was running rampant, preventing colonies from building up. And it is not just pathogen-caused brood disease that may cause a problem. Toxic pollen (such as that of California Buckeye), nutritionally inadequate pollen, smokestack pollution, chilling of the brood due to anything that causes high adult mortality (virus, nosema, pesticides), or pesticide/miticide residues can all affect the colony similarly, in that they may reduce larval survivability.
Practical application: any factor that reduces larval survivability (such as chilling, poor nutrition, toxins, or disease) will decrease the rate of recruitment, and have a profound effect upon not only the rate of colony buildup, but unless the problem is resolved, also upon its ultimate population size.
Adult Survivorship
The rate of colony buildup is also determined by the rate of attrition of the adult bees. Ideally, springtime workers can be expected to live for an average of about 35 days. During spring buildup, adult survivorship is critical to colony success. I find that infection by either viruses or nosema can prevent a successful spring turnover due to their decreasing adult survivorship [5].
It doesn't take much of a reduction in adult survivorship to exhibit a profound effect (Fig. 11):
Figure 11. In order to create this graph, I shifted Harris' survivorship curves either longer or shorter by 5 days (roughly a 14% increase or decrease in average survivorship). Note how even a few days increase or reduction in average worker longevity has a profound effect upon colony buildup and eventual maximum population.
Practical application: any factor that negatively affects either larval or adult worker survivorship can make a huge difference in eventual colony size and honey production.
Take Home Message
Once a broodnest is established and the population has grown to the extent that the queen can hit her stride in egglaying (which takes a cluster covering at least 7 frames), the honey bee colony has the potential to grow at a linear rate of increase of nearly 2 frames of bees per week. But things don't always go well for growing colonies. As beekeepers, we can provide husbandry to minimize any breaks in the momentum of colony buildup, as well put by Jeffrey in 1959 [6]:
...in Britain colonies are ordinarily increasing in size for only about three months out of the twelve, and in late summer and throughout the long autumn, winter and early spring, numbers are steadily declining This would apparently point to two important principles in commercially successful bee-keeping: first, that the bee-keeper ought to guard carefully against any break in that swift and steady upward surge in the number of bees during April, May and June--for a break at this time cannot be fully retrieved later--and in particular it is suggested that queenless intervals should be most carefully avoided; and secondly, steps should be taken to reduce to a minimum the rate of decline during those other nine long months.
Next month: I'll continue with the swarming impulse
Acknowledgements
As always, my thanks to Lloyd Harris and Peter Borst.
Citations And Footnotes
[1] These hiccups in egglaying are broken out by individual queen in Fig. 1 of my previous article
[2] Riessberger U, & K Crailsheim (1887) Short-term effect of different weather conditions upon the behaviour of forager and nurse honey bees (Apis mellifera carnica Pollmann). Apidologie 28: 411-426. Open access.
[3] Schmickl T & K Crailsheim (2001) Cannibalism and early capping: strategy of honeybee colonies in times of experimental pollen shortages. J Comp Physiol A 187(7):541-547.
[4] For symptoms of some of the "new" brood diseases, see https://scientificbeekeeping.com/sick-bees-part-18a-colony-collaspse-revisited/
[5] See Figure 11 in Part 3 of this series.
[6] Jeffree, EP (1959) Op cit.
See also Jeffree, EP (1955) Observations on the growth and decline of honey bee colonies. Journal of Economic Entomology. 48: 732-726.
Category: Bee Behavior and Biology
Tags: adult survivorship, brood survivorship, cold weather, rainy weather, spring, starvation | brood survivorship Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/brood-survivorship/ |
Reevaluating Beebread: Part 3 - For Preservation or Digestion?
First published in: American Bee Journal, December 2015
Reevaluating Beebread: Part 3
For Preservation Or Digestion?
Randy Oliver
ScientificBeekeeping.com
First published in ABJ Dec 2015
CONTENTS
Anderson's Investigatory Approach
Previous Research
Identification Of The Microbes Involved (via DNA Sequencing)
Bacterial Abundance During The Fermentation Process
Nurse Bee Feeding Preference By Age Of Beebread
The Pollen To Microbe Biomass Ratio
The Degree Of Digestion Of Hive-Stored Pollen
Dr. Anderson's Conclusions
Summary
Next
References And Notes
We've now identified the bacterial players. So let's see what Dr. Kirk Anderson's lab has found to date about why bees turn raw pollen into beebread.
In this article, I'm going to briefly summarize Dr. Anderson's well-designed investigations [1]. My readers know that I can be critical of sloppy science; conversely, I feel that truly exemplary scientific research should receive kudos. The investigation by Kirk and his associates meets this standard, and is a textbook example of good scientific research and writing. Kirk laid out his investigation methodically, questioning each premise of the "predigestion hypothesis," and seeing whether there was actual evidence either supporting or refuting the claim. I will quote from Kirk's papers extensively in italics [2].
Anderson's Investigatory Approach
Scientists typically specify the hypothesis to be tested and lay out their game plan:
It was hypothesized that co-evolved microbes orchestrate the long-term conversion of stored pollen into a more nutritious food source, a process involving microbial succession, anaerobic breakdown of materials, the release of pollen cell contents and/or predigestion by moulds. Here, we use a multifaceted approach to determine whether hive-stored pollen of honey bees involves significant nutrient conversion or 'pre-digestion' by microbes. To this end, we explore [reordered]
whether the differences in bacterial richness and diversity between newly collected and hive-stored pollen are consistent with a preservation or nutrient conversion environment
the absolute number of bacteria in stored pollen,
the association between bacterial abundance and pollen storage time,
the time period associated with pollen storage prior to ingestion by nurse bees,
the pollen to microbe biomass ratio, and
the degree of digestion of hive-stored pollen
Previous Research
Hypothesis to be tested: whether the fermentation of beebread requires inoculation of the pollen with symbiotic "core" gut bacteria via the crop as proposed by Vasquez and Olofsson [3]: "Our research has identified the bacteria involved and revealed that bees, in producing bee bread, add all the beneficial [lactic acid bacteria] to the pollen when they collect it at the site of the flower."
Vasquez and Olofsson's early research was very exciting, but they apparently overstated the case in claiming that bees added all the beneficial lactic acid bacteria to pollen, and especially that those bacteria came from the crop. Scientists already knew that pollen, and especially nectar, typically contains lactic acid and other bacteria prior to being visited by bees [4]. And subsequent research by others found that there were very few bacteria in the bee crop [5]. The question then is whether the pollen loads of returning foragers showed signs of being spiked with the core gut bacteria.
What Anderson found: In previous work, we determined that freshly-collected pollen from returning foragers or beebread contains incidental amounts of core hind-gut bacteria, suggesting that this core gut community does not contribute substantially to the conversion or preservation of pollen stores... This new finding contrasts markedly with the previous culture-dependent view...
Note: Dr. Anderson writes in a meticulous and precise scientific manner, appropriate for the journals in which he publishes (I again commend him for his exemplary backing up of each of his claims with accurate citations and supplemental data). It is polite scientific convention to say that a finding "contrasts markedly" with a previous view; a layman might say "man, did those guys get it wrong."
Identification Of The Microbes Involved (Via DNA Sequencing)
Hypotheses to test: if pollen is indeed inoculated by the bees with core gut bacteria in order to ferment it into beebread, then the bacterial species composition in beebread would shift towards core bacteria during the fermentation process.
Anderson found that: "The bacterial communities found in hive-stored pollen did not differ from those of newly collected pollen, but both sample types varied significantly by season." He found that only a small percentage of the bacteria found in freshly-gathered pollen loads were core hind-gut bacteria (in some cases as little as 3/10ths of a percent). Even more telling was that fermented beebread contained an even lower proportion of core gut bacteria than did newly-collected pollen.
Instead, the most common bacteria found in beebread were strains of Lactobacillus kunkeei. This floral/fruit bacterium thrives in fructose-rich aerobic environments, producing lactic acid as a metabolic byproduct, which has the benefit of making its environment inhospitable to competing yeasts and bacteria. Bees create an ideal environment for L. kunkeei by enriching pollen with fructose-rich nectar-thus its rapid preservation of beebread by the process of acidic "pickling." L. kunkeei is one of the few bacteria that can survive (perhaps in a dormant state) in honey and beebread, likely quickly rejuvenating when exposed to diluted nectar or honey in the crop.
Kirk and others [6]) have found that the bacterial community in bees may differ a bit from hive to hive, and by season or forage, but there is always a "core" hindgut biota (apparently passed via a fecal/oral route of some sort) [7]. The story is as yet far from complete, but it appears that honey bees have a commensal or mutualistic relationship with these core species, but also utilize free-living flower bacteria, such as L. kunkeei, to their advantage. An interesting recent study by Blum [8], working with the fruit fly Drosophila, points out that a host does not necessarily need to maintain a population of endosymbionts, but may instead continually replenish it via its food:
The Drosophila system may represent an alternative mutualism strategy that we term "quotidian replenishment," which is intended to indicate the need for daily replenishment to obtain a consistent [bacterial] community in the animal. In this model, the symbiotic community in Drosophila is maintained through frequent ingestion from an external reservoir of bacteria [its food]... Furthermore, our study shows that one member of the microbiome, Lactobacillus plantarum, protects the fly from intestinal pathogens. These results suggest that, although not always present, the microbiota can promote salubrious [9] effects for the host.
It appears that the honey bee may use a combination of vertical transmission (colony to daughter colony) of the core endosymbionts, coupled with the advantageous use of naturally-occurring floral bacteria (similar to the way that humans make sauerkraut or silage). Of interest is that some free-living bacteria can exert salubrious [10] effects on host immunity (which opens the market for bee probiotics) [11].
Bacterial Abundance During The Fermentation Process
Hypothesis tested: if pollen is indeed digested by core bacteria during the fermentation of beebread, then the number of those bacteria would increase during the process.
What Anderson found: that bacterial abundance increased only during the first two days of fermentation, and then decreased thereafter (Fig. 1). This finding does not support the digestion hypothesis, instead indicating that the formation of lactic acid acts to protect the pollen in beebread from microbial degradation.
Figure 1. After a day's fermentation, the bacterial count of stored pollen increased greatly from that of fresh incoming pollen, and then dropped sharply as the beebread became too acidic for further microbial growth. After Anderson (2014) [[i]].
[i] Kirk shared the raw data so that I could chart it out in a manner more understandable to the layman. See the original paper for his graph, which contains more information.
Nurse Bee Feeding Preference By Age Of Beebread
Hypothesis to be tested: if fermentation improved the nutritional quality of pollen, then it would follow that nurse bees would preferentially consume beebread that had fully fermented.
The Method: Kirk's team meticulously tracked the daily deposition or consumption of pollen in every cell of an active brood frame from each of 8 colonies over 5 days, repeated with different colonies in March, April, and May.
What Anderson found: The results are shown in Fig. 2. Although these measurements were taken during times of pollen surplus (as indicated by the fact that nearly 90% of the beebread cells were over 96 hrs old), the nurse bees appeared to preferentially consume either fresh incoming or slightly fermented pollen to aged beebread. This observation does not support the hypothesis that fermentation improves pollen nutritional quality.
Figure 2. Measurements were taken of the ages of beebread cells in the combs; the orange columns indicate the average number of cells present for each age class of beebread. The capped lines indicate the proportion of that age class of pollen consumed each day. There was apparently an aversion by bees to consume pollen that had undergone extended fermentation [[i]].
[i] Or perhaps a preference for fresh, or slightly fermented, pollen. The overall expected consumption rate for each age class of beebread predicted to be consumed at random based on its abundance on the frames was 9.3%. Compare that to the measured consumption rates shown. Kirk has shown me additional (as yet unpublished) data gathered this spring that shows that the relative consumption rate continues to drop for beebread aged 6, 7, or more days.
Note: despite the observation that bees clearly prefer fresher beebread to older, due to the overwhelming presence of aged beebread in the combs of the colonies he observed, the majority of total beebread consumed (other than the unmeasured consumption of freshly-gathered pollen) was over 96 hrs old, suggesting perhaps that bees make an effort to "rotate the stores."
The Pollen To Microbe Biomass Ratio
And now Anderson, in a stroke of brilliance, shot right to the crucial question: are there even enough bacteria present in beebread to exert a digestive effect? Bacteria lack teeth, and thus depend upon the enzymes that they produce in order to digest foodstuffs. Pollen does not make it easy for microbes to get to the good stuff inside the protective outer shell.
A pollen grain is enclosed in a tough coat called the exine. The exine is composed of a highly decay-resistant biopolymer called sporopollenin. Sporopollenin is so resistant to bacterial enzymes that "Pollen walls...often survive intact and recognizable for millions of years in bog and sediment deposits" [14]. The only place for bacteria to gain access to the nutritious innards of the pollen grain is through the (generally) one or more germination pores in the exine (these also serve as routes for water uptake). These pores are protected by a membrane called the intine, composed of cellulose and pectin. It is this layer that bacteria would need to digest their way through.
Kirk recognized that for bacteria to breach the intine of the pollen pores, that there would need to be a lot of them producing enzymes at those surfaces. So are there enough present? As I'm want to say, let's do the math! In this case, Kirk did it for us.
Hypothesis: that there are enough enzyme-producing bacteria present in beebread relative to the surface area of the pollen grains to digest their way through the pollen shells.
Kirk's math: He was generous on his estimate of the number of microbes present in mature beebread, quadrupling his actual colony counts to allow for culture bias and fungi, arriving at about 36,900 microbes per gram of pollen. He then counted pollen grains under a scope, estimating about 90 million pollen grains per gram. This works out to about 1 microbe per 2500 pollen grains (Fig. 3). To place this into biological perspective, a single grain of pollen in the bee hindgut is often covered with hundreds or thousands of bacteria (Fig. 4), busily digesting the remnants left over from the digestion that took place in the bee midgut.
As an imaginary visual analogy, I calculated that the proportion of bacteria per surface area of the pollen grains works out to the spatial equivalent of a single BB placed on a football field [15]--hardly enough to produce the enzymes necessary to digest their way through the pollen exine or intine.
Figure 3. A scanning electron micrograph of dried beebread. The pink substance is dried simple sugars, which constitute about 40-50% by weight. Note the distinct lack of bacteria. Electron micrographs courtesy Kirk Anderson.
Figure 4. For comparison, these pollen grains from a nurse bee hindgut are covered with live bacteria (stained purple).
Conclusion: there simply aren't enough microbes present in beebread to cause any significant degree of digestion of the pollen grain contents. Kirk succinctly concludes that: "Hive-stored pollen lacks the microbial biomass needed to alter pollen nutrition."
The Degree Of Digestion Of Hive-Stored Pollen
Kirk is hardly the first bee researcher to point out that beebread contains few microbes. Back in 1983 Klungess and Peng [15], using microscopy, found few microorganisms in fresh beebread (but more in dark, old beebread). They concluded that:
The substances, presumably nectar or diluted honey and enzymes from the ventriculus and salivary gland, that bees add to pollen during packing on to the corbiculae [pollen baskets] and into cells, and the bee bread ripening process, do not break down the pollen contents. Nor do the microorganisms associated with fresh and old bee bread appear to cause destruction of pollen intine or the cytoplasm. .. It is, therefore, proposed that the substances added to pollen by bees during storage function as a preservative. We found no visible evidence that these substances pre-digest the pollen so as to make the nutrients more available to bees during subsequent digestion and absorption.
Compare this to Peng's previous finding that most (but not all) pollen grains are rapidly digested during their passage through the nurse bee midgut, which contains few microbes [16].
Hypothesis: if bacteria indeed digest the pollen grains in beebread, this should be easily observed through microscopy.
Anderson's finding: "There were no discernible morphological differences between newly collected and hive-stored pollen."
This should be something that any beekeeper could easily verify for him/herself. So I looked at aged beebread from my own hives under the scope (at 400 and 1000x), and also found very few microorganisms or digested pollen grains (Figs. 5-7).
Figure 5. Pollen grains in aged beebread under light microscopy. Note the relative absence of yeast or bacteria, and the unbreached (not misshapen) exines and intact colored contents of the pollen grains.
Figure 6. Pollen grains from beebread that I diluted with a weak sugar solution and allowed to ferment for 10 days. Note the abundant yeast and bacterial cells in the background (unfortunately there was not enough depth of field to bring both the pollen and microbes simultaneously into focus). Despite being exposed to over a week of vigorous aerobic fermentation, these pollen grains remain intact and undigested. Compare these intact grains to those below.
Figure 7. A sample of digested pollen from the hindgut of a nurse bee. Note how most of the pollen shells are empty (no longer yellow inside) and distorted, indicating digestion of the contents.
Conclusion: the bee midgut can quickly empty pollen grains and digest the contents. But such digestion does not occur when bacteria and yeast ferment pollen into beebread.
Dr. Anderson's Conclusions
Our combined results do not support the hypothesis that hive-stored pollen of honey bees involves nutrient conversion or predigestion by microbes prior to consumption.
The bacterial communities found in hive-stored pollen did not differ from those of newly collected pollen, but both sample types varied significantly by season. This result indicates the lack of an emergent 'core' bacterial community co-evolved to predigest pollen.
Relative to other plant material involving microbial digestion or extensive fermentation, hive-stored pollen contains very few microbes.
The absolute number of bacteria in hive-stored pollen decreases with storage time, indicating that it is not a suitable medium for microbial growth.
The preferential consumption of freshly collected pollen indicates that bees have not evolved to rely on microbes or other time-related factors for pollen predigestion.
The microbe to pollen grain ratio is many orders of magnitude removed from that required to alter hive-stored pollen.
Regardless of sampled season or the taxonomic character of microbial communities, microscopic examination revealed no intermediate stage of pollen digestion in hive-stored pollen.
Based on these collective findings, we suggest that stored pollen is a preservative environment governed largely by nonmicrobial additions of nectar, honey and bee glandular secretions.
Summary
Flowers and pollinators have coevolved over millions of years, and along with them microbes always at the ready to consume them, or perhaps establish symbiotic relationships. Since microbes are invisible to the naked eye, it is difficult for us to grasp their degree of prevalence in the environment, or to understand their contribution to bee nutrition and health.
There may be a million bacteria (along with yeasts and other fungi) per milliliter in nectar when bees first collect it--fresh nectar is often already starting to ferment [18]. Pollen contains somewhat fewer microbes, but is still very biologically active when first gathered. The greatest concentration of microbes in the hive is in the residual undigested material in the bees' hindguts--that of a single bee may contain hundreds of millions of bacteria [19].
Kirk points out that the fluctuation of pollen availability has likely "selected for the quick turnover of the most readily available pollen nutrients into a 'nutritional reservoir' of living tissue (i.e. larva and worker fat bodies). In such a state, nutritional reserves are better protected from microbial digestion, more quickly shared among hive members and easier to digest than hive-stored pollen."
The above observation reminds us that hungry nurse bees readily consume larvae that they had previously been lavishing with jelly when it was abundant. The larvae thus function as a living protein reserve that through cannibalism can be quickly converted back into jelly or used to replenish fat bodies.
The honey bee, similar to humans, stores surplus food (that can't be immediately consumed) for later consumption (mainly to survive the winter). Like us, bees have figured out similar ways to prevent that food from being decomposed by microbes. Both nectar and pollen are prepared for prolonged storage by using a combination of high sugar concentration for osmotic preservative effect (similar to making jam), acidification via bacterial lactic acid production (pickling), and the addition of salivary antimicrobial compounds such as glucose oxidase (food preservatives).
Two key bacteria in this preservation process are the acid-resistant and osmotolerant [20] Lactobacillus kunkeei and Parasaccharibacter apium, both of which appear to be instrumental in hive hygiene, food storage, and larval health.
The microbial community in the hive is dynamic and evolving, not only in the gut of every bee during its short life, but also hour by hour during the fermentation of beebread. The microbiomes of the hive rapidly "adapt to changing diets and conditions not only by shifting community membership but also by changing gene content via horizontal gene transfer." Bacteria, by continually swapping genes, can adapt and evolve at a rate inconceivable to humans.
In the extended flower-pollinator community, pollinators vector microbes (including pathogens) with a remarkably high degree of efficiency. Graystock [21] found surprisingly efficient transmission of pathogens from bee to bee during flower visitations--the same would be expected to apply to hive or gut bacteria. This is due to the fact that the toilet hygiene of flying insects is rudimentary at best, resulting in plenty of fecal bacteria being inadvertently transferred to flower surfaces during pollinator visits (after all, just think about the degree of pollen transfer from flower to flower). And such transmission can be interspecific--any bee, fly, butterfly, beetle, or wasp can carry floral or pathogenic microbes from one flower to another. The total amount of microbial interchange within the entire flower/pollinator environment is mind boggling to consider, and makes for a highly dynamic system of microbial and pathogen interactions that we are only beginning to understand.
Next
The biological and chemical processes that take place during the fermentation of beebread, yeasts and fungi, probiotics, and the Anderson labs' current research projects.
References And Notes
[1] Published as Anderson, KE, MJ CarrolL, T Sheehan, BM Mott, P Maes and V Corby-Harris (2014) Hive-stored pollen of honey bees: many lines of evidence are consistent with pollen preservation, not nutrient conversion. Molecular Ecology 23: 5904-5917.
[2] Mainly from the above citation, but also from other published and as yet unpublished research. I also took the liberty to edit or reorder the quotations from his papers for readability.
[3] Vasquez A, Olofsson TC (2011) The honey crop - the holy grail when antibiotics fail. Microbiology Today, 38, 226-229.
[4] Fridman S, et al (2012) Bacterial communities in floral nectar. Environ. Microbiol. Rep 4:97-104.
[5] See my previous articles in this series.
[6] Disayathanoowat, T, et al (2012) T-RFLP analysis of bacterial communities in the midguts of Apis mellifera and Apis cerana honey bees in Thailand. Journal of Apicultural Research 51(4): 312-319.
[7] Don't be grossed out--the same thing happens with humans and many other animals.
[8] Blum JE, et al (2013) Frequent replenishment sustains the beneficial microbiome of Drosophila melanogaster. mBio 4(6):e00860-13. doi: 10.1128/mBio.00860-13
[9] Salubrious-healthful, beneficial, wholesome. Man, I gotta add this descriptive word to my vocabulary!
[10] I couldn't wait.
[11] Again, I've yet to see any hard data that any probiotic currently on the market is of benefit to bees. But I wouldn't be the least surprised if some were developed in the near future. But don't just go feeding any untested probiotic--a recent study found that some can seriously harm bees:
Ptaszynska, AA, et al (2015) Are commercial probiotics and prebiotics effective in the treatment and prevention of honeybee nosemosis C? Parasitol Res DOI 10.1007/s00436-015-4761-z Open access.
[12] Kirk shared the raw data so that I could chart it out in a manner more understandable to the layman. See the original paper for his graph, which contains more information.
[13] Or perhaps a preference for fresh, or slightly fermented, pollen. The overall expected consumption rate for each age class of beebread predicted to be consumed at random based on its abundance on the frames was 9.3%. Compare that to the measured consumption rates shown. Kirk has shown me additional (as yet unpublished) data gathered this spring that shows that the relative consumption rate continues to drop for beebread aged 6, 7, or more days.
Note: despite the observation that bees clearly prefer fresher beebread to older, due to the overwhelming presence of aged beebread in the combs of the colonies he observed, the majority of total beebread consumed (other than the unmeasured consumption of freshly-gathered pollen) was over 96 hrs old, suggesting perhaps that bees make an effort to "rotate the stores."
[14] Roulston, THI and JH Cane (2000) Pollen nutritional content and digestibility for animals. Plant Systematics 222: 187-209.
[15] By my math.
[16] Klungness L. M., Peng Y.-S. (1983) A scanning electron microscopic study of pollen loads collected and stored by honeybees. J. Apicul. Res. 22: 264-271.
[17] Peng YS, ME Nasr, et al (1985) The digestion of dandelion pollen by adult worker honeybees. Physiol. Entomol. 10: 75-82.
[18] Castillo, C, et al (2012) Seasonal variation in the titers and biosynthesis of the primer pheromone ethyl oleate in honey bees. J Insect Physiol 58(8):1112-21.
[19] Estimate, Kirk Anderson, pers comm.
[20] Osmotolerance is the ability to live in high-sugar environment that would dessicate other microbes.
[21] Graystock P, et al (2015) Parasites in bloom: flowers aid dispersal and transmission of pollinator parasites within and between bee species. Proc. R. Soc. B 282: 20151371. http://dx.doi.org/10.1098/rspb.2015.1371
Category: Bee Nutrition
Tags: beebread, digestion, DNA sequencing, Dr. Anderson, fermentation, hive-stored pollen, microbe biomass | beebread Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/beebread/ |
Reevaluating Beebread: Part 3 - For Preservation or Digestion?
First published in: American Bee Journal, December 2015
Reevaluating Beebread: Part 3
For Preservation Or Digestion?
Randy Oliver
ScientificBeekeeping.com
First published in ABJ Dec 2015
CONTENTS
Anderson's Investigatory Approach
Previous Research
Identification Of The Microbes Involved (via DNA Sequencing)
Bacterial Abundance During The Fermentation Process
Nurse Bee Feeding Preference By Age Of Beebread
The Pollen To Microbe Biomass Ratio
The Degree Of Digestion Of Hive-Stored Pollen
Dr. Anderson's Conclusions
Summary
Next
References And Notes
We've now identified the bacterial players. So let's see what Dr. Kirk Anderson's lab has found to date about why bees turn raw pollen into beebread.
In this article, I'm going to briefly summarize Dr. Anderson's well-designed investigations [1]. My readers know that I can be critical of sloppy science; conversely, I feel that truly exemplary scientific research should receive kudos. The investigation by Kirk and his associates meets this standard, and is a textbook example of good scientific research and writing. Kirk laid out his investigation methodically, questioning each premise of the "predigestion hypothesis," and seeing whether there was actual evidence either supporting or refuting the claim. I will quote from Kirk's papers extensively in italics [2].
Anderson's Investigatory Approach
Scientists typically specify the hypothesis to be tested and lay out their game plan:
It was hypothesized that co-evolved microbes orchestrate the long-term conversion of stored pollen into a more nutritious food source, a process involving microbial succession, anaerobic breakdown of materials, the release of pollen cell contents and/or predigestion by moulds. Here, we use a multifaceted approach to determine whether hive-stored pollen of honey bees involves significant nutrient conversion or 'pre-digestion' by microbes. To this end, we explore [reordered]
whether the differences in bacterial richness and diversity between newly collected and hive-stored pollen are consistent with a preservation or nutrient conversion environment
the absolute number of bacteria in stored pollen,
the association between bacterial abundance and pollen storage time,
the time period associated with pollen storage prior to ingestion by nurse bees,
the pollen to microbe biomass ratio, and
the degree of digestion of hive-stored pollen
Previous Research
Hypothesis to be tested: whether the fermentation of beebread requires inoculation of the pollen with symbiotic "core" gut bacteria via the crop as proposed by Vasquez and Olofsson [3]: "Our research has identified the bacteria involved and revealed that bees, in producing bee bread, add all the beneficial [lactic acid bacteria] to the pollen when they collect it at the site of the flower."
Vasquez and Olofsson's early research was very exciting, but they apparently overstated the case in claiming that bees added all the beneficial lactic acid bacteria to pollen, and especially that those bacteria came from the crop. Scientists already knew that pollen, and especially nectar, typically contains lactic acid and other bacteria prior to being visited by bees [4]. And subsequent research by others found that there were very few bacteria in the bee crop [5]. The question then is whether the pollen loads of returning foragers showed signs of being spiked with the core gut bacteria.
What Anderson found: In previous work, we determined that freshly-collected pollen from returning foragers or beebread contains incidental amounts of core hind-gut bacteria, suggesting that this core gut community does not contribute substantially to the conversion or preservation of pollen stores... This new finding contrasts markedly with the previous culture-dependent view...
Note: Dr. Anderson writes in a meticulous and precise scientific manner, appropriate for the journals in which he publishes (I again commend him for his exemplary backing up of each of his claims with accurate citations and supplemental data). It is polite scientific convention to say that a finding "contrasts markedly" with a previous view; a layman might say "man, did those guys get it wrong."
Identification Of The Microbes Involved (Via DNA Sequencing)
Hypotheses to test: if pollen is indeed inoculated by the bees with core gut bacteria in order to ferment it into beebread, then the bacterial species composition in beebread would shift towards core bacteria during the fermentation process.
Anderson found that: "The bacterial communities found in hive-stored pollen did not differ from those of newly collected pollen, but both sample types varied significantly by season." He found that only a small percentage of the bacteria found in freshly-gathered pollen loads were core hind-gut bacteria (in some cases as little as 3/10ths of a percent). Even more telling was that fermented beebread contained an even lower proportion of core gut bacteria than did newly-collected pollen.
Instead, the most common bacteria found in beebread were strains of Lactobacillus kunkeei. This floral/fruit bacterium thrives in fructose-rich aerobic environments, producing lactic acid as a metabolic byproduct, which has the benefit of making its environment inhospitable to competing yeasts and bacteria. Bees create an ideal environment for L. kunkeei by enriching pollen with fructose-rich nectar-thus its rapid preservation of beebread by the process of acidic "pickling." L. kunkeei is one of the few bacteria that can survive (perhaps in a dormant state) in honey and beebread, likely quickly rejuvenating when exposed to diluted nectar or honey in the crop.
Kirk and others [6]) have found that the bacterial community in bees may differ a bit from hive to hive, and by season or forage, but there is always a "core" hindgut biota (apparently passed via a fecal/oral route of some sort) [7]. The story is as yet far from complete, but it appears that honey bees have a commensal or mutualistic relationship with these core species, but also utilize free-living flower bacteria, such as L. kunkeei, to their advantage. An interesting recent study by Blum [8], working with the fruit fly Drosophila, points out that a host does not necessarily need to maintain a population of endosymbionts, but may instead continually replenish it via its food:
The Drosophila system may represent an alternative mutualism strategy that we term "quotidian replenishment," which is intended to indicate the need for daily replenishment to obtain a consistent [bacterial] community in the animal. In this model, the symbiotic community in Drosophila is maintained through frequent ingestion from an external reservoir of bacteria [its food]... Furthermore, our study shows that one member of the microbiome, Lactobacillus plantarum, protects the fly from intestinal pathogens. These results suggest that, although not always present, the microbiota can promote salubrious [9] effects for the host.
It appears that the honey bee may use a combination of vertical transmission (colony to daughter colony) of the core endosymbionts, coupled with the advantageous use of naturally-occurring floral bacteria (similar to the way that humans make sauerkraut or silage). Of interest is that some free-living bacteria can exert salubrious [10] effects on host immunity (which opens the market for bee probiotics) [11].
Bacterial Abundance During The Fermentation Process
Hypothesis tested: if pollen is indeed digested by core bacteria during the fermentation of beebread, then the number of those bacteria would increase during the process.
What Anderson found: that bacterial abundance increased only during the first two days of fermentation, and then decreased thereafter (Fig. 1). This finding does not support the digestion hypothesis, instead indicating that the formation of lactic acid acts to protect the pollen in beebread from microbial degradation.
Figure 1. After a day's fermentation, the bacterial count of stored pollen increased greatly from that of fresh incoming pollen, and then dropped sharply as the beebread became too acidic for further microbial growth. After Anderson (2014) [[i]].
[i] Kirk shared the raw data so that I could chart it out in a manner more understandable to the layman. See the original paper for his graph, which contains more information.
Nurse Bee Feeding Preference By Age Of Beebread
Hypothesis to be tested: if fermentation improved the nutritional quality of pollen, then it would follow that nurse bees would preferentially consume beebread that had fully fermented.
The Method: Kirk's team meticulously tracked the daily deposition or consumption of pollen in every cell of an active brood frame from each of 8 colonies over 5 days, repeated with different colonies in March, April, and May.
What Anderson found: The results are shown in Fig. 2. Although these measurements were taken during times of pollen surplus (as indicated by the fact that nearly 90% of the beebread cells were over 96 hrs old), the nurse bees appeared to preferentially consume either fresh incoming or slightly fermented pollen to aged beebread. This observation does not support the hypothesis that fermentation improves pollen nutritional quality.
Figure 2. Measurements were taken of the ages of beebread cells in the combs; the orange columns indicate the average number of cells present for each age class of beebread. The capped lines indicate the proportion of that age class of pollen consumed each day. There was apparently an aversion by bees to consume pollen that had undergone extended fermentation [[i]].
[i] Or perhaps a preference for fresh, or slightly fermented, pollen. The overall expected consumption rate for each age class of beebread predicted to be consumed at random based on its abundance on the frames was 9.3%. Compare that to the measured consumption rates shown. Kirk has shown me additional (as yet unpublished) data gathered this spring that shows that the relative consumption rate continues to drop for beebread aged 6, 7, or more days.
Note: despite the observation that bees clearly prefer fresher beebread to older, due to the overwhelming presence of aged beebread in the combs of the colonies he observed, the majority of total beebread consumed (other than the unmeasured consumption of freshly-gathered pollen) was over 96 hrs old, suggesting perhaps that bees make an effort to "rotate the stores."
The Pollen To Microbe Biomass Ratio
And now Anderson, in a stroke of brilliance, shot right to the crucial question: are there even enough bacteria present in beebread to exert a digestive effect? Bacteria lack teeth, and thus depend upon the enzymes that they produce in order to digest foodstuffs. Pollen does not make it easy for microbes to get to the good stuff inside the protective outer shell.
A pollen grain is enclosed in a tough coat called the exine. The exine is composed of a highly decay-resistant biopolymer called sporopollenin. Sporopollenin is so resistant to bacterial enzymes that "Pollen walls...often survive intact and recognizable for millions of years in bog and sediment deposits" [14]. The only place for bacteria to gain access to the nutritious innards of the pollen grain is through the (generally) one or more germination pores in the exine (these also serve as routes for water uptake). These pores are protected by a membrane called the intine, composed of cellulose and pectin. It is this layer that bacteria would need to digest their way through.
Kirk recognized that for bacteria to breach the intine of the pollen pores, that there would need to be a lot of them producing enzymes at those surfaces. So are there enough present? As I'm want to say, let's do the math! In this case, Kirk did it for us.
Hypothesis: that there are enough enzyme-producing bacteria present in beebread relative to the surface area of the pollen grains to digest their way through the pollen shells.
Kirk's math: He was generous on his estimate of the number of microbes present in mature beebread, quadrupling his actual colony counts to allow for culture bias and fungi, arriving at about 36,900 microbes per gram of pollen. He then counted pollen grains under a scope, estimating about 90 million pollen grains per gram. This works out to about 1 microbe per 2500 pollen grains (Fig. 3). To place this into biological perspective, a single grain of pollen in the bee hindgut is often covered with hundreds or thousands of bacteria (Fig. 4), busily digesting the remnants left over from the digestion that took place in the bee midgut.
As an imaginary visual analogy, I calculated that the proportion of bacteria per surface area of the pollen grains works out to the spatial equivalent of a single BB placed on a football field [15]--hardly enough to produce the enzymes necessary to digest their way through the pollen exine or intine.
Figure 3. A scanning electron micrograph of dried beebread. The pink substance is dried simple sugars, which constitute about 40-50% by weight. Note the distinct lack of bacteria. Electron micrographs courtesy Kirk Anderson.
Figure 4. For comparison, these pollen grains from a nurse bee hindgut are covered with live bacteria (stained purple).
Conclusion: there simply aren't enough microbes present in beebread to cause any significant degree of digestion of the pollen grain contents. Kirk succinctly concludes that: "Hive-stored pollen lacks the microbial biomass needed to alter pollen nutrition."
The Degree Of Digestion Of Hive-Stored Pollen
Kirk is hardly the first bee researcher to point out that beebread contains few microbes. Back in 1983 Klungess and Peng [15], using microscopy, found few microorganisms in fresh beebread (but more in dark, old beebread). They concluded that:
The substances, presumably nectar or diluted honey and enzymes from the ventriculus and salivary gland, that bees add to pollen during packing on to the corbiculae [pollen baskets] and into cells, and the bee bread ripening process, do not break down the pollen contents. Nor do the microorganisms associated with fresh and old bee bread appear to cause destruction of pollen intine or the cytoplasm. .. It is, therefore, proposed that the substances added to pollen by bees during storage function as a preservative. We found no visible evidence that these substances pre-digest the pollen so as to make the nutrients more available to bees during subsequent digestion and absorption.
Compare this to Peng's previous finding that most (but not all) pollen grains are rapidly digested during their passage through the nurse bee midgut, which contains few microbes [16].
Hypothesis: if bacteria indeed digest the pollen grains in beebread, this should be easily observed through microscopy.
Anderson's finding: "There were no discernible morphological differences between newly collected and hive-stored pollen."
This should be something that any beekeeper could easily verify for him/herself. So I looked at aged beebread from my own hives under the scope (at 400 and 1000x), and also found very few microorganisms or digested pollen grains (Figs. 5-7).
Figure 5. Pollen grains in aged beebread under light microscopy. Note the relative absence of yeast or bacteria, and the unbreached (not misshapen) exines and intact colored contents of the pollen grains.
Figure 6. Pollen grains from beebread that I diluted with a weak sugar solution and allowed to ferment for 10 days. Note the abundant yeast and bacterial cells in the background (unfortunately there was not enough depth of field to bring both the pollen and microbes simultaneously into focus). Despite being exposed to over a week of vigorous aerobic fermentation, these pollen grains remain intact and undigested. Compare these intact grains to those below.
Figure 7. A sample of digested pollen from the hindgut of a nurse bee. Note how most of the pollen shells are empty (no longer yellow inside) and distorted, indicating digestion of the contents.
Conclusion: the bee midgut can quickly empty pollen grains and digest the contents. But such digestion does not occur when bacteria and yeast ferment pollen into beebread.
Dr. Anderson's Conclusions
Our combined results do not support the hypothesis that hive-stored pollen of honey bees involves nutrient conversion or predigestion by microbes prior to consumption.
The bacterial communities found in hive-stored pollen did not differ from those of newly collected pollen, but both sample types varied significantly by season. This result indicates the lack of an emergent 'core' bacterial community co-evolved to predigest pollen.
Relative to other plant material involving microbial digestion or extensive fermentation, hive-stored pollen contains very few microbes.
The absolute number of bacteria in hive-stored pollen decreases with storage time, indicating that it is not a suitable medium for microbial growth.
The preferential consumption of freshly collected pollen indicates that bees have not evolved to rely on microbes or other time-related factors for pollen predigestion.
The microbe to pollen grain ratio is many orders of magnitude removed from that required to alter hive-stored pollen.
Regardless of sampled season or the taxonomic character of microbial communities, microscopic examination revealed no intermediate stage of pollen digestion in hive-stored pollen.
Based on these collective findings, we suggest that stored pollen is a preservative environment governed largely by nonmicrobial additions of nectar, honey and bee glandular secretions.
Summary
Flowers and pollinators have coevolved over millions of years, and along with them microbes always at the ready to consume them, or perhaps establish symbiotic relationships. Since microbes are invisible to the naked eye, it is difficult for us to grasp their degree of prevalence in the environment, or to understand their contribution to bee nutrition and health.
There may be a million bacteria (along with yeasts and other fungi) per milliliter in nectar when bees first collect it--fresh nectar is often already starting to ferment [18]. Pollen contains somewhat fewer microbes, but is still very biologically active when first gathered. The greatest concentration of microbes in the hive is in the residual undigested material in the bees' hindguts--that of a single bee may contain hundreds of millions of bacteria [19].
Kirk points out that the fluctuation of pollen availability has likely "selected for the quick turnover of the most readily available pollen nutrients into a 'nutritional reservoir' of living tissue (i.e. larva and worker fat bodies). In such a state, nutritional reserves are better protected from microbial digestion, more quickly shared among hive members and easier to digest than hive-stored pollen."
The above observation reminds us that hungry nurse bees readily consume larvae that they had previously been lavishing with jelly when it was abundant. The larvae thus function as a living protein reserve that through cannibalism can be quickly converted back into jelly or used to replenish fat bodies.
The honey bee, similar to humans, stores surplus food (that can't be immediately consumed) for later consumption (mainly to survive the winter). Like us, bees have figured out similar ways to prevent that food from being decomposed by microbes. Both nectar and pollen are prepared for prolonged storage by using a combination of high sugar concentration for osmotic preservative effect (similar to making jam), acidification via bacterial lactic acid production (pickling), and the addition of salivary antimicrobial compounds such as glucose oxidase (food preservatives).
Two key bacteria in this preservation process are the acid-resistant and osmotolerant [20] Lactobacillus kunkeei and Parasaccharibacter apium, both of which appear to be instrumental in hive hygiene, food storage, and larval health.
The microbial community in the hive is dynamic and evolving, not only in the gut of every bee during its short life, but also hour by hour during the fermentation of beebread. The microbiomes of the hive rapidly "adapt to changing diets and conditions not only by shifting community membership but also by changing gene content via horizontal gene transfer." Bacteria, by continually swapping genes, can adapt and evolve at a rate inconceivable to humans.
In the extended flower-pollinator community, pollinators vector microbes (including pathogens) with a remarkably high degree of efficiency. Graystock [21] found surprisingly efficient transmission of pathogens from bee to bee during flower visitations--the same would be expected to apply to hive or gut bacteria. This is due to the fact that the toilet hygiene of flying insects is rudimentary at best, resulting in plenty of fecal bacteria being inadvertently transferred to flower surfaces during pollinator visits (after all, just think about the degree of pollen transfer from flower to flower). And such transmission can be interspecific--any bee, fly, butterfly, beetle, or wasp can carry floral or pathogenic microbes from one flower to another. The total amount of microbial interchange within the entire flower/pollinator environment is mind boggling to consider, and makes for a highly dynamic system of microbial and pathogen interactions that we are only beginning to understand.
Next
The biological and chemical processes that take place during the fermentation of beebread, yeasts and fungi, probiotics, and the Anderson labs' current research projects.
References And Notes
[1] Published as Anderson, KE, MJ CarrolL, T Sheehan, BM Mott, P Maes and V Corby-Harris (2014) Hive-stored pollen of honey bees: many lines of evidence are consistent with pollen preservation, not nutrient conversion. Molecular Ecology 23: 5904-5917.
[2] Mainly from the above citation, but also from other published and as yet unpublished research. I also took the liberty to edit or reorder the quotations from his papers for readability.
[3] Vasquez A, Olofsson TC (2011) The honey crop - the holy grail when antibiotics fail. Microbiology Today, 38, 226-229.
[4] Fridman S, et al (2012) Bacterial communities in floral nectar. Environ. Microbiol. Rep 4:97-104.
[5] See my previous articles in this series.
[6] Disayathanoowat, T, et al (2012) T-RFLP analysis of bacterial communities in the midguts of Apis mellifera and Apis cerana honey bees in Thailand. Journal of Apicultural Research 51(4): 312-319.
[7] Don't be grossed out--the same thing happens with humans and many other animals.
[8] Blum JE, et al (2013) Frequent replenishment sustains the beneficial microbiome of Drosophila melanogaster. mBio 4(6):e00860-13. doi: 10.1128/mBio.00860-13
[9] Salubrious-healthful, beneficial, wholesome. Man, I gotta add this descriptive word to my vocabulary!
[10] I couldn't wait.
[11] Again, I've yet to see any hard data that any probiotic currently on the market is of benefit to bees. But I wouldn't be the least surprised if some were developed in the near future. But don't just go feeding any untested probiotic--a recent study found that some can seriously harm bees:
Ptaszynska, AA, et al (2015) Are commercial probiotics and prebiotics effective in the treatment and prevention of honeybee nosemosis C? Parasitol Res DOI 10.1007/s00436-015-4761-z Open access.
[12] Kirk shared the raw data so that I could chart it out in a manner more understandable to the layman. See the original paper for his graph, which contains more information.
[13] Or perhaps a preference for fresh, or slightly fermented, pollen. The overall expected consumption rate for each age class of beebread predicted to be consumed at random based on its abundance on the frames was 9.3%. Compare that to the measured consumption rates shown. Kirk has shown me additional (as yet unpublished) data gathered this spring that shows that the relative consumption rate continues to drop for beebread aged 6, 7, or more days.
Note: despite the observation that bees clearly prefer fresher beebread to older, due to the overwhelming presence of aged beebread in the combs of the colonies he observed, the majority of total beebread consumed (other than the unmeasured consumption of freshly-gathered pollen) was over 96 hrs old, suggesting perhaps that bees make an effort to "rotate the stores."
[14] Roulston, THI and JH Cane (2000) Pollen nutritional content and digestibility for animals. Plant Systematics 222: 187-209.
[15] By my math.
[16] Klungness L. M., Peng Y.-S. (1983) A scanning electron microscopic study of pollen loads collected and stored by honeybees. J. Apicul. Res. 22: 264-271.
[17] Peng YS, ME Nasr, et al (1985) The digestion of dandelion pollen by adult worker honeybees. Physiol. Entomol. 10: 75-82.
[18] Castillo, C, et al (2012) Seasonal variation in the titers and biosynthesis of the primer pheromone ethyl oleate in honey bees. J Insect Physiol 58(8):1112-21.
[19] Estimate, Kirk Anderson, pers comm.
[20] Osmotolerance is the ability to live in high-sugar environment that would dessicate other microbes.
[21] Graystock P, et al (2015) Parasites in bloom: flowers aid dispersal and transmission of pollinator parasites within and between bee species. Proc. R. Soc. B 282: 20151371. http://dx.doi.org/10.1098/rspb.2015.1371
Category: Bee Nutrition
Tags: beebread, digestion, DNA sequencing, Dr. Anderson, fermentation, hive-stored pollen, microbe biomass | digestion Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/digestion/ |
Reevaluating Beebread: Part 3 - For Preservation or Digestion?
First published in: American Bee Journal, December 2015
Reevaluating Beebread: Part 3
For Preservation Or Digestion?
Randy Oliver
ScientificBeekeeping.com
First published in ABJ Dec 2015
CONTENTS
Anderson's Investigatory Approach
Previous Research
Identification Of The Microbes Involved (via DNA Sequencing)
Bacterial Abundance During The Fermentation Process
Nurse Bee Feeding Preference By Age Of Beebread
The Pollen To Microbe Biomass Ratio
The Degree Of Digestion Of Hive-Stored Pollen
Dr. Anderson's Conclusions
Summary
Next
References And Notes
We've now identified the bacterial players. So let's see what Dr. Kirk Anderson's lab has found to date about why bees turn raw pollen into beebread.
In this article, I'm going to briefly summarize Dr. Anderson's well-designed investigations [1]. My readers know that I can be critical of sloppy science; conversely, I feel that truly exemplary scientific research should receive kudos. The investigation by Kirk and his associates meets this standard, and is a textbook example of good scientific research and writing. Kirk laid out his investigation methodically, questioning each premise of the "predigestion hypothesis," and seeing whether there was actual evidence either supporting or refuting the claim. I will quote from Kirk's papers extensively in italics [2].
Anderson's Investigatory Approach
Scientists typically specify the hypothesis to be tested and lay out their game plan:
It was hypothesized that co-evolved microbes orchestrate the long-term conversion of stored pollen into a more nutritious food source, a process involving microbial succession, anaerobic breakdown of materials, the release of pollen cell contents and/or predigestion by moulds. Here, we use a multifaceted approach to determine whether hive-stored pollen of honey bees involves significant nutrient conversion or 'pre-digestion' by microbes. To this end, we explore [reordered]
whether the differences in bacterial richness and diversity between newly collected and hive-stored pollen are consistent with a preservation or nutrient conversion environment
the absolute number of bacteria in stored pollen,
the association between bacterial abundance and pollen storage time,
the time period associated with pollen storage prior to ingestion by nurse bees,
the pollen to microbe biomass ratio, and
the degree of digestion of hive-stored pollen
Previous Research
Hypothesis to be tested: whether the fermentation of beebread requires inoculation of the pollen with symbiotic "core" gut bacteria via the crop as proposed by Vasquez and Olofsson [3]: "Our research has identified the bacteria involved and revealed that bees, in producing bee bread, add all the beneficial [lactic acid bacteria] to the pollen when they collect it at the site of the flower."
Vasquez and Olofsson's early research was very exciting, but they apparently overstated the case in claiming that bees added all the beneficial lactic acid bacteria to pollen, and especially that those bacteria came from the crop. Scientists already knew that pollen, and especially nectar, typically contains lactic acid and other bacteria prior to being visited by bees [4]. And subsequent research by others found that there were very few bacteria in the bee crop [5]. The question then is whether the pollen loads of returning foragers showed signs of being spiked with the core gut bacteria.
What Anderson found: In previous work, we determined that freshly-collected pollen from returning foragers or beebread contains incidental amounts of core hind-gut bacteria, suggesting that this core gut community does not contribute substantially to the conversion or preservation of pollen stores... This new finding contrasts markedly with the previous culture-dependent view...
Note: Dr. Anderson writes in a meticulous and precise scientific manner, appropriate for the journals in which he publishes (I again commend him for his exemplary backing up of each of his claims with accurate citations and supplemental data). It is polite scientific convention to say that a finding "contrasts markedly" with a previous view; a layman might say "man, did those guys get it wrong."
Identification Of The Microbes Involved (Via DNA Sequencing)
Hypotheses to test: if pollen is indeed inoculated by the bees with core gut bacteria in order to ferment it into beebread, then the bacterial species composition in beebread would shift towards core bacteria during the fermentation process.
Anderson found that: "The bacterial communities found in hive-stored pollen did not differ from those of newly collected pollen, but both sample types varied significantly by season." He found that only a small percentage of the bacteria found in freshly-gathered pollen loads were core hind-gut bacteria (in some cases as little as 3/10ths of a percent). Even more telling was that fermented beebread contained an even lower proportion of core gut bacteria than did newly-collected pollen.
Instead, the most common bacteria found in beebread were strains of Lactobacillus kunkeei. This floral/fruit bacterium thrives in fructose-rich aerobic environments, producing lactic acid as a metabolic byproduct, which has the benefit of making its environment inhospitable to competing yeasts and bacteria. Bees create an ideal environment for L. kunkeei by enriching pollen with fructose-rich nectar-thus its rapid preservation of beebread by the process of acidic "pickling." L. kunkeei is one of the few bacteria that can survive (perhaps in a dormant state) in honey and beebread, likely quickly rejuvenating when exposed to diluted nectar or honey in the crop.
Kirk and others [6]) have found that the bacterial community in bees may differ a bit from hive to hive, and by season or forage, but there is always a "core" hindgut biota (apparently passed via a fecal/oral route of some sort) [7]. The story is as yet far from complete, but it appears that honey bees have a commensal or mutualistic relationship with these core species, but also utilize free-living flower bacteria, such as L. kunkeei, to their advantage. An interesting recent study by Blum [8], working with the fruit fly Drosophila, points out that a host does not necessarily need to maintain a population of endosymbionts, but may instead continually replenish it via its food:
The Drosophila system may represent an alternative mutualism strategy that we term "quotidian replenishment," which is intended to indicate the need for daily replenishment to obtain a consistent [bacterial] community in the animal. In this model, the symbiotic community in Drosophila is maintained through frequent ingestion from an external reservoir of bacteria [its food]... Furthermore, our study shows that one member of the microbiome, Lactobacillus plantarum, protects the fly from intestinal pathogens. These results suggest that, although not always present, the microbiota can promote salubrious [9] effects for the host.
It appears that the honey bee may use a combination of vertical transmission (colony to daughter colony) of the core endosymbionts, coupled with the advantageous use of naturally-occurring floral bacteria (similar to the way that humans make sauerkraut or silage). Of interest is that some free-living bacteria can exert salubrious [10] effects on host immunity (which opens the market for bee probiotics) [11].
Bacterial Abundance During The Fermentation Process
Hypothesis tested: if pollen is indeed digested by core bacteria during the fermentation of beebread, then the number of those bacteria would increase during the process.
What Anderson found: that bacterial abundance increased only during the first two days of fermentation, and then decreased thereafter (Fig. 1). This finding does not support the digestion hypothesis, instead indicating that the formation of lactic acid acts to protect the pollen in beebread from microbial degradation.
Figure 1. After a day's fermentation, the bacterial count of stored pollen increased greatly from that of fresh incoming pollen, and then dropped sharply as the beebread became too acidic for further microbial growth. After Anderson (2014) [[i]].
[i] Kirk shared the raw data so that I could chart it out in a manner more understandable to the layman. See the original paper for his graph, which contains more information.
Nurse Bee Feeding Preference By Age Of Beebread
Hypothesis to be tested: if fermentation improved the nutritional quality of pollen, then it would follow that nurse bees would preferentially consume beebread that had fully fermented.
The Method: Kirk's team meticulously tracked the daily deposition or consumption of pollen in every cell of an active brood frame from each of 8 colonies over 5 days, repeated with different colonies in March, April, and May.
What Anderson found: The results are shown in Fig. 2. Although these measurements were taken during times of pollen surplus (as indicated by the fact that nearly 90% of the beebread cells were over 96 hrs old), the nurse bees appeared to preferentially consume either fresh incoming or slightly fermented pollen to aged beebread. This observation does not support the hypothesis that fermentation improves pollen nutritional quality.
Figure 2. Measurements were taken of the ages of beebread cells in the combs; the orange columns indicate the average number of cells present for each age class of beebread. The capped lines indicate the proportion of that age class of pollen consumed each day. There was apparently an aversion by bees to consume pollen that had undergone extended fermentation [[i]].
[i] Or perhaps a preference for fresh, or slightly fermented, pollen. The overall expected consumption rate for each age class of beebread predicted to be consumed at random based on its abundance on the frames was 9.3%. Compare that to the measured consumption rates shown. Kirk has shown me additional (as yet unpublished) data gathered this spring that shows that the relative consumption rate continues to drop for beebread aged 6, 7, or more days.
Note: despite the observation that bees clearly prefer fresher beebread to older, due to the overwhelming presence of aged beebread in the combs of the colonies he observed, the majority of total beebread consumed (other than the unmeasured consumption of freshly-gathered pollen) was over 96 hrs old, suggesting perhaps that bees make an effort to "rotate the stores."
The Pollen To Microbe Biomass Ratio
And now Anderson, in a stroke of brilliance, shot right to the crucial question: are there even enough bacteria present in beebread to exert a digestive effect? Bacteria lack teeth, and thus depend upon the enzymes that they produce in order to digest foodstuffs. Pollen does not make it easy for microbes to get to the good stuff inside the protective outer shell.
A pollen grain is enclosed in a tough coat called the exine. The exine is composed of a highly decay-resistant biopolymer called sporopollenin. Sporopollenin is so resistant to bacterial enzymes that "Pollen walls...often survive intact and recognizable for millions of years in bog and sediment deposits" [14]. The only place for bacteria to gain access to the nutritious innards of the pollen grain is through the (generally) one or more germination pores in the exine (these also serve as routes for water uptake). These pores are protected by a membrane called the intine, composed of cellulose and pectin. It is this layer that bacteria would need to digest their way through.
Kirk recognized that for bacteria to breach the intine of the pollen pores, that there would need to be a lot of them producing enzymes at those surfaces. So are there enough present? As I'm want to say, let's do the math! In this case, Kirk did it for us.
Hypothesis: that there are enough enzyme-producing bacteria present in beebread relative to the surface area of the pollen grains to digest their way through the pollen shells.
Kirk's math: He was generous on his estimate of the number of microbes present in mature beebread, quadrupling his actual colony counts to allow for culture bias and fungi, arriving at about 36,900 microbes per gram of pollen. He then counted pollen grains under a scope, estimating about 90 million pollen grains per gram. This works out to about 1 microbe per 2500 pollen grains (Fig. 3). To place this into biological perspective, a single grain of pollen in the bee hindgut is often covered with hundreds or thousands of bacteria (Fig. 4), busily digesting the remnants left over from the digestion that took place in the bee midgut.
As an imaginary visual analogy, I calculated that the proportion of bacteria per surface area of the pollen grains works out to the spatial equivalent of a single BB placed on a football field [15]--hardly enough to produce the enzymes necessary to digest their way through the pollen exine or intine.
Figure 3. A scanning electron micrograph of dried beebread. The pink substance is dried simple sugars, which constitute about 40-50% by weight. Note the distinct lack of bacteria. Electron micrographs courtesy Kirk Anderson.
Figure 4. For comparison, these pollen grains from a nurse bee hindgut are covered with live bacteria (stained purple).
Conclusion: there simply aren't enough microbes present in beebread to cause any significant degree of digestion of the pollen grain contents. Kirk succinctly concludes that: "Hive-stored pollen lacks the microbial biomass needed to alter pollen nutrition."
The Degree Of Digestion Of Hive-Stored Pollen
Kirk is hardly the first bee researcher to point out that beebread contains few microbes. Back in 1983 Klungess and Peng [15], using microscopy, found few microorganisms in fresh beebread (but more in dark, old beebread). They concluded that:
The substances, presumably nectar or diluted honey and enzymes from the ventriculus and salivary gland, that bees add to pollen during packing on to the corbiculae [pollen baskets] and into cells, and the bee bread ripening process, do not break down the pollen contents. Nor do the microorganisms associated with fresh and old bee bread appear to cause destruction of pollen intine or the cytoplasm. .. It is, therefore, proposed that the substances added to pollen by bees during storage function as a preservative. We found no visible evidence that these substances pre-digest the pollen so as to make the nutrients more available to bees during subsequent digestion and absorption.
Compare this to Peng's previous finding that most (but not all) pollen grains are rapidly digested during their passage through the nurse bee midgut, which contains few microbes [16].
Hypothesis: if bacteria indeed digest the pollen grains in beebread, this should be easily observed through microscopy.
Anderson's finding: "There were no discernible morphological differences between newly collected and hive-stored pollen."
This should be something that any beekeeper could easily verify for him/herself. So I looked at aged beebread from my own hives under the scope (at 400 and 1000x), and also found very few microorganisms or digested pollen grains (Figs. 5-7).
Figure 5. Pollen grains in aged beebread under light microscopy. Note the relative absence of yeast or bacteria, and the unbreached (not misshapen) exines and intact colored contents of the pollen grains.
Figure 6. Pollen grains from beebread that I diluted with a weak sugar solution and allowed to ferment for 10 days. Note the abundant yeast and bacterial cells in the background (unfortunately there was not enough depth of field to bring both the pollen and microbes simultaneously into focus). Despite being exposed to over a week of vigorous aerobic fermentation, these pollen grains remain intact and undigested. Compare these intact grains to those below.
Figure 7. A sample of digested pollen from the hindgut of a nurse bee. Note how most of the pollen shells are empty (no longer yellow inside) and distorted, indicating digestion of the contents.
Conclusion: the bee midgut can quickly empty pollen grains and digest the contents. But such digestion does not occur when bacteria and yeast ferment pollen into beebread.
Dr. Anderson's Conclusions
Our combined results do not support the hypothesis that hive-stored pollen of honey bees involves nutrient conversion or predigestion by microbes prior to consumption.
The bacterial communities found in hive-stored pollen did not differ from those of newly collected pollen, but both sample types varied significantly by season. This result indicates the lack of an emergent 'core' bacterial community co-evolved to predigest pollen.
Relative to other plant material involving microbial digestion or extensive fermentation, hive-stored pollen contains very few microbes.
The absolute number of bacteria in hive-stored pollen decreases with storage time, indicating that it is not a suitable medium for microbial growth.
The preferential consumption of freshly collected pollen indicates that bees have not evolved to rely on microbes or other time-related factors for pollen predigestion.
The microbe to pollen grain ratio is many orders of magnitude removed from that required to alter hive-stored pollen.
Regardless of sampled season or the taxonomic character of microbial communities, microscopic examination revealed no intermediate stage of pollen digestion in hive-stored pollen.
Based on these collective findings, we suggest that stored pollen is a preservative environment governed largely by nonmicrobial additions of nectar, honey and bee glandular secretions.
Summary
Flowers and pollinators have coevolved over millions of years, and along with them microbes always at the ready to consume them, or perhaps establish symbiotic relationships. Since microbes are invisible to the naked eye, it is difficult for us to grasp their degree of prevalence in the environment, or to understand their contribution to bee nutrition and health.
There may be a million bacteria (along with yeasts and other fungi) per milliliter in nectar when bees first collect it--fresh nectar is often already starting to ferment [18]. Pollen contains somewhat fewer microbes, but is still very biologically active when first gathered. The greatest concentration of microbes in the hive is in the residual undigested material in the bees' hindguts--that of a single bee may contain hundreds of millions of bacteria [19].
Kirk points out that the fluctuation of pollen availability has likely "selected for the quick turnover of the most readily available pollen nutrients into a 'nutritional reservoir' of living tissue (i.e. larva and worker fat bodies). In such a state, nutritional reserves are better protected from microbial digestion, more quickly shared among hive members and easier to digest than hive-stored pollen."
The above observation reminds us that hungry nurse bees readily consume larvae that they had previously been lavishing with jelly when it was abundant. The larvae thus function as a living protein reserve that through cannibalism can be quickly converted back into jelly or used to replenish fat bodies.
The honey bee, similar to humans, stores surplus food (that can't be immediately consumed) for later consumption (mainly to survive the winter). Like us, bees have figured out similar ways to prevent that food from being decomposed by microbes. Both nectar and pollen are prepared for prolonged storage by using a combination of high sugar concentration for osmotic preservative effect (similar to making jam), acidification via bacterial lactic acid production (pickling), and the addition of salivary antimicrobial compounds such as glucose oxidase (food preservatives).
Two key bacteria in this preservation process are the acid-resistant and osmotolerant [20] Lactobacillus kunkeei and Parasaccharibacter apium, both of which appear to be instrumental in hive hygiene, food storage, and larval health.
The microbial community in the hive is dynamic and evolving, not only in the gut of every bee during its short life, but also hour by hour during the fermentation of beebread. The microbiomes of the hive rapidly "adapt to changing diets and conditions not only by shifting community membership but also by changing gene content via horizontal gene transfer." Bacteria, by continually swapping genes, can adapt and evolve at a rate inconceivable to humans.
In the extended flower-pollinator community, pollinators vector microbes (including pathogens) with a remarkably high degree of efficiency. Graystock [21] found surprisingly efficient transmission of pathogens from bee to bee during flower visitations--the same would be expected to apply to hive or gut bacteria. This is due to the fact that the toilet hygiene of flying insects is rudimentary at best, resulting in plenty of fecal bacteria being inadvertently transferred to flower surfaces during pollinator visits (after all, just think about the degree of pollen transfer from flower to flower). And such transmission can be interspecific--any bee, fly, butterfly, beetle, or wasp can carry floral or pathogenic microbes from one flower to another. The total amount of microbial interchange within the entire flower/pollinator environment is mind boggling to consider, and makes for a highly dynamic system of microbial and pathogen interactions that we are only beginning to understand.
Next
The biological and chemical processes that take place during the fermentation of beebread, yeasts and fungi, probiotics, and the Anderson labs' current research projects.
References And Notes
[1] Published as Anderson, KE, MJ CarrolL, T Sheehan, BM Mott, P Maes and V Corby-Harris (2014) Hive-stored pollen of honey bees: many lines of evidence are consistent with pollen preservation, not nutrient conversion. Molecular Ecology 23: 5904-5917.
[2] Mainly from the above citation, but also from other published and as yet unpublished research. I also took the liberty to edit or reorder the quotations from his papers for readability.
[3] Vasquez A, Olofsson TC (2011) The honey crop - the holy grail when antibiotics fail. Microbiology Today, 38, 226-229.
[4] Fridman S, et al (2012) Bacterial communities in floral nectar. Environ. Microbiol. Rep 4:97-104.
[5] See my previous articles in this series.
[6] Disayathanoowat, T, et al (2012) T-RFLP analysis of bacterial communities in the midguts of Apis mellifera and Apis cerana honey bees in Thailand. Journal of Apicultural Research 51(4): 312-319.
[7] Don't be grossed out--the same thing happens with humans and many other animals.
[8] Blum JE, et al (2013) Frequent replenishment sustains the beneficial microbiome of Drosophila melanogaster. mBio 4(6):e00860-13. doi: 10.1128/mBio.00860-13
[9] Salubrious-healthful, beneficial, wholesome. Man, I gotta add this descriptive word to my vocabulary!
[10] I couldn't wait.
[11] Again, I've yet to see any hard data that any probiotic currently on the market is of benefit to bees. But I wouldn't be the least surprised if some were developed in the near future. But don't just go feeding any untested probiotic--a recent study found that some can seriously harm bees:
Ptaszynska, AA, et al (2015) Are commercial probiotics and prebiotics effective in the treatment and prevention of honeybee nosemosis C? Parasitol Res DOI 10.1007/s00436-015-4761-z Open access.
[12] Kirk shared the raw data so that I could chart it out in a manner more understandable to the layman. See the original paper for his graph, which contains more information.
[13] Or perhaps a preference for fresh, or slightly fermented, pollen. The overall expected consumption rate for each age class of beebread predicted to be consumed at random based on its abundance on the frames was 9.3%. Compare that to the measured consumption rates shown. Kirk has shown me additional (as yet unpublished) data gathered this spring that shows that the relative consumption rate continues to drop for beebread aged 6, 7, or more days.
Note: despite the observation that bees clearly prefer fresher beebread to older, due to the overwhelming presence of aged beebread in the combs of the colonies he observed, the majority of total beebread consumed (other than the unmeasured consumption of freshly-gathered pollen) was over 96 hrs old, suggesting perhaps that bees make an effort to "rotate the stores."
[14] Roulston, THI and JH Cane (2000) Pollen nutritional content and digestibility for animals. Plant Systematics 222: 187-209.
[15] By my math.
[16] Klungness L. M., Peng Y.-S. (1983) A scanning electron microscopic study of pollen loads collected and stored by honeybees. J. Apicul. Res. 22: 264-271.
[17] Peng YS, ME Nasr, et al (1985) The digestion of dandelion pollen by adult worker honeybees. Physiol. Entomol. 10: 75-82.
[18] Castillo, C, et al (2012) Seasonal variation in the titers and biosynthesis of the primer pheromone ethyl oleate in honey bees. J Insect Physiol 58(8):1112-21.
[19] Estimate, Kirk Anderson, pers comm.
[20] Osmotolerance is the ability to live in high-sugar environment that would dessicate other microbes.
[21] Graystock P, et al (2015) Parasites in bloom: flowers aid dispersal and transmission of pollinator parasites within and between bee species. Proc. R. Soc. B 282: 20151371. http://dx.doi.org/10.1098/rspb.2015.1371
Category: Bee Nutrition
Tags: beebread, digestion, DNA sequencing, Dr. Anderson, fermentation, hive-stored pollen, microbe biomass | microbe biomass Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/microbe-biomass/ |
Reevaluating Beebread: Part 3 - For Preservation or Digestion?
First published in: American Bee Journal, December 2015
Reevaluating Beebread: Part 3
For Preservation Or Digestion?
Randy Oliver
ScientificBeekeeping.com
First published in ABJ Dec 2015
CONTENTS
Anderson's Investigatory Approach
Previous Research
Identification Of The Microbes Involved (via DNA Sequencing)
Bacterial Abundance During The Fermentation Process
Nurse Bee Feeding Preference By Age Of Beebread
The Pollen To Microbe Biomass Ratio
The Degree Of Digestion Of Hive-Stored Pollen
Dr. Anderson's Conclusions
Summary
Next
References And Notes
We've now identified the bacterial players. So let's see what Dr. Kirk Anderson's lab has found to date about why bees turn raw pollen into beebread.
In this article, I'm going to briefly summarize Dr. Anderson's well-designed investigations [1]. My readers know that I can be critical of sloppy science; conversely, I feel that truly exemplary scientific research should receive kudos. The investigation by Kirk and his associates meets this standard, and is a textbook example of good scientific research and writing. Kirk laid out his investigation methodically, questioning each premise of the "predigestion hypothesis," and seeing whether there was actual evidence either supporting or refuting the claim. I will quote from Kirk's papers extensively in italics [2].
Anderson's Investigatory Approach
Scientists typically specify the hypothesis to be tested and lay out their game plan:
It was hypothesized that co-evolved microbes orchestrate the long-term conversion of stored pollen into a more nutritious food source, a process involving microbial succession, anaerobic breakdown of materials, the release of pollen cell contents and/or predigestion by moulds. Here, we use a multifaceted approach to determine whether hive-stored pollen of honey bees involves significant nutrient conversion or 'pre-digestion' by microbes. To this end, we explore [reordered]
whether the differences in bacterial richness and diversity between newly collected and hive-stored pollen are consistent with a preservation or nutrient conversion environment
the absolute number of bacteria in stored pollen,
the association between bacterial abundance and pollen storage time,
the time period associated with pollen storage prior to ingestion by nurse bees,
the pollen to microbe biomass ratio, and
the degree of digestion of hive-stored pollen
Previous Research
Hypothesis to be tested: whether the fermentation of beebread requires inoculation of the pollen with symbiotic "core" gut bacteria via the crop as proposed by Vasquez and Olofsson [3]: "Our research has identified the bacteria involved and revealed that bees, in producing bee bread, add all the beneficial [lactic acid bacteria] to the pollen when they collect it at the site of the flower."
Vasquez and Olofsson's early research was very exciting, but they apparently overstated the case in claiming that bees added all the beneficial lactic acid bacteria to pollen, and especially that those bacteria came from the crop. Scientists already knew that pollen, and especially nectar, typically contains lactic acid and other bacteria prior to being visited by bees [4]. And subsequent research by others found that there were very few bacteria in the bee crop [5]. The question then is whether the pollen loads of returning foragers showed signs of being spiked with the core gut bacteria.
What Anderson found: In previous work, we determined that freshly-collected pollen from returning foragers or beebread contains incidental amounts of core hind-gut bacteria, suggesting that this core gut community does not contribute substantially to the conversion or preservation of pollen stores... This new finding contrasts markedly with the previous culture-dependent view...
Note: Dr. Anderson writes in a meticulous and precise scientific manner, appropriate for the journals in which he publishes (I again commend him for his exemplary backing up of each of his claims with accurate citations and supplemental data). It is polite scientific convention to say that a finding "contrasts markedly" with a previous view; a layman might say "man, did those guys get it wrong."
Identification Of The Microbes Involved (Via DNA Sequencing)
Hypotheses to test: if pollen is indeed inoculated by the bees with core gut bacteria in order to ferment it into beebread, then the bacterial species composition in beebread would shift towards core bacteria during the fermentation process.
Anderson found that: "The bacterial communities found in hive-stored pollen did not differ from those of newly collected pollen, but both sample types varied significantly by season." He found that only a small percentage of the bacteria found in freshly-gathered pollen loads were core hind-gut bacteria (in some cases as little as 3/10ths of a percent). Even more telling was that fermented beebread contained an even lower proportion of core gut bacteria than did newly-collected pollen.
Instead, the most common bacteria found in beebread were strains of Lactobacillus kunkeei. This floral/fruit bacterium thrives in fructose-rich aerobic environments, producing lactic acid as a metabolic byproduct, which has the benefit of making its environment inhospitable to competing yeasts and bacteria. Bees create an ideal environment for L. kunkeei by enriching pollen with fructose-rich nectar-thus its rapid preservation of beebread by the process of acidic "pickling." L. kunkeei is one of the few bacteria that can survive (perhaps in a dormant state) in honey and beebread, likely quickly rejuvenating when exposed to diluted nectar or honey in the crop.
Kirk and others [6]) have found that the bacterial community in bees may differ a bit from hive to hive, and by season or forage, but there is always a "core" hindgut biota (apparently passed via a fecal/oral route of some sort) [7]. The story is as yet far from complete, but it appears that honey bees have a commensal or mutualistic relationship with these core species, but also utilize free-living flower bacteria, such as L. kunkeei, to their advantage. An interesting recent study by Blum [8], working with the fruit fly Drosophila, points out that a host does not necessarily need to maintain a population of endosymbionts, but may instead continually replenish it via its food:
The Drosophila system may represent an alternative mutualism strategy that we term "quotidian replenishment," which is intended to indicate the need for daily replenishment to obtain a consistent [bacterial] community in the animal. In this model, the symbiotic community in Drosophila is maintained through frequent ingestion from an external reservoir of bacteria [its food]... Furthermore, our study shows that one member of the microbiome, Lactobacillus plantarum, protects the fly from intestinal pathogens. These results suggest that, although not always present, the microbiota can promote salubrious [9] effects for the host.
It appears that the honey bee may use a combination of vertical transmission (colony to daughter colony) of the core endosymbionts, coupled with the advantageous use of naturally-occurring floral bacteria (similar to the way that humans make sauerkraut or silage). Of interest is that some free-living bacteria can exert salubrious [10] effects on host immunity (which opens the market for bee probiotics) [11].
Bacterial Abundance During The Fermentation Process
Hypothesis tested: if pollen is indeed digested by core bacteria during the fermentation of beebread, then the number of those bacteria would increase during the process.
What Anderson found: that bacterial abundance increased only during the first two days of fermentation, and then decreased thereafter (Fig. 1). This finding does not support the digestion hypothesis, instead indicating that the formation of lactic acid acts to protect the pollen in beebread from microbial degradation.
Figure 1. After a day's fermentation, the bacterial count of stored pollen increased greatly from that of fresh incoming pollen, and then dropped sharply as the beebread became too acidic for further microbial growth. After Anderson (2014) [[i]].
[i] Kirk shared the raw data so that I could chart it out in a manner more understandable to the layman. See the original paper for his graph, which contains more information.
Nurse Bee Feeding Preference By Age Of Beebread
Hypothesis to be tested: if fermentation improved the nutritional quality of pollen, then it would follow that nurse bees would preferentially consume beebread that had fully fermented.
The Method: Kirk's team meticulously tracked the daily deposition or consumption of pollen in every cell of an active brood frame from each of 8 colonies over 5 days, repeated with different colonies in March, April, and May.
What Anderson found: The results are shown in Fig. 2. Although these measurements were taken during times of pollen surplus (as indicated by the fact that nearly 90% of the beebread cells were over 96 hrs old), the nurse bees appeared to preferentially consume either fresh incoming or slightly fermented pollen to aged beebread. This observation does not support the hypothesis that fermentation improves pollen nutritional quality.
Figure 2. Measurements were taken of the ages of beebread cells in the combs; the orange columns indicate the average number of cells present for each age class of beebread. The capped lines indicate the proportion of that age class of pollen consumed each day. There was apparently an aversion by bees to consume pollen that had undergone extended fermentation [[i]].
[i] Or perhaps a preference for fresh, or slightly fermented, pollen. The overall expected consumption rate for each age class of beebread predicted to be consumed at random based on its abundance on the frames was 9.3%. Compare that to the measured consumption rates shown. Kirk has shown me additional (as yet unpublished) data gathered this spring that shows that the relative consumption rate continues to drop for beebread aged 6, 7, or more days.
Note: despite the observation that bees clearly prefer fresher beebread to older, due to the overwhelming presence of aged beebread in the combs of the colonies he observed, the majority of total beebread consumed (other than the unmeasured consumption of freshly-gathered pollen) was over 96 hrs old, suggesting perhaps that bees make an effort to "rotate the stores."
The Pollen To Microbe Biomass Ratio
And now Anderson, in a stroke of brilliance, shot right to the crucial question: are there even enough bacteria present in beebread to exert a digestive effect? Bacteria lack teeth, and thus depend upon the enzymes that they produce in order to digest foodstuffs. Pollen does not make it easy for microbes to get to the good stuff inside the protective outer shell.
A pollen grain is enclosed in a tough coat called the exine. The exine is composed of a highly decay-resistant biopolymer called sporopollenin. Sporopollenin is so resistant to bacterial enzymes that "Pollen walls...often survive intact and recognizable for millions of years in bog and sediment deposits" [14]. The only place for bacteria to gain access to the nutritious innards of the pollen grain is through the (generally) one or more germination pores in the exine (these also serve as routes for water uptake). These pores are protected by a membrane called the intine, composed of cellulose and pectin. It is this layer that bacteria would need to digest their way through.
Kirk recognized that for bacteria to breach the intine of the pollen pores, that there would need to be a lot of them producing enzymes at those surfaces. So are there enough present? As I'm want to say, let's do the math! In this case, Kirk did it for us.
Hypothesis: that there are enough enzyme-producing bacteria present in beebread relative to the surface area of the pollen grains to digest their way through the pollen shells.
Kirk's math: He was generous on his estimate of the number of microbes present in mature beebread, quadrupling his actual colony counts to allow for culture bias and fungi, arriving at about 36,900 microbes per gram of pollen. He then counted pollen grains under a scope, estimating about 90 million pollen grains per gram. This works out to about 1 microbe per 2500 pollen grains (Fig. 3). To place this into biological perspective, a single grain of pollen in the bee hindgut is often covered with hundreds or thousands of bacteria (Fig. 4), busily digesting the remnants left over from the digestion that took place in the bee midgut.
As an imaginary visual analogy, I calculated that the proportion of bacteria per surface area of the pollen grains works out to the spatial equivalent of a single BB placed on a football field [15]--hardly enough to produce the enzymes necessary to digest their way through the pollen exine or intine.
Figure 3. A scanning electron micrograph of dried beebread. The pink substance is dried simple sugars, which constitute about 40-50% by weight. Note the distinct lack of bacteria. Electron micrographs courtesy Kirk Anderson.
Figure 4. For comparison, these pollen grains from a nurse bee hindgut are covered with live bacteria (stained purple).
Conclusion: there simply aren't enough microbes present in beebread to cause any significant degree of digestion of the pollen grain contents. Kirk succinctly concludes that: "Hive-stored pollen lacks the microbial biomass needed to alter pollen nutrition."
The Degree Of Digestion Of Hive-Stored Pollen
Kirk is hardly the first bee researcher to point out that beebread contains few microbes. Back in 1983 Klungess and Peng [15], using microscopy, found few microorganisms in fresh beebread (but more in dark, old beebread). They concluded that:
The substances, presumably nectar or diluted honey and enzymes from the ventriculus and salivary gland, that bees add to pollen during packing on to the corbiculae [pollen baskets] and into cells, and the bee bread ripening process, do not break down the pollen contents. Nor do the microorganisms associated with fresh and old bee bread appear to cause destruction of pollen intine or the cytoplasm. .. It is, therefore, proposed that the substances added to pollen by bees during storage function as a preservative. We found no visible evidence that these substances pre-digest the pollen so as to make the nutrients more available to bees during subsequent digestion and absorption.
Compare this to Peng's previous finding that most (but not all) pollen grains are rapidly digested during their passage through the nurse bee midgut, which contains few microbes [16].
Hypothesis: if bacteria indeed digest the pollen grains in beebread, this should be easily observed through microscopy.
Anderson's finding: "There were no discernible morphological differences between newly collected and hive-stored pollen."
This should be something that any beekeeper could easily verify for him/herself. So I looked at aged beebread from my own hives under the scope (at 400 and 1000x), and also found very few microorganisms or digested pollen grains (Figs. 5-7).
Figure 5. Pollen grains in aged beebread under light microscopy. Note the relative absence of yeast or bacteria, and the unbreached (not misshapen) exines and intact colored contents of the pollen grains.
Figure 6. Pollen grains from beebread that I diluted with a weak sugar solution and allowed to ferment for 10 days. Note the abundant yeast and bacterial cells in the background (unfortunately there was not enough depth of field to bring both the pollen and microbes simultaneously into focus). Despite being exposed to over a week of vigorous aerobic fermentation, these pollen grains remain intact and undigested. Compare these intact grains to those below.
Figure 7. A sample of digested pollen from the hindgut of a nurse bee. Note how most of the pollen shells are empty (no longer yellow inside) and distorted, indicating digestion of the contents.
Conclusion: the bee midgut can quickly empty pollen grains and digest the contents. But such digestion does not occur when bacteria and yeast ferment pollen into beebread.
Dr. Anderson's Conclusions
Our combined results do not support the hypothesis that hive-stored pollen of honey bees involves nutrient conversion or predigestion by microbes prior to consumption.
The bacterial communities found in hive-stored pollen did not differ from those of newly collected pollen, but both sample types varied significantly by season. This result indicates the lack of an emergent 'core' bacterial community co-evolved to predigest pollen.
Relative to other plant material involving microbial digestion or extensive fermentation, hive-stored pollen contains very few microbes.
The absolute number of bacteria in hive-stored pollen decreases with storage time, indicating that it is not a suitable medium for microbial growth.
The preferential consumption of freshly collected pollen indicates that bees have not evolved to rely on microbes or other time-related factors for pollen predigestion.
The microbe to pollen grain ratio is many orders of magnitude removed from that required to alter hive-stored pollen.
Regardless of sampled season or the taxonomic character of microbial communities, microscopic examination revealed no intermediate stage of pollen digestion in hive-stored pollen.
Based on these collective findings, we suggest that stored pollen is a preservative environment governed largely by nonmicrobial additions of nectar, honey and bee glandular secretions.
Summary
Flowers and pollinators have coevolved over millions of years, and along with them microbes always at the ready to consume them, or perhaps establish symbiotic relationships. Since microbes are invisible to the naked eye, it is difficult for us to grasp their degree of prevalence in the environment, or to understand their contribution to bee nutrition and health.
There may be a million bacteria (along with yeasts and other fungi) per milliliter in nectar when bees first collect it--fresh nectar is often already starting to ferment [18]. Pollen contains somewhat fewer microbes, but is still very biologically active when first gathered. The greatest concentration of microbes in the hive is in the residual undigested material in the bees' hindguts--that of a single bee may contain hundreds of millions of bacteria [19].
Kirk points out that the fluctuation of pollen availability has likely "selected for the quick turnover of the most readily available pollen nutrients into a 'nutritional reservoir' of living tissue (i.e. larva and worker fat bodies). In such a state, nutritional reserves are better protected from microbial digestion, more quickly shared among hive members and easier to digest than hive-stored pollen."
The above observation reminds us that hungry nurse bees readily consume larvae that they had previously been lavishing with jelly when it was abundant. The larvae thus function as a living protein reserve that through cannibalism can be quickly converted back into jelly or used to replenish fat bodies.
The honey bee, similar to humans, stores surplus food (that can't be immediately consumed) for later consumption (mainly to survive the winter). Like us, bees have figured out similar ways to prevent that food from being decomposed by microbes. Both nectar and pollen are prepared for prolonged storage by using a combination of high sugar concentration for osmotic preservative effect (similar to making jam), acidification via bacterial lactic acid production (pickling), and the addition of salivary antimicrobial compounds such as glucose oxidase (food preservatives).
Two key bacteria in this preservation process are the acid-resistant and osmotolerant [20] Lactobacillus kunkeei and Parasaccharibacter apium, both of which appear to be instrumental in hive hygiene, food storage, and larval health.
The microbial community in the hive is dynamic and evolving, not only in the gut of every bee during its short life, but also hour by hour during the fermentation of beebread. The microbiomes of the hive rapidly "adapt to changing diets and conditions not only by shifting community membership but also by changing gene content via horizontal gene transfer." Bacteria, by continually swapping genes, can adapt and evolve at a rate inconceivable to humans.
In the extended flower-pollinator community, pollinators vector microbes (including pathogens) with a remarkably high degree of efficiency. Graystock [21] found surprisingly efficient transmission of pathogens from bee to bee during flower visitations--the same would be expected to apply to hive or gut bacteria. This is due to the fact that the toilet hygiene of flying insects is rudimentary at best, resulting in plenty of fecal bacteria being inadvertently transferred to flower surfaces during pollinator visits (after all, just think about the degree of pollen transfer from flower to flower). And such transmission can be interspecific--any bee, fly, butterfly, beetle, or wasp can carry floral or pathogenic microbes from one flower to another. The total amount of microbial interchange within the entire flower/pollinator environment is mind boggling to consider, and makes for a highly dynamic system of microbial and pathogen interactions that we are only beginning to understand.
Next
The biological and chemical processes that take place during the fermentation of beebread, yeasts and fungi, probiotics, and the Anderson labs' current research projects.
References And Notes
[1] Published as Anderson, KE, MJ CarrolL, T Sheehan, BM Mott, P Maes and V Corby-Harris (2014) Hive-stored pollen of honey bees: many lines of evidence are consistent with pollen preservation, not nutrient conversion. Molecular Ecology 23: 5904-5917.
[2] Mainly from the above citation, but also from other published and as yet unpublished research. I also took the liberty to edit or reorder the quotations from his papers for readability.
[3] Vasquez A, Olofsson TC (2011) The honey crop - the holy grail when antibiotics fail. Microbiology Today, 38, 226-229.
[4] Fridman S, et al (2012) Bacterial communities in floral nectar. Environ. Microbiol. Rep 4:97-104.
[5] See my previous articles in this series.
[6] Disayathanoowat, T, et al (2012) T-RFLP analysis of bacterial communities in the midguts of Apis mellifera and Apis cerana honey bees in Thailand. Journal of Apicultural Research 51(4): 312-319.
[7] Don't be grossed out--the same thing happens with humans and many other animals.
[8] Blum JE, et al (2013) Frequent replenishment sustains the beneficial microbiome of Drosophila melanogaster. mBio 4(6):e00860-13. doi: 10.1128/mBio.00860-13
[9] Salubrious-healthful, beneficial, wholesome. Man, I gotta add this descriptive word to my vocabulary!
[10] I couldn't wait.
[11] Again, I've yet to see any hard data that any probiotic currently on the market is of benefit to bees. But I wouldn't be the least surprised if some were developed in the near future. But don't just go feeding any untested probiotic--a recent study found that some can seriously harm bees:
Ptaszynska, AA, et al (2015) Are commercial probiotics and prebiotics effective in the treatment and prevention of honeybee nosemosis C? Parasitol Res DOI 10.1007/s00436-015-4761-z Open access.
[12] Kirk shared the raw data so that I could chart it out in a manner more understandable to the layman. See the original paper for his graph, which contains more information.
[13] Or perhaps a preference for fresh, or slightly fermented, pollen. The overall expected consumption rate for each age class of beebread predicted to be consumed at random based on its abundance on the frames was 9.3%. Compare that to the measured consumption rates shown. Kirk has shown me additional (as yet unpublished) data gathered this spring that shows that the relative consumption rate continues to drop for beebread aged 6, 7, or more days.
Note: despite the observation that bees clearly prefer fresher beebread to older, due to the overwhelming presence of aged beebread in the combs of the colonies he observed, the majority of total beebread consumed (other than the unmeasured consumption of freshly-gathered pollen) was over 96 hrs old, suggesting perhaps that bees make an effort to "rotate the stores."
[14] Roulston, THI and JH Cane (2000) Pollen nutritional content and digestibility for animals. Plant Systematics 222: 187-209.
[15] By my math.
[16] Klungness L. M., Peng Y.-S. (1983) A scanning electron microscopic study of pollen loads collected and stored by honeybees. J. Apicul. Res. 22: 264-271.
[17] Peng YS, ME Nasr, et al (1985) The digestion of dandelion pollen by adult worker honeybees. Physiol. Entomol. 10: 75-82.
[18] Castillo, C, et al (2012) Seasonal variation in the titers and biosynthesis of the primer pheromone ethyl oleate in honey bees. J Insect Physiol 58(8):1112-21.
[19] Estimate, Kirk Anderson, pers comm.
[20] Osmotolerance is the ability to live in high-sugar environment that would dessicate other microbes.
[21] Graystock P, et al (2015) Parasites in bloom: flowers aid dispersal and transmission of pollinator parasites within and between bee species. Proc. R. Soc. B 282: 20151371. http://dx.doi.org/10.1098/rspb.2015.1371
Category: Bee Nutrition
Tags: beebread, digestion, DNA sequencing, Dr. Anderson, fermentation, hive-stored pollen, microbe biomass | fermentation Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/fermentation/ |
Reevaluating Beebread: Part 3 - For Preservation or Digestion?
First published in: American Bee Journal, December 2015
Reevaluating Beebread: Part 3
For Preservation Or Digestion?
Randy Oliver
ScientificBeekeeping.com
First published in ABJ Dec 2015
CONTENTS
Anderson's Investigatory Approach
Previous Research
Identification Of The Microbes Involved (via DNA Sequencing)
Bacterial Abundance During The Fermentation Process
Nurse Bee Feeding Preference By Age Of Beebread
The Pollen To Microbe Biomass Ratio
The Degree Of Digestion Of Hive-Stored Pollen
Dr. Anderson's Conclusions
Summary
Next
References And Notes
We've now identified the bacterial players. So let's see what Dr. Kirk Anderson's lab has found to date about why bees turn raw pollen into beebread.
In this article, I'm going to briefly summarize Dr. Anderson's well-designed investigations [1]. My readers know that I can be critical of sloppy science; conversely, I feel that truly exemplary scientific research should receive kudos. The investigation by Kirk and his associates meets this standard, and is a textbook example of good scientific research and writing. Kirk laid out his investigation methodically, questioning each premise of the "predigestion hypothesis," and seeing whether there was actual evidence either supporting or refuting the claim. I will quote from Kirk's papers extensively in italics [2].
Anderson's Investigatory Approach
Scientists typically specify the hypothesis to be tested and lay out their game plan:
It was hypothesized that co-evolved microbes orchestrate the long-term conversion of stored pollen into a more nutritious food source, a process involving microbial succession, anaerobic breakdown of materials, the release of pollen cell contents and/or predigestion by moulds. Here, we use a multifaceted approach to determine whether hive-stored pollen of honey bees involves significant nutrient conversion or 'pre-digestion' by microbes. To this end, we explore [reordered]
whether the differences in bacterial richness and diversity between newly collected and hive-stored pollen are consistent with a preservation or nutrient conversion environment
the absolute number of bacteria in stored pollen,
the association between bacterial abundance and pollen storage time,
the time period associated with pollen storage prior to ingestion by nurse bees,
the pollen to microbe biomass ratio, and
the degree of digestion of hive-stored pollen
Previous Research
Hypothesis to be tested: whether the fermentation of beebread requires inoculation of the pollen with symbiotic "core" gut bacteria via the crop as proposed by Vasquez and Olofsson [3]: "Our research has identified the bacteria involved and revealed that bees, in producing bee bread, add all the beneficial [lactic acid bacteria] to the pollen when they collect it at the site of the flower."
Vasquez and Olofsson's early research was very exciting, but they apparently overstated the case in claiming that bees added all the beneficial lactic acid bacteria to pollen, and especially that those bacteria came from the crop. Scientists already knew that pollen, and especially nectar, typically contains lactic acid and other bacteria prior to being visited by bees [4]. And subsequent research by others found that there were very few bacteria in the bee crop [5]. The question then is whether the pollen loads of returning foragers showed signs of being spiked with the core gut bacteria.
What Anderson found: In previous work, we determined that freshly-collected pollen from returning foragers or beebread contains incidental amounts of core hind-gut bacteria, suggesting that this core gut community does not contribute substantially to the conversion or preservation of pollen stores... This new finding contrasts markedly with the previous culture-dependent view...
Note: Dr. Anderson writes in a meticulous and precise scientific manner, appropriate for the journals in which he publishes (I again commend him for his exemplary backing up of each of his claims with accurate citations and supplemental data). It is polite scientific convention to say that a finding "contrasts markedly" with a previous view; a layman might say "man, did those guys get it wrong."
Identification Of The Microbes Involved (Via DNA Sequencing)
Hypotheses to test: if pollen is indeed inoculated by the bees with core gut bacteria in order to ferment it into beebread, then the bacterial species composition in beebread would shift towards core bacteria during the fermentation process.
Anderson found that: "The bacterial communities found in hive-stored pollen did not differ from those of newly collected pollen, but both sample types varied significantly by season." He found that only a small percentage of the bacteria found in freshly-gathered pollen loads were core hind-gut bacteria (in some cases as little as 3/10ths of a percent). Even more telling was that fermented beebread contained an even lower proportion of core gut bacteria than did newly-collected pollen.
Instead, the most common bacteria found in beebread were strains of Lactobacillus kunkeei. This floral/fruit bacterium thrives in fructose-rich aerobic environments, producing lactic acid as a metabolic byproduct, which has the benefit of making its environment inhospitable to competing yeasts and bacteria. Bees create an ideal environment for L. kunkeei by enriching pollen with fructose-rich nectar-thus its rapid preservation of beebread by the process of acidic "pickling." L. kunkeei is one of the few bacteria that can survive (perhaps in a dormant state) in honey and beebread, likely quickly rejuvenating when exposed to diluted nectar or honey in the crop.
Kirk and others [6]) have found that the bacterial community in bees may differ a bit from hive to hive, and by season or forage, but there is always a "core" hindgut biota (apparently passed via a fecal/oral route of some sort) [7]. The story is as yet far from complete, but it appears that honey bees have a commensal or mutualistic relationship with these core species, but also utilize free-living flower bacteria, such as L. kunkeei, to their advantage. An interesting recent study by Blum [8], working with the fruit fly Drosophila, points out that a host does not necessarily need to maintain a population of endosymbionts, but may instead continually replenish it via its food:
The Drosophila system may represent an alternative mutualism strategy that we term "quotidian replenishment," which is intended to indicate the need for daily replenishment to obtain a consistent [bacterial] community in the animal. In this model, the symbiotic community in Drosophila is maintained through frequent ingestion from an external reservoir of bacteria [its food]... Furthermore, our study shows that one member of the microbiome, Lactobacillus plantarum, protects the fly from intestinal pathogens. These results suggest that, although not always present, the microbiota can promote salubrious [9] effects for the host.
It appears that the honey bee may use a combination of vertical transmission (colony to daughter colony) of the core endosymbionts, coupled with the advantageous use of naturally-occurring floral bacteria (similar to the way that humans make sauerkraut or silage). Of interest is that some free-living bacteria can exert salubrious [10] effects on host immunity (which opens the market for bee probiotics) [11].
Bacterial Abundance During The Fermentation Process
Hypothesis tested: if pollen is indeed digested by core bacteria during the fermentation of beebread, then the number of those bacteria would increase during the process.
What Anderson found: that bacterial abundance increased only during the first two days of fermentation, and then decreased thereafter (Fig. 1). This finding does not support the digestion hypothesis, instead indicating that the formation of lactic acid acts to protect the pollen in beebread from microbial degradation.
Figure 1. After a day's fermentation, the bacterial count of stored pollen increased greatly from that of fresh incoming pollen, and then dropped sharply as the beebread became too acidic for further microbial growth. After Anderson (2014) [[i]].
[i] Kirk shared the raw data so that I could chart it out in a manner more understandable to the layman. See the original paper for his graph, which contains more information.
Nurse Bee Feeding Preference By Age Of Beebread
Hypothesis to be tested: if fermentation improved the nutritional quality of pollen, then it would follow that nurse bees would preferentially consume beebread that had fully fermented.
The Method: Kirk's team meticulously tracked the daily deposition or consumption of pollen in every cell of an active brood frame from each of 8 colonies over 5 days, repeated with different colonies in March, April, and May.
What Anderson found: The results are shown in Fig. 2. Although these measurements were taken during times of pollen surplus (as indicated by the fact that nearly 90% of the beebread cells were over 96 hrs old), the nurse bees appeared to preferentially consume either fresh incoming or slightly fermented pollen to aged beebread. This observation does not support the hypothesis that fermentation improves pollen nutritional quality.
Figure 2. Measurements were taken of the ages of beebread cells in the combs; the orange columns indicate the average number of cells present for each age class of beebread. The capped lines indicate the proportion of that age class of pollen consumed each day. There was apparently an aversion by bees to consume pollen that had undergone extended fermentation [[i]].
[i] Or perhaps a preference for fresh, or slightly fermented, pollen. The overall expected consumption rate for each age class of beebread predicted to be consumed at random based on its abundance on the frames was 9.3%. Compare that to the measured consumption rates shown. Kirk has shown me additional (as yet unpublished) data gathered this spring that shows that the relative consumption rate continues to drop for beebread aged 6, 7, or more days.
Note: despite the observation that bees clearly prefer fresher beebread to older, due to the overwhelming presence of aged beebread in the combs of the colonies he observed, the majority of total beebread consumed (other than the unmeasured consumption of freshly-gathered pollen) was over 96 hrs old, suggesting perhaps that bees make an effort to "rotate the stores."
The Pollen To Microbe Biomass Ratio
And now Anderson, in a stroke of brilliance, shot right to the crucial question: are there even enough bacteria present in beebread to exert a digestive effect? Bacteria lack teeth, and thus depend upon the enzymes that they produce in order to digest foodstuffs. Pollen does not make it easy for microbes to get to the good stuff inside the protective outer shell.
A pollen grain is enclosed in a tough coat called the exine. The exine is composed of a highly decay-resistant biopolymer called sporopollenin. Sporopollenin is so resistant to bacterial enzymes that "Pollen walls...often survive intact and recognizable for millions of years in bog and sediment deposits" [14]. The only place for bacteria to gain access to the nutritious innards of the pollen grain is through the (generally) one or more germination pores in the exine (these also serve as routes for water uptake). These pores are protected by a membrane called the intine, composed of cellulose and pectin. It is this layer that bacteria would need to digest their way through.
Kirk recognized that for bacteria to breach the intine of the pollen pores, that there would need to be a lot of them producing enzymes at those surfaces. So are there enough present? As I'm want to say, let's do the math! In this case, Kirk did it for us.
Hypothesis: that there are enough enzyme-producing bacteria present in beebread relative to the surface area of the pollen grains to digest their way through the pollen shells.
Kirk's math: He was generous on his estimate of the number of microbes present in mature beebread, quadrupling his actual colony counts to allow for culture bias and fungi, arriving at about 36,900 microbes per gram of pollen. He then counted pollen grains under a scope, estimating about 90 million pollen grains per gram. This works out to about 1 microbe per 2500 pollen grains (Fig. 3). To place this into biological perspective, a single grain of pollen in the bee hindgut is often covered with hundreds or thousands of bacteria (Fig. 4), busily digesting the remnants left over from the digestion that took place in the bee midgut.
As an imaginary visual analogy, I calculated that the proportion of bacteria per surface area of the pollen grains works out to the spatial equivalent of a single BB placed on a football field [15]--hardly enough to produce the enzymes necessary to digest their way through the pollen exine or intine.
Figure 3. A scanning electron micrograph of dried beebread. The pink substance is dried simple sugars, which constitute about 40-50% by weight. Note the distinct lack of bacteria. Electron micrographs courtesy Kirk Anderson.
Figure 4. For comparison, these pollen grains from a nurse bee hindgut are covered with live bacteria (stained purple).
Conclusion: there simply aren't enough microbes present in beebread to cause any significant degree of digestion of the pollen grain contents. Kirk succinctly concludes that: "Hive-stored pollen lacks the microbial biomass needed to alter pollen nutrition."
The Degree Of Digestion Of Hive-Stored Pollen
Kirk is hardly the first bee researcher to point out that beebread contains few microbes. Back in 1983 Klungess and Peng [15], using microscopy, found few microorganisms in fresh beebread (but more in dark, old beebread). They concluded that:
The substances, presumably nectar or diluted honey and enzymes from the ventriculus and salivary gland, that bees add to pollen during packing on to the corbiculae [pollen baskets] and into cells, and the bee bread ripening process, do not break down the pollen contents. Nor do the microorganisms associated with fresh and old bee bread appear to cause destruction of pollen intine or the cytoplasm. .. It is, therefore, proposed that the substances added to pollen by bees during storage function as a preservative. We found no visible evidence that these substances pre-digest the pollen so as to make the nutrients more available to bees during subsequent digestion and absorption.
Compare this to Peng's previous finding that most (but not all) pollen grains are rapidly digested during their passage through the nurse bee midgut, which contains few microbes [16].
Hypothesis: if bacteria indeed digest the pollen grains in beebread, this should be easily observed through microscopy.
Anderson's finding: "There were no discernible morphological differences between newly collected and hive-stored pollen."
This should be something that any beekeeper could easily verify for him/herself. So I looked at aged beebread from my own hives under the scope (at 400 and 1000x), and also found very few microorganisms or digested pollen grains (Figs. 5-7).
Figure 5. Pollen grains in aged beebread under light microscopy. Note the relative absence of yeast or bacteria, and the unbreached (not misshapen) exines and intact colored contents of the pollen grains.
Figure 6. Pollen grains from beebread that I diluted with a weak sugar solution and allowed to ferment for 10 days. Note the abundant yeast and bacterial cells in the background (unfortunately there was not enough depth of field to bring both the pollen and microbes simultaneously into focus). Despite being exposed to over a week of vigorous aerobic fermentation, these pollen grains remain intact and undigested. Compare these intact grains to those below.
Figure 7. A sample of digested pollen from the hindgut of a nurse bee. Note how most of the pollen shells are empty (no longer yellow inside) and distorted, indicating digestion of the contents.
Conclusion: the bee midgut can quickly empty pollen grains and digest the contents. But such digestion does not occur when bacteria and yeast ferment pollen into beebread.
Dr. Anderson's Conclusions
Our combined results do not support the hypothesis that hive-stored pollen of honey bees involves nutrient conversion or predigestion by microbes prior to consumption.
The bacterial communities found in hive-stored pollen did not differ from those of newly collected pollen, but both sample types varied significantly by season. This result indicates the lack of an emergent 'core' bacterial community co-evolved to predigest pollen.
Relative to other plant material involving microbial digestion or extensive fermentation, hive-stored pollen contains very few microbes.
The absolute number of bacteria in hive-stored pollen decreases with storage time, indicating that it is not a suitable medium for microbial growth.
The preferential consumption of freshly collected pollen indicates that bees have not evolved to rely on microbes or other time-related factors for pollen predigestion.
The microbe to pollen grain ratio is many orders of magnitude removed from that required to alter hive-stored pollen.
Regardless of sampled season or the taxonomic character of microbial communities, microscopic examination revealed no intermediate stage of pollen digestion in hive-stored pollen.
Based on these collective findings, we suggest that stored pollen is a preservative environment governed largely by nonmicrobial additions of nectar, honey and bee glandular secretions.
Summary
Flowers and pollinators have coevolved over millions of years, and along with them microbes always at the ready to consume them, or perhaps establish symbiotic relationships. Since microbes are invisible to the naked eye, it is difficult for us to grasp their degree of prevalence in the environment, or to understand their contribution to bee nutrition and health.
There may be a million bacteria (along with yeasts and other fungi) per milliliter in nectar when bees first collect it--fresh nectar is often already starting to ferment [18]. Pollen contains somewhat fewer microbes, but is still very biologically active when first gathered. The greatest concentration of microbes in the hive is in the residual undigested material in the bees' hindguts--that of a single bee may contain hundreds of millions of bacteria [19].
Kirk points out that the fluctuation of pollen availability has likely "selected for the quick turnover of the most readily available pollen nutrients into a 'nutritional reservoir' of living tissue (i.e. larva and worker fat bodies). In such a state, nutritional reserves are better protected from microbial digestion, more quickly shared among hive members and easier to digest than hive-stored pollen."
The above observation reminds us that hungry nurse bees readily consume larvae that they had previously been lavishing with jelly when it was abundant. The larvae thus function as a living protein reserve that through cannibalism can be quickly converted back into jelly or used to replenish fat bodies.
The honey bee, similar to humans, stores surplus food (that can't be immediately consumed) for later consumption (mainly to survive the winter). Like us, bees have figured out similar ways to prevent that food from being decomposed by microbes. Both nectar and pollen are prepared for prolonged storage by using a combination of high sugar concentration for osmotic preservative effect (similar to making jam), acidification via bacterial lactic acid production (pickling), and the addition of salivary antimicrobial compounds such as glucose oxidase (food preservatives).
Two key bacteria in this preservation process are the acid-resistant and osmotolerant [20] Lactobacillus kunkeei and Parasaccharibacter apium, both of which appear to be instrumental in hive hygiene, food storage, and larval health.
The microbial community in the hive is dynamic and evolving, not only in the gut of every bee during its short life, but also hour by hour during the fermentation of beebread. The microbiomes of the hive rapidly "adapt to changing diets and conditions not only by shifting community membership but also by changing gene content via horizontal gene transfer." Bacteria, by continually swapping genes, can adapt and evolve at a rate inconceivable to humans.
In the extended flower-pollinator community, pollinators vector microbes (including pathogens) with a remarkably high degree of efficiency. Graystock [21] found surprisingly efficient transmission of pathogens from bee to bee during flower visitations--the same would be expected to apply to hive or gut bacteria. This is due to the fact that the toilet hygiene of flying insects is rudimentary at best, resulting in plenty of fecal bacteria being inadvertently transferred to flower surfaces during pollinator visits (after all, just think about the degree of pollen transfer from flower to flower). And such transmission can be interspecific--any bee, fly, butterfly, beetle, or wasp can carry floral or pathogenic microbes from one flower to another. The total amount of microbial interchange within the entire flower/pollinator environment is mind boggling to consider, and makes for a highly dynamic system of microbial and pathogen interactions that we are only beginning to understand.
Next
The biological and chemical processes that take place during the fermentation of beebread, yeasts and fungi, probiotics, and the Anderson labs' current research projects.
References And Notes
[1] Published as Anderson, KE, MJ CarrolL, T Sheehan, BM Mott, P Maes and V Corby-Harris (2014) Hive-stored pollen of honey bees: many lines of evidence are consistent with pollen preservation, not nutrient conversion. Molecular Ecology 23: 5904-5917.
[2] Mainly from the above citation, but also from other published and as yet unpublished research. I also took the liberty to edit or reorder the quotations from his papers for readability.
[3] Vasquez A, Olofsson TC (2011) The honey crop - the holy grail when antibiotics fail. Microbiology Today, 38, 226-229.
[4] Fridman S, et al (2012) Bacterial communities in floral nectar. Environ. Microbiol. Rep 4:97-104.
[5] See my previous articles in this series.
[6] Disayathanoowat, T, et al (2012) T-RFLP analysis of bacterial communities in the midguts of Apis mellifera and Apis cerana honey bees in Thailand. Journal of Apicultural Research 51(4): 312-319.
[7] Don't be grossed out--the same thing happens with humans and many other animals.
[8] Blum JE, et al (2013) Frequent replenishment sustains the beneficial microbiome of Drosophila melanogaster. mBio 4(6):e00860-13. doi: 10.1128/mBio.00860-13
[9] Salubrious-healthful, beneficial, wholesome. Man, I gotta add this descriptive word to my vocabulary!
[10] I couldn't wait.
[11] Again, I've yet to see any hard data that any probiotic currently on the market is of benefit to bees. But I wouldn't be the least surprised if some were developed in the near future. But don't just go feeding any untested probiotic--a recent study found that some can seriously harm bees:
Ptaszynska, AA, et al (2015) Are commercial probiotics and prebiotics effective in the treatment and prevention of honeybee nosemosis C? Parasitol Res DOI 10.1007/s00436-015-4761-z Open access.
[12] Kirk shared the raw data so that I could chart it out in a manner more understandable to the layman. See the original paper for his graph, which contains more information.
[13] Or perhaps a preference for fresh, or slightly fermented, pollen. The overall expected consumption rate for each age class of beebread predicted to be consumed at random based on its abundance on the frames was 9.3%. Compare that to the measured consumption rates shown. Kirk has shown me additional (as yet unpublished) data gathered this spring that shows that the relative consumption rate continues to drop for beebread aged 6, 7, or more days.
Note: despite the observation that bees clearly prefer fresher beebread to older, due to the overwhelming presence of aged beebread in the combs of the colonies he observed, the majority of total beebread consumed (other than the unmeasured consumption of freshly-gathered pollen) was over 96 hrs old, suggesting perhaps that bees make an effort to "rotate the stores."
[14] Roulston, THI and JH Cane (2000) Pollen nutritional content and digestibility for animals. Plant Systematics 222: 187-209.
[15] By my math.
[16] Klungness L. M., Peng Y.-S. (1983) A scanning electron microscopic study of pollen loads collected and stored by honeybees. J. Apicul. Res. 22: 264-271.
[17] Peng YS, ME Nasr, et al (1985) The digestion of dandelion pollen by adult worker honeybees. Physiol. Entomol. 10: 75-82.
[18] Castillo, C, et al (2012) Seasonal variation in the titers and biosynthesis of the primer pheromone ethyl oleate in honey bees. J Insect Physiol 58(8):1112-21.
[19] Estimate, Kirk Anderson, pers comm.
[20] Osmotolerance is the ability to live in high-sugar environment that would dessicate other microbes.
[21] Graystock P, et al (2015) Parasites in bloom: flowers aid dispersal and transmission of pollinator parasites within and between bee species. Proc. R. Soc. B 282: 20151371. http://dx.doi.org/10.1098/rspb.2015.1371
Category: Bee Nutrition
Tags: beebread, digestion, DNA sequencing, Dr. Anderson, fermentation, hive-stored pollen, microbe biomass | DNA sequencing Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/dna-sequencing/ |
Effect of Amitraz on Buildup of Nucs
First published in: American Bee Journal, October 2014
Effect Of Amitraz On Buildup Of Nucs
Randy Oliver
ScientificBeekeeping.com
First published in ABJ October 2014
Introduction And Objectives
I was surprised by the slow buildup and lack of drawing of foundation by the nucs in my 2013/14 Pollen Supp Trial. Although the colonies were started during a dearth, due to the near-continual feeding of syrup, I fully expected them to build more rapidly. They didn't start to build to any extent until shortly after we removed the Apivar strips, but since I had not run a control group without Apivar, I had no way of knowing whether there was any connection.
As I mulled over the question, I came across additional information that furthered my curiosity as to whether amitraz might exhibit negative effects upon colonies (see Amitraz: Red Flags or Red Herrings? in this same issue).
So I decided to run a trial this summer to see whether the application of Apivar strips had a negative effect upon either colony buildup or the drawing of foundation.
Principal Investigator: Randy Oliver, assisted by Eric and Ian Oliver
Funding sources: I hope to be reimbursed for this trial by a grant from the North Dakota Department of Agriculture, solicited for me by the North Dakota Beekeepers Association.
Experimental Design:
Set up 36 5-frame nucs with freshly-mated tested queens, of two different maternal lines, equalized for strength, in pairs by queen mother. All hives 10-frame deep singles.
Reduce varroa levels to near nil by "natural" miticides known to leave few persistent residues.
Randomly assign 1 hive in each pair to receive a single Apivar strip for the duration of the trial (Treatment); open the other hive in each pair but apply no strip (Controls).
Add 5 frames of foundation and feed colonies for buildup, adding a second box of foundation to all when the first colony drew out its combs in the first box.
Allow colonies to grow, and then grade them for gain in strength and amount of combs drawn.
Trial Log
June 4, 2014 Moved 20 recently-mated queenright nucs to the test yard, which already contained 20 similar nucs from a different queen mother (both Italian mongrels). All nucs oxalic'd at Day 19; all checked for good patterns of worker brood. The nucs were set in pairs, each pair consisting of two nucs headed by sister queens.
June 6 Equalized all into 5-frames in a single. Typically 4 frames with brood.
June 9 Equalized.
June 12 Equalized and treated all with 1/2 MAQS.
June 19 Checked one hive for mites--4 in 1/2 cup bee sample-too many.
June 20 Equalized. Treated all with 1 Hopguard II strip.
June 27 Colonies drawing and filling foundation well. Large hive-to-hive variation in the amount of chewed Hopguard paper at the front of hives. Took composite mite samples of 1/2 cup of bees from 6 pairs of hives. Only 2 mites total in >1800 bees.
June 30 Final equalization of colonies, checked for queenrightness (2 colonies superseding, removed them and 2 others from trial), removed excess frames of bees, leaving each colony with 5 frames of brood, covered solid with bees. Good nectar flow on.
Experimental note: These nucs were considerably stronger than those in the previous trial, since they started with 5 full frames of brood. The experiment also began earlier in the season (July 1 vs. Aug 8), and during a nectar flow rather than a dearth.
July 1 Time Point 0 Good nectar flow on. Overnight, nearly every colony had built several combs underneath the lids (Figs. 1, 2, and 3).
Figure 1. All colonies were vigorously drawing comb on a natural nectar flow and ready to rock and roll. Remains of Hopguard II strip visible.
Figure 2. Colonies were in pairs, each pair headed by sister queens. We flipped a coin to decide which of each pair received an Apivar strip, and inserted one strip near the center of each treated hive. Here's Ian adding the frames of wax-coated plastic foundation to the 5-frame nucs.
Figure 3. Start of trial, treatment randomly assigned to each pair. I would have preferred a less-crowded test yard, but this one was near home.
July 7 Spot checked. Some colonies drawing foundation, nectar flow tapering off. Fed each colony 1/2 gal of 1:1 sucrose syrup.
July 21 All colonies appeared strong and building. The strongest had all 10 frames drawn and were heavy; the weakest had not yet drawn all 10 frames, nor covered them. The main flow is tapering off. Fed 1/2 gal 1:1 sucrose syrup. Added deep super of foundation to each colony.
Experimental note: the strong nectar flow after the start of the trial was unexpected, based upon the previous history of this yard.
July 24 Fed 1/2 gal 1:1 sucrose syrup.
Aug 8 Time Point 1 Main flow appears to be over, but still mixed pollens coming in. Since there were large differences in strength, we decided to perform the end point assessment. Graded all colonies (by Randy) in morning (by 9:15), blinded as to treatment. Graded for seams of bees and number of well/drawn combs of foundation (out of possible 15).
Results
The final grading took place at Day 38. The Control colonies averaged 8.8 (SEM 0.3) seams of bees; the Apivar-treated colonies averaged 8.5 (0.3). There was no significant difference between the two (Mann-Whitney p = 0.61), as reflected in the histogram of colony strengths in Fig. 4.
Figure 4. There was no apparent difference in buildup due to treatment with Apivar.
There was no difference between groups in the number of combs of foundation drawn- 5.9 (SEM 0.6) in the Controls; 5.7 (0.5) in the Apivar-treated group.
Discussion
The application of one Apivar strip to a strong 5-frame nuc on a decent nectar flow did not appear to inhibit either colony buildup or the drawing of foundation. I am toying with continuing this trial, periodically replacing the Apivar strips, through next spring, to see whether there are any other observable effects upon the colonies.
Acknowledgements
Thanks to Bonnie and Brent Woodworth and the North Dakota Beekeepers Association for their support of my research.
Category: Pesticide Issues
Tags: amitraz, nucs | nucs Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/nucs/ |
Reevaluating Beebread: Part 3 - For Preservation or Digestion?
First published in: American Bee Journal, December 2015
Reevaluating Beebread: Part 3
For Preservation Or Digestion?
Randy Oliver
ScientificBeekeeping.com
First published in ABJ Dec 2015
CONTENTS
Anderson's Investigatory Approach
Previous Research
Identification Of The Microbes Involved (via DNA Sequencing)
Bacterial Abundance During The Fermentation Process
Nurse Bee Feeding Preference By Age Of Beebread
The Pollen To Microbe Biomass Ratio
The Degree Of Digestion Of Hive-Stored Pollen
Dr. Anderson's Conclusions
Summary
Next
References And Notes
We've now identified the bacterial players. So let's see what Dr. Kirk Anderson's lab has found to date about why bees turn raw pollen into beebread.
In this article, I'm going to briefly summarize Dr. Anderson's well-designed investigations [1]. My readers know that I can be critical of sloppy science; conversely, I feel that truly exemplary scientific research should receive kudos. The investigation by Kirk and his associates meets this standard, and is a textbook example of good scientific research and writing. Kirk laid out his investigation methodically, questioning each premise of the "predigestion hypothesis," and seeing whether there was actual evidence either supporting or refuting the claim. I will quote from Kirk's papers extensively in italics [2].
Anderson's Investigatory Approach
Scientists typically specify the hypothesis to be tested and lay out their game plan:
It was hypothesized that co-evolved microbes orchestrate the long-term conversion of stored pollen into a more nutritious food source, a process involving microbial succession, anaerobic breakdown of materials, the release of pollen cell contents and/or predigestion by moulds. Here, we use a multifaceted approach to determine whether hive-stored pollen of honey bees involves significant nutrient conversion or 'pre-digestion' by microbes. To this end, we explore [reordered]
whether the differences in bacterial richness and diversity between newly collected and hive-stored pollen are consistent with a preservation or nutrient conversion environment
the absolute number of bacteria in stored pollen,
the association between bacterial abundance and pollen storage time,
the time period associated with pollen storage prior to ingestion by nurse bees,
the pollen to microbe biomass ratio, and
the degree of digestion of hive-stored pollen
Previous Research
Hypothesis to be tested: whether the fermentation of beebread requires inoculation of the pollen with symbiotic "core" gut bacteria via the crop as proposed by Vasquez and Olofsson [3]: "Our research has identified the bacteria involved and revealed that bees, in producing bee bread, add all the beneficial [lactic acid bacteria] to the pollen when they collect it at the site of the flower."
Vasquez and Olofsson's early research was very exciting, but they apparently overstated the case in claiming that bees added all the beneficial lactic acid bacteria to pollen, and especially that those bacteria came from the crop. Scientists already knew that pollen, and especially nectar, typically contains lactic acid and other bacteria prior to being visited by bees [4]. And subsequent research by others found that there were very few bacteria in the bee crop [5]. The question then is whether the pollen loads of returning foragers showed signs of being spiked with the core gut bacteria.
What Anderson found: In previous work, we determined that freshly-collected pollen from returning foragers or beebread contains incidental amounts of core hind-gut bacteria, suggesting that this core gut community does not contribute substantially to the conversion or preservation of pollen stores... This new finding contrasts markedly with the previous culture-dependent view...
Note: Dr. Anderson writes in a meticulous and precise scientific manner, appropriate for the journals in which he publishes (I again commend him for his exemplary backing up of each of his claims with accurate citations and supplemental data). It is polite scientific convention to say that a finding "contrasts markedly" with a previous view; a layman might say "man, did those guys get it wrong."
Identification Of The Microbes Involved (Via DNA Sequencing)
Hypotheses to test: if pollen is indeed inoculated by the bees with core gut bacteria in order to ferment it into beebread, then the bacterial species composition in beebread would shift towards core bacteria during the fermentation process.
Anderson found that: "The bacterial communities found in hive-stored pollen did not differ from those of newly collected pollen, but both sample types varied significantly by season." He found that only a small percentage of the bacteria found in freshly-gathered pollen loads were core hind-gut bacteria (in some cases as little as 3/10ths of a percent). Even more telling was that fermented beebread contained an even lower proportion of core gut bacteria than did newly-collected pollen.
Instead, the most common bacteria found in beebread were strains of Lactobacillus kunkeei. This floral/fruit bacterium thrives in fructose-rich aerobic environments, producing lactic acid as a metabolic byproduct, which has the benefit of making its environment inhospitable to competing yeasts and bacteria. Bees create an ideal environment for L. kunkeei by enriching pollen with fructose-rich nectar-thus its rapid preservation of beebread by the process of acidic "pickling." L. kunkeei is one of the few bacteria that can survive (perhaps in a dormant state) in honey and beebread, likely quickly rejuvenating when exposed to diluted nectar or honey in the crop.
Kirk and others [6]) have found that the bacterial community in bees may differ a bit from hive to hive, and by season or forage, but there is always a "core" hindgut biota (apparently passed via a fecal/oral route of some sort) [7]. The story is as yet far from complete, but it appears that honey bees have a commensal or mutualistic relationship with these core species, but also utilize free-living flower bacteria, such as L. kunkeei, to their advantage. An interesting recent study by Blum [8], working with the fruit fly Drosophila, points out that a host does not necessarily need to maintain a population of endosymbionts, but may instead continually replenish it via its food:
The Drosophila system may represent an alternative mutualism strategy that we term "quotidian replenishment," which is intended to indicate the need for daily replenishment to obtain a consistent [bacterial] community in the animal. In this model, the symbiotic community in Drosophila is maintained through frequent ingestion from an external reservoir of bacteria [its food]... Furthermore, our study shows that one member of the microbiome, Lactobacillus plantarum, protects the fly from intestinal pathogens. These results suggest that, although not always present, the microbiota can promote salubrious [9] effects for the host.
It appears that the honey bee may use a combination of vertical transmission (colony to daughter colony) of the core endosymbionts, coupled with the advantageous use of naturally-occurring floral bacteria (similar to the way that humans make sauerkraut or silage). Of interest is that some free-living bacteria can exert salubrious [10] effects on host immunity (which opens the market for bee probiotics) [11].
Bacterial Abundance During The Fermentation Process
Hypothesis tested: if pollen is indeed digested by core bacteria during the fermentation of beebread, then the number of those bacteria would increase during the process.
What Anderson found: that bacterial abundance increased only during the first two days of fermentation, and then decreased thereafter (Fig. 1). This finding does not support the digestion hypothesis, instead indicating that the formation of lactic acid acts to protect the pollen in beebread from microbial degradation.
Figure 1. After a day's fermentation, the bacterial count of stored pollen increased greatly from that of fresh incoming pollen, and then dropped sharply as the beebread became too acidic for further microbial growth. After Anderson (2014) [[i]].
[i] Kirk shared the raw data so that I could chart it out in a manner more understandable to the layman. See the original paper for his graph, which contains more information.
Nurse Bee Feeding Preference By Age Of Beebread
Hypothesis to be tested: if fermentation improved the nutritional quality of pollen, then it would follow that nurse bees would preferentially consume beebread that had fully fermented.
The Method: Kirk's team meticulously tracked the daily deposition or consumption of pollen in every cell of an active brood frame from each of 8 colonies over 5 days, repeated with different colonies in March, April, and May.
What Anderson found: The results are shown in Fig. 2. Although these measurements were taken during times of pollen surplus (as indicated by the fact that nearly 90% of the beebread cells were over 96 hrs old), the nurse bees appeared to preferentially consume either fresh incoming or slightly fermented pollen to aged beebread. This observation does not support the hypothesis that fermentation improves pollen nutritional quality.
Figure 2. Measurements were taken of the ages of beebread cells in the combs; the orange columns indicate the average number of cells present for each age class of beebread. The capped lines indicate the proportion of that age class of pollen consumed each day. There was apparently an aversion by bees to consume pollen that had undergone extended fermentation [[i]].
[i] Or perhaps a preference for fresh, or slightly fermented, pollen. The overall expected consumption rate for each age class of beebread predicted to be consumed at random based on its abundance on the frames was 9.3%. Compare that to the measured consumption rates shown. Kirk has shown me additional (as yet unpublished) data gathered this spring that shows that the relative consumption rate continues to drop for beebread aged 6, 7, or more days.
Note: despite the observation that bees clearly prefer fresher beebread to older, due to the overwhelming presence of aged beebread in the combs of the colonies he observed, the majority of total beebread consumed (other than the unmeasured consumption of freshly-gathered pollen) was over 96 hrs old, suggesting perhaps that bees make an effort to "rotate the stores."
The Pollen To Microbe Biomass Ratio
And now Anderson, in a stroke of brilliance, shot right to the crucial question: are there even enough bacteria present in beebread to exert a digestive effect? Bacteria lack teeth, and thus depend upon the enzymes that they produce in order to digest foodstuffs. Pollen does not make it easy for microbes to get to the good stuff inside the protective outer shell.
A pollen grain is enclosed in a tough coat called the exine. The exine is composed of a highly decay-resistant biopolymer called sporopollenin. Sporopollenin is so resistant to bacterial enzymes that "Pollen walls...often survive intact and recognizable for millions of years in bog and sediment deposits" [14]. The only place for bacteria to gain access to the nutritious innards of the pollen grain is through the (generally) one or more germination pores in the exine (these also serve as routes for water uptake). These pores are protected by a membrane called the intine, composed of cellulose and pectin. It is this layer that bacteria would need to digest their way through.
Kirk recognized that for bacteria to breach the intine of the pollen pores, that there would need to be a lot of them producing enzymes at those surfaces. So are there enough present? As I'm want to say, let's do the math! In this case, Kirk did it for us.
Hypothesis: that there are enough enzyme-producing bacteria present in beebread relative to the surface area of the pollen grains to digest their way through the pollen shells.
Kirk's math: He was generous on his estimate of the number of microbes present in mature beebread, quadrupling his actual colony counts to allow for culture bias and fungi, arriving at about 36,900 microbes per gram of pollen. He then counted pollen grains under a scope, estimating about 90 million pollen grains per gram. This works out to about 1 microbe per 2500 pollen grains (Fig. 3). To place this into biological perspective, a single grain of pollen in the bee hindgut is often covered with hundreds or thousands of bacteria (Fig. 4), busily digesting the remnants left over from the digestion that took place in the bee midgut.
As an imaginary visual analogy, I calculated that the proportion of bacteria per surface area of the pollen grains works out to the spatial equivalent of a single BB placed on a football field [15]--hardly enough to produce the enzymes necessary to digest their way through the pollen exine or intine.
Figure 3. A scanning electron micrograph of dried beebread. The pink substance is dried simple sugars, which constitute about 40-50% by weight. Note the distinct lack of bacteria. Electron micrographs courtesy Kirk Anderson.
Figure 4. For comparison, these pollen grains from a nurse bee hindgut are covered with live bacteria (stained purple).
Conclusion: there simply aren't enough microbes present in beebread to cause any significant degree of digestion of the pollen grain contents. Kirk succinctly concludes that: "Hive-stored pollen lacks the microbial biomass needed to alter pollen nutrition."
The Degree Of Digestion Of Hive-Stored Pollen
Kirk is hardly the first bee researcher to point out that beebread contains few microbes. Back in 1983 Klungess and Peng [15], using microscopy, found few microorganisms in fresh beebread (but more in dark, old beebread). They concluded that:
The substances, presumably nectar or diluted honey and enzymes from the ventriculus and salivary gland, that bees add to pollen during packing on to the corbiculae [pollen baskets] and into cells, and the bee bread ripening process, do not break down the pollen contents. Nor do the microorganisms associated with fresh and old bee bread appear to cause destruction of pollen intine or the cytoplasm. .. It is, therefore, proposed that the substances added to pollen by bees during storage function as a preservative. We found no visible evidence that these substances pre-digest the pollen so as to make the nutrients more available to bees during subsequent digestion and absorption.
Compare this to Peng's previous finding that most (but not all) pollen grains are rapidly digested during their passage through the nurse bee midgut, which contains few microbes [16].
Hypothesis: if bacteria indeed digest the pollen grains in beebread, this should be easily observed through microscopy.
Anderson's finding: "There were no discernible morphological differences between newly collected and hive-stored pollen."
This should be something that any beekeeper could easily verify for him/herself. So I looked at aged beebread from my own hives under the scope (at 400 and 1000x), and also found very few microorganisms or digested pollen grains (Figs. 5-7).
Figure 5. Pollen grains in aged beebread under light microscopy. Note the relative absence of yeast or bacteria, and the unbreached (not misshapen) exines and intact colored contents of the pollen grains.
Figure 6. Pollen grains from beebread that I diluted with a weak sugar solution and allowed to ferment for 10 days. Note the abundant yeast and bacterial cells in the background (unfortunately there was not enough depth of field to bring both the pollen and microbes simultaneously into focus). Despite being exposed to over a week of vigorous aerobic fermentation, these pollen grains remain intact and undigested. Compare these intact grains to those below.
Figure 7. A sample of digested pollen from the hindgut of a nurse bee. Note how most of the pollen shells are empty (no longer yellow inside) and distorted, indicating digestion of the contents.
Conclusion: the bee midgut can quickly empty pollen grains and digest the contents. But such digestion does not occur when bacteria and yeast ferment pollen into beebread.
Dr. Anderson's Conclusions
Our combined results do not support the hypothesis that hive-stored pollen of honey bees involves nutrient conversion or predigestion by microbes prior to consumption.
The bacterial communities found in hive-stored pollen did not differ from those of newly collected pollen, but both sample types varied significantly by season. This result indicates the lack of an emergent 'core' bacterial community co-evolved to predigest pollen.
Relative to other plant material involving microbial digestion or extensive fermentation, hive-stored pollen contains very few microbes.
The absolute number of bacteria in hive-stored pollen decreases with storage time, indicating that it is not a suitable medium for microbial growth.
The preferential consumption of freshly collected pollen indicates that bees have not evolved to rely on microbes or other time-related factors for pollen predigestion.
The microbe to pollen grain ratio is many orders of magnitude removed from that required to alter hive-stored pollen.
Regardless of sampled season or the taxonomic character of microbial communities, microscopic examination revealed no intermediate stage of pollen digestion in hive-stored pollen.
Based on these collective findings, we suggest that stored pollen is a preservative environment governed largely by nonmicrobial additions of nectar, honey and bee glandular secretions.
Summary
Flowers and pollinators have coevolved over millions of years, and along with them microbes always at the ready to consume them, or perhaps establish symbiotic relationships. Since microbes are invisible to the naked eye, it is difficult for us to grasp their degree of prevalence in the environment, or to understand their contribution to bee nutrition and health.
There may be a million bacteria (along with yeasts and other fungi) per milliliter in nectar when bees first collect it--fresh nectar is often already starting to ferment [18]. Pollen contains somewhat fewer microbes, but is still very biologically active when first gathered. The greatest concentration of microbes in the hive is in the residual undigested material in the bees' hindguts--that of a single bee may contain hundreds of millions of bacteria [19].
Kirk points out that the fluctuation of pollen availability has likely "selected for the quick turnover of the most readily available pollen nutrients into a 'nutritional reservoir' of living tissue (i.e. larva and worker fat bodies). In such a state, nutritional reserves are better protected from microbial digestion, more quickly shared among hive members and easier to digest than hive-stored pollen."
The above observation reminds us that hungry nurse bees readily consume larvae that they had previously been lavishing with jelly when it was abundant. The larvae thus function as a living protein reserve that through cannibalism can be quickly converted back into jelly or used to replenish fat bodies.
The honey bee, similar to humans, stores surplus food (that can't be immediately consumed) for later consumption (mainly to survive the winter). Like us, bees have figured out similar ways to prevent that food from being decomposed by microbes. Both nectar and pollen are prepared for prolonged storage by using a combination of high sugar concentration for osmotic preservative effect (similar to making jam), acidification via bacterial lactic acid production (pickling), and the addition of salivary antimicrobial compounds such as glucose oxidase (food preservatives).
Two key bacteria in this preservation process are the acid-resistant and osmotolerant [20] Lactobacillus kunkeei and Parasaccharibacter apium, both of which appear to be instrumental in hive hygiene, food storage, and larval health.
The microbial community in the hive is dynamic and evolving, not only in the gut of every bee during its short life, but also hour by hour during the fermentation of beebread. The microbiomes of the hive rapidly "adapt to changing diets and conditions not only by shifting community membership but also by changing gene content via horizontal gene transfer." Bacteria, by continually swapping genes, can adapt and evolve at a rate inconceivable to humans.
In the extended flower-pollinator community, pollinators vector microbes (including pathogens) with a remarkably high degree of efficiency. Graystock [21] found surprisingly efficient transmission of pathogens from bee to bee during flower visitations--the same would be expected to apply to hive or gut bacteria. This is due to the fact that the toilet hygiene of flying insects is rudimentary at best, resulting in plenty of fecal bacteria being inadvertently transferred to flower surfaces during pollinator visits (after all, just think about the degree of pollen transfer from flower to flower). And such transmission can be interspecific--any bee, fly, butterfly, beetle, or wasp can carry floral or pathogenic microbes from one flower to another. The total amount of microbial interchange within the entire flower/pollinator environment is mind boggling to consider, and makes for a highly dynamic system of microbial and pathogen interactions that we are only beginning to understand.
Next
The biological and chemical processes that take place during the fermentation of beebread, yeasts and fungi, probiotics, and the Anderson labs' current research projects.
References And Notes
[1] Published as Anderson, KE, MJ CarrolL, T Sheehan, BM Mott, P Maes and V Corby-Harris (2014) Hive-stored pollen of honey bees: many lines of evidence are consistent with pollen preservation, not nutrient conversion. Molecular Ecology 23: 5904-5917.
[2] Mainly from the above citation, but also from other published and as yet unpublished research. I also took the liberty to edit or reorder the quotations from his papers for readability.
[3] Vasquez A, Olofsson TC (2011) The honey crop - the holy grail when antibiotics fail. Microbiology Today, 38, 226-229.
[4] Fridman S, et al (2012) Bacterial communities in floral nectar. Environ. Microbiol. Rep 4:97-104.
[5] See my previous articles in this series.
[6] Disayathanoowat, T, et al (2012) T-RFLP analysis of bacterial communities in the midguts of Apis mellifera and Apis cerana honey bees in Thailand. Journal of Apicultural Research 51(4): 312-319.
[7] Don't be grossed out--the same thing happens with humans and many other animals.
[8] Blum JE, et al (2013) Frequent replenishment sustains the beneficial microbiome of Drosophila melanogaster. mBio 4(6):e00860-13. doi: 10.1128/mBio.00860-13
[9] Salubrious-healthful, beneficial, wholesome. Man, I gotta add this descriptive word to my vocabulary!
[10] I couldn't wait.
[11] Again, I've yet to see any hard data that any probiotic currently on the market is of benefit to bees. But I wouldn't be the least surprised if some were developed in the near future. But don't just go feeding any untested probiotic--a recent study found that some can seriously harm bees:
Ptaszynska, AA, et al (2015) Are commercial probiotics and prebiotics effective in the treatment and prevention of honeybee nosemosis C? Parasitol Res DOI 10.1007/s00436-015-4761-z Open access.
[12] Kirk shared the raw data so that I could chart it out in a manner more understandable to the layman. See the original paper for his graph, which contains more information.
[13] Or perhaps a preference for fresh, or slightly fermented, pollen. The overall expected consumption rate for each age class of beebread predicted to be consumed at random based on its abundance on the frames was 9.3%. Compare that to the measured consumption rates shown. Kirk has shown me additional (as yet unpublished) data gathered this spring that shows that the relative consumption rate continues to drop for beebread aged 6, 7, or more days.
Note: despite the observation that bees clearly prefer fresher beebread to older, due to the overwhelming presence of aged beebread in the combs of the colonies he observed, the majority of total beebread consumed (other than the unmeasured consumption of freshly-gathered pollen) was over 96 hrs old, suggesting perhaps that bees make an effort to "rotate the stores."
[14] Roulston, THI and JH Cane (2000) Pollen nutritional content and digestibility for animals. Plant Systematics 222: 187-209.
[15] By my math.
[16] Klungness L. M., Peng Y.-S. (1983) A scanning electron microscopic study of pollen loads collected and stored by honeybees. J. Apicul. Res. 22: 264-271.
[17] Peng YS, ME Nasr, et al (1985) The digestion of dandelion pollen by adult worker honeybees. Physiol. Entomol. 10: 75-82.
[18] Castillo, C, et al (2012) Seasonal variation in the titers and biosynthesis of the primer pheromone ethyl oleate in honey bees. J Insect Physiol 58(8):1112-21.
[19] Estimate, Kirk Anderson, pers comm.
[20] Osmotolerance is the ability to live in high-sugar environment that would dessicate other microbes.
[21] Graystock P, et al (2015) Parasites in bloom: flowers aid dispersal and transmission of pollinator parasites within and between bee species. Proc. R. Soc. B 282: 20151371. http://dx.doi.org/10.1098/rspb.2015.1371
Category: Bee Nutrition
Tags: beebread, digestion, DNA sequencing, Dr. Anderson, fermentation, hive-stored pollen, microbe biomass | Dr. Anderson Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/dr-anderson/ |
Mite Management Update 2013
First published in: American Bee Journal, August 2013
Monitoring Mites by Sampling
Frame-to-Frame Consistency of Samples
Mite Recovery of the Alcohol Wash
Sticky Boards
Natural Mite Drop vs. Alcohol Wash
Discussion
Experimenting with MAQS Strips
References and Footnotes
Mite Management Update 2013
Randy Oliver
ScientificBeekeeping.com
First published in ABJ August 2013
It's that time of year again to get a jump on varroa mites before it's too late. This raises two questions: how to measure the degree of mite infestation in your hives, and how to treat if the levels are excessive. In this article I'll share some of what I've learned in the past year.
It's common consensus that if the mite infestation rate (the percentage of bees actually parasitized by a mite) is kept low, that the colony can generally deal with the "varroa/virus complex." It is only when that infestation rate exceeds some "economic threshold" that the combination of the direct damage due to varroa parasitism, combined with the mite's vectoring of viruses within the hive, create the explosive virus epidemics that cause noticeable colony morbidity or mortality.
For my apiaries in the California foothills, I've found that if I keep the mite infestation rate below the 2% level (2 mites per 100 bees) that my colonies thrive. But should that rate reach 5%, then I start seeing the brood fall apart. By the time the rate reaches 15%, the colony is generally seriously on the way downhill, and even with treatment may not recover.
The most critical time to monitor and reduce the mite level is in late summer and fall, since this is when the generation of bees that form the winter cluster is raised. If there is a virus epidemic in the hive in fall, the colony will likely not survive the winter.
Surprisingly, many beekeepers allow their apiaries to enter the winter with excessive mite loads (Fig. 1).
Figure 1. Data from samples from cooperating beekeepers across the country indicate that mite levels in many apiaries exceed the economic treatment threshold in fall. Note that in 2010 the average sampled hive contained nearly 10 mites per 100 bees in November! It is not surprising that such colonies suffer from elevated winter mortality. Graph from [[i]].
[i] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
Last year I ran some trials in which I was required to withhold mite treatments. I do not yet have the data from one trial in which 70% of the colonies died, but those results should help us greatly in understanding the dynamics of the varroa/virus complex.
But I do have some data to share from a smaller trial in which I measured mite levels and colony frame strength over the course of the winter (Fig. 2).
Figure 2. For these 36 colonies, there was a clear relationship between November mite levels and loss of colony strength over winter. The mean starting strength was 9.2 frames covered with bees (range 6.5-13) on Sept. 12.
Monitoring Mites By Sampling
So how does one determine what the actual infestation rate of a colony is? The only definitive assessment is to kill all the bees in the hive, wash all the mites from them, and then count all the bees and mites one by one. And then, you'd need to open all the sealed brood and count the mites in each cell. Obviously, Joe Beekeeper is not going to do that!
So we generally use either:
An indirect method of sampling, such as natural mite drop.
A more direct whole-hive method such as drop accelerated by sugar dust or chemical treatment.
A direct counting of the number of mites in a sample of adult bees or in worker or brood cells.
All the above methods are detailed at my website.
I've found the sampling of drone brood to be totally unreliable, and no beekeeper that I know is going to open hundreds of worker cells to count mites. The accelerated drop method works well, but it requires a screened bottom board, two trips to the hive, and must be adjusted for the number of frames actually covered by bees.
So that leaves as the most practical methods, the natural mite drop onto sticky boards, or one of the "jar" methods--ether roll, alcohol or detergent wash, or the "sugar shake." I tend to favor the jar methods, since they are quick, require only one trip to the hive, are direct rather than indirect methods, and do not require adjustment for the strength of the colony.
The other reason that I favor the direct methods of sampling is that they reflect the actual biological relevance of the mite infestation. The percentage of bees that are carrying a mite is more relevant to the immune suppression and virus transmission by the mite than is the rate at which mites are falling from the combs on any particular day. Direct measurement also does not need to be adjusted for colony strength.
Although many commercial beekeepers favor the ether roll, I found it to be inconsistent. That leaves the alcohol and detergent washes and the sugar shake, which give roughly the same results. The alcohol is also handy because it will preserve bees for later sampling for nosema, or at a wash table back at the shop. On the other hand, the sugar shake does not require the killing of any bees, but does take a strong arm if you plan to do more than a few tests.
So allow me to now compare the alcohol wash and the natural drop methods. First, let me check our assumptions for the validity of the sampling and the wash.
Frame-To-Frame Consistency Of Samples
Dr. Frank Eischen of the U.S. ARS was kind enough to share with me a data set from 2005 in which he had counted the numbers of bees and mites in samples of bees shaken from two different frames from the brood nest of each hive. I took the 168 paired samples [2], which averaged 512 bees per sample, and determined the difference in the mite infestation rates between the samples. The mean mite infestation was 6 mites per 100 bees (6% infestation rate), ranging from zero to 58/100 (Fig. 3).
Figure 3. Frequency distribution of the differences in mites/100 bees in samples taken from two different frames from the broodnest of a hive. In 85% of the cases, the count was within 3 mites/100 bees. Data originally from Dr. Frank Eischen.
The above data suggest that there is not a great deal of frame-to-frame variation in the mite infestation rate of house bees (my own limited data suggest the same). Since I use a treatment threshold of 2 mites/100 bees, I checked the 54 cases in which a colony tested at 2 or fewer mites/100 in the first sample. In only three cases out of those 54 did the second frame contain of more than 5 mites/100 bees.
Practical applications: any frame from the broodnest appears to be adequate for sampling. At low infestation rates, any sample is unlikely to underestimate a serious infestation. I tend to pull an outer brood frame in order to minimize the chance of disturbing or inadvertently killing the queen. So long as you consistently pull a frame from the same area of the broodnest, you can then compare consistent samples.
Mite Recovery Of The Alcohol Wash
The question to me then is how well the "Mite Wash" bottle developed by Dr. Medhat Nasr (Fig.4) actually recovered the mites on the bees. So I shook a bunch of samples of bees three times in a row to eventually recover all the mites. I shook at a rate of about three shakes per count, for the count of twenty, for a total of about 60 shakes. I shook vigorously enough to dislodge stingers from the bees (Fig. 5). At the end of each shaking I jiggled the bottle to keep the mites from being caught in the bees as the alcohol drained to the lower jar (see [3] for details on the method).
Figure 4. Using the mite wash bottle. When I'm really cooking, I can sample hives at a turnaround time of less than four minutes per hive.
Figure 5. Mites are easy to see and quickly count in the Mite Wash bottle. Note the presence of the dislodged stinger at lower right, which is a good indicator for whether you are shaking vigorously enough. The 21 mites in this sample of 1/2 cup of bees would indicate an infestation rate in the ballpark of 7 mites/100 bees (7% rate). This is far above my treatment threshold.
Table 1. Recovery of mites by alcohol wash in a "Mite Wash" bottle. I averaged 87% recovery in the first wash.
You can see that determining the mite infestation rate of a colony has a certain amount of built in error. There is frame-to-frame variability, variation in the number of bees in the sample cup, and variation in the recovery rate of mites. However, it appears to me that the washing the mites from a sample of bees from the broodnest gives a pretty good ballpark representation of actual mite infestation rates. I would certainly not trust any individual sample. But in practical experience, I find that a second shake from the same colony generally comes up within a mite or two at low infestation rates. Please note that one need not fabricate a Mite Wash bottle to perform an alcohol wash--a kitchen sieve in a bowl also works just fine!
Sticky Boards
Lots of beekeepers use stickyboards because they don't have to open the hive, which is a plus. But if you're over 40, then you've got to deal with the fact that it's danged hard and dismally tedious to discriminate the mites from the hive trash, and then keep a running total of counted mites without either missing some or counting others twice (Fig. 6). In addition, sticky board counts still must be adjusted not only for colony strength, but also for the time of year and amount of brood present in order to see how they relate to the threshold for treatment [4].
Figure 6. Counting mites among the hive trash on a sticky board is a tedious process that requires sharp eyes or supplementary magnification. The natural mite drop is an indirect indicator of the mite infestation rate, since the count is largely dependent upon the amount of brood emergence on that day. This portion of the sticky board shows five adult mites clearly, one adult partially hidden by a piece of hive trash, and one partial mite shell.
But what I really I wondered was just how consistently the natural mite drop reflected the actual infestation rate of the adult bees in the hive?
I had the opportunity last summer to run a trial in which I took sticky board counts of natural mite fall as well as alcohol washes from the same hives sometimes on the same days over a period of time. I was immediately surprised by the large day-to-day variation in natural mite drop, and wondered whether it had anything to do with temperature, humidity, or rain, so I downloaded the records of the local weather station. Below are the average daily mite drop counts for 12 hives over the course of 10 days, recording the average and maximum temperature for the day, minimum humidity, and whether it rained (Fig. 7).
Figure 7. Mean daily mite drop for 10 hives relative to environmental factors. There was rain in the apiary on 5 August. Although temperature and humidity varied a fair amount, I don't see any particular relationship between environmental factors and natural mite drop.
Note that in the above graph that the mite levels went up and down considerably from day to day, which was surprising, since I think that it's safe to assume that the mite infestation rate of the apiary did not vary that much on a daily basis. This raised the question in my mind as to how consistent the counts were for each individual hive, which would tell me how much I could trust any single count. I've plotted the data below (Fig. 8).
Figure 8. Sticky board counts for six hives over time. Note that on any particular day, the count can easily go up or down by a factor of two!
Clearly, natural mite drop is highly variable from day to day. So I wondered whether the same would apply to an alcohol wash.
Natural Mite Drop Vs. Alcohol Wash
As luck would have it, I had also collected data or alcohol washes of 1/2 cup of bees from the same colonies, sometimes on the same days that I took sticky board counts (Fig. 9).
Figure 9. Alcohol washes for the same hives overlapping the dates of the preceding graph. Note a couple of things: the reduced variability of alcohol washes, and that the plots of the two methods for determining mite infestation rate do not match for each colony (the color for each hive is matched in the two charts).
From a practical standpoint, the most important question is which method most closely reflects the actual infestation rate in the hive. Since the alcohol wash is a direct measurement of the actual number of mites per 100 bees, it would likely have the most biological (and practical) relevance. So let's compare the two for my full [5] data set (Fig. 10).
Figure 10. Comparisons of natural mite drops on sticky boards to alcohol wash of 1/2 cup of bees, late July and early August. The alarming thing is those natural drop counts in the pink shaded area at the bottom, in which natural mite drop substantially underestimated a serious infestation rate in the hive (more than 5 mites/100 bees). Of less concern were those stickyboard counts in the blue area, which overestimated the problem.
As you can see above, the two monitoring methods followed the same general trend--natural mite fall tended to go up as the actual mite infestation rate rose. The problem is that in a fair percentage of the cases, natural drop did not reflect the brewing of a serious mite infestation!
Practical application: I've lost faith in the natural mite drop as a means of monitoring mite levels. It is handy when used to determine whether a miticide gives a quick knock down, but not so much to indicate the biologically relevant level of mite infestation. If one does use stickyboards as their only monitoring method, might I suggest that you take counts over a period of time.
Discussion
Beekeepers and researchers have long looked for an easy, consistent, and accurate method of estimating the mite infestation rate within a hive [[i]]. Each method has advantages and drawbacks. Whole-hive sampling methods (natural drop, accelerated drop) are more likely to detect mites at low infestation rates, since the entire hive population is sampled. But at higher infestation rates, the consistency of the natural mite drop appears to fall apart (perhaps because of the number of variables involved). The difference between the natural drop and the accelerated drop is that the first is an indirect measurement, whereas with a high-efficacy accelerant, the other is more of a direct method.
The "jar" techniques of removing mites from a sample of 200-400 bees from the broodnest are all direct methods, and all appear to be consistently reliable. I tend to favor these methods since they only require one trip to the hive, don't require sharp eyes and excessive counting, and the results give the beekeeper a true indication of the degree of mite stress to the bees in the broodnest.
I don't have strong feelings for or against any of the jar methods. Sugar shake resonates with hobbyists, since the method doesn't require the killing of any bees, but it does take more shaking, and in my tests mite recovery was less than that of the wash methods. I was disappointed in my early testing of the ether roll, but since it is commonly (and apparently successfully) used by many commercial beekeepers, perhaps I was premature in my dismissal of it as a reliable method.
The wash methods (alcohol or detergent) work quite well, with alcohol being a bit less messy. The Nasr mite wash bottle is a handy field tool, but still leaves something to be desired, since its design tends to allow mites to be trapped in the bees as the alcohol washes down, depressing the recovery rate. This defect can be corrected with a shaker table, in which alcohol-immersed bees are always held above the bottom of the container by a screen (personal experience). I hope to further experiment in improving methods for performing the alcohol wash in the field, perhaps building upon an original design for a wash bottle that I published in 2006 [7].
Experimenting With MAQS Strips
My three favorite mite treatments are now thymol (applied as Apiguard thymol gel), oxalic acid (applied as a dribble), and formic acid (applied in Mite Away Quick Strips-MAQS). I'm quite taken by MAQS, since it is effective, can be applied with honey supers on, and leaves no residues in the hive. As with any new product, there is a learning curve. So let me share some of the results of my own experimentation.
In the first place, after hearing of beekeepers who suffered queen loss issues after applying the full two-strip ("knockout") treatment, I've only applied single strips to a hive ("knockback"), and haven't noticed any queen issues (I'm curious now as to whether some of those beekeepers inadvertently tore the slow-release paper on the strips, which can result in an excessive initial spike in formic vapors).
Last summer I experimented with testing the efficacy of both single-strip and half-strip applications. All applications were made between late August and late September during dry 90degF weather (Fig. 11). The mite infestation rate was measured by alcohol wash of 1/2 cup of bees for the 22 August data, and from1/3 cup of bees at the other time points. I took mite measurements at time of treatment, again at 16-20 days, and in some cases at 35 days after treatment. Measurements at those time intervals (roughly after one or two mite reproductive cycles) were timed in order to pick up the effect that formic treatment might have on the male mites under the cappings. All applications were to double deep strong colonies with 3/4" entrances unless otherwise noted. The strips were laid crosswise between the brood chambers.
Figure 11. Temperatures during the tests.
The results of my testing of a single MAQS follow (Figs. 12 & 13):
Figure 12. Mites levels in highly-infested hives late in the season at time of treatment and at intervals thereafter. Red bars are initial mite levels, blue and green bars represent mite levels after one or two mite reproductive cycles, respectively. Note the greater degree of mite reduction by the treatment in the later-applied treatments. I apologize for not having data for control colonies [[i]].
[i] In order to run a truly valid test of efficacy, one would need to simultaneously measure the mite levels in adjacent untreated control hives, to see whether mite levels would have dropped off spontaneously. I apologize for not having such data. My pitiful excuse is that I initially set up the trial with controls and took mite washes, but midway into taking the 16-day checkback samples, I suddenly realized that I needed to get to the airport for a conference, s0 skipped taking samples from the control group. I missed the flight anyway : (
As a beekeeper, however, I know that the mite levels of the rest of the colonies in my operation typically continue to rise at this time of year, so although I would not be able to publish this data in a refereed journal, I feel that it may be of value to beekeepers whose goal is simply to get below a target infestation rate.
Figure 13. The same data as above, but normalized to indicate the percentage reduction from initial mite level. Note that the efficacy increased at later treatment dates (up to 90%), presumably due to the colonies reducing the amount of brood present as they settled down in our dry fall weather.
Since in my mite management strategy we only look for a 50-60% mite knockback with treatments (to make the treatments easier on the bees, and to avoid mite resistance to the treatments), we've been quite happy with the efficacy of a single strip of MAQS. The question then was, how effective would a half strip be? So I applied a half of a single strip to doubles and recently-started singles (~6-frame strength) (Figs. 14 & 15).
Figure 14. Half of one MAQS didn't do much good in a double, but was remarkably effective in small singles in hot weather.
Figure 15. Same as before; note the high efficacy of a half strip in weak singles.
The undersides of the hive covers of those weak singles get quite warm--I measured inside temperatures exceeding 130degF on the wood against which the half MAQS was pressed. I fully expected that such temperatures would rapidly evaporate the formic vapors out of the gel. I was surprised to find that even two weeks after application, the strips remained soft and intensely redolent of formic -unlike those between brood chambers, which quickly dry and harden. I suspect that this is due to at least three factors--the lid sealing off the top surface of the strip from evaporation, the bees sealing the four edges of the strip with propolis (Fig. 16), and the bees' behavior of placing drops of water on the top bars for evaporative cooling in hot weather.
For whatever reasons, such reduction and prolongation of the formic acid evaporation may have helped in reducing queen loss, and perhaps the efficacy of mite kill. We treated a couple of dozen weak singles, and only observed queen supersedure in two that had queens with preexisting problems.
Figure 16. A half of a MAQS applied directly under a dark lid to a strong single during 90degF weather.
References And Footnotes
[1] http://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2011_National_Survey_Report.pdf
[2] I censored one clear outlier.
[3] https://scientificbeekeeping.com/sick-bees-part-11-mite-monitoring-methods/
[4] https://secure.fera.defra.gov.uk/beebase/public/BeeDiseases/varroaCalculator.cfm
[5] The trial from which I took this data was for a bee health product that was applied to the colonies mid trial (it had a minimal effect on mite drop for a few days). I didn't want that effect to influence the plots over time, so I only used the data from the control hives for the first graphs. But for comparing the two methods of sampling, I could use the full data set, since for each data point I was only comparing the actual mite presence in each hive at that moment in time.
[6] Various researchers have compared sampling methods. A review of the research through the year 2000 can be found in :
Devlin, SM (2001) Comparative analyses of sampling methods for varroa mites (Varroa destructor Anderson and Trueman) on honey bees (Apis mellifera L.). M.S. Thesis, Simon Fraser University.
More recently, Dr. Pierre Giovanazzo has presented data at conferences that suggested that natural mite drop was more indicative than alcohol wash.
However, data from Dr. Rob Currie indicate that alcohol wash accurately reflects the buildup of the mite infestation rate over the course of the year. http://capabees.org/content/uploads/2013/02/varroathreshold.pdf
[7] https://scientificbeekeeping.com/fighting-varroa-reconnaissance-mite-sampling/
[8] In order to run a truly valid test of efficacy, one would need to simultaneously measure the mite levels in adjacent untreated control hives, to see whether mite levels would have dropped off spontaneously. I apologize for not having such data. My pitiful excuse is that I initially set up the trial with controls and took mite washes, but midway into taking the 16-day checkback samples, I suddenly realized that I needed to get to the airport for a conference, s0 skipped taking samples from the control group. I missed the flight anyway : (
As a beekeeper, however, I know that the mite levels of the rest of the colonies in my operation typically continue to rise at this time of year, so although I would not be able to publish this data in a refereed journal, I feel that it may be of value to beekeepers whose goal is simply to get below a target infestation rate.
Category: Varroa Management
Tags: alcohol wash, MAQS strips, mite drop, mites | MAQS strips Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/maqs-strips/ |
Reflections on the Honey Bee Health Summit
First published in: American Bee Journal, August 2013
Reflections On The Honey Bee Health Summit
(And Other Random Thoughts)
Randy Oliver
ScientificBeekeeping.com
First Published in ABJ in August 2013
Into The Belly of the Beast
Plant Breeders
Drop the Demonization
Let's Be Logical
Take Home Sound Bites
Colony Health
The Varroa/Virus Complex
Pesticide Issues
Agriculture and Nutrition
Toxins
Sentinel Apiaries
Weighing the Costs and Benefits
The Varroa/Virus Complex
Watch What You Say
The Two Worlds of Beekeeping
The Evolution of Beekeeping
The Forage Issue, or Weeds, Bees Love'em
Economics and Meeting the Demand for Almond Pollination
The Nitty Gritty
We Need a New "Silent Spring"
Action Items and Resources
Disclaimer
References
In early June, Project Apis m. held a Honey Bee Health Summit hosted by Monsanto at the company's research headquarters in St. Louis, Missouri. The organizers invited speakers and stakeholders from the scientific community, the major beekeeping organizations, the pesticide companies, the EPA, various agricultural companies, the almond and cotton boards, economists, etc. Monsanto also opened the conference to any interested employees, picked up the transportation tab for them to attend, and filmed the proceedings for live webcast open to all 20,000 Monsanto employees worldwide.
Into The Belly Of The Beast
Many of us found it hard to believe that we were actually sitting in the "belly of the Beast"--Monsanto being popularly (and perhaps unjustly) demonized by many activists (especially in my home state of California). But the Summit wasn't about winning us over-rather its purpose was to allow the major stakeholders in beekeeping and agriculture to interact, to put each others' issues into perspective, and to make suggestions for improvement. Let me make clear that the Summit was not a corporate sales pitch, and that there were few presentations by Monsanto itself--the Summit was about honey bee health, the problems that beekeepers are having with Big Ag, and about the survival of our industry.
Monsanto was a logical choice as a corporate host for the conference, since the Israeli start up Beeologics recently asked (an important point) the company to acquire it in order to bring their RNAi technology to market for the benefit of the bee industry. Monsanto, in return, got access to Beeologic's proprietary RNAi technology in order to help it to develop the next generation of plant protection products, which, if successful, should reduce the need for toxic insecticides. Monsanto hired beloved apiary inspector and writer Jerry Hayes (The Classroom) to head its honey bee division, and recently completed its first large-scale field research project (in which I was a collaborator) which will likely give us the best insight into the causes of colony winter mortality to date (collected the very winter of the meltdown of bees for almond pollination).
Plant Breeders
I have no intention of making this article a fluff piece for Monsanto, but feel that the reader might benefit from some background information. At the research facility, one certainly gets the impression that the focus of Monsanto is upon plant breeding. We found a group of cheerful [1] and very interested scientists and technicians busily at work breeding better cultivars of crops (a thousand scientists at this facility alone). I should make clear that most of Monsanto's breeding work in not dependent upon genetic engineering (surprisingly, Monsanto produces seeds for organic, as well as conventional production).
In order to produce these cultivars, Monsanto breeders cross, say, a highly productive corn cultivar with a variety resistant to a particular blight. But first they sequence the crop plant's genome to look for genetic markers for the most desirable traits. This process is called "marker assisted selection," and is completely acceptable for organic certification. They then use an amazing machine to take each of the hundreds of thousands of seeds from the progeny of the crosses, and grind off a tiny snip of the seed coat which is then genetically analyzed for the desired markers. This process cuts out the need to grow to maturity the vast majority of those seeds in order to determine whether they carry the desired combination of traits or not.
I asked some of the scientists about the popular Bt (genetically engineered) trait for pest control, and reports that some insects are becoming resistant. The breeders felt that they will be able to keep ahead of resistance by employing slightly different cry toxins (each of course is carefully tested to ensure that it is not toxic to humans or bees).
Then to further speed up the tedious process of plant breeding, there are acres of greenhouses atop the buildings, which allow the breeders to grow three generations of that crop plant each season, thus tripling the rate at which better cultivars can be developed. Monsanto invests more money in plant breeding than all its major competitors combined, to the tune of $4 million dollars a day, 365 days a year!
Drop The Demonization
I'm not writing this article to defend Monsanto or any other corporate agribusiness (personally, I have an innate distrust of mega corporations and abhor the consolidation of agribusiness). Rather, I'm pointing out that Monsanto employees hardly consider what they do to be "evil." Far from it, the ones that I spoke with are excited to be developing new cultivars that produce more food on healthier plants with less water, fertilizer, or pesticides (Fig. 1).
Figure 1. Considerable progress has been made in lessening the environmental footprint of the growing of major crops such as corn. Field to MarketTM graphically illustrates such improvement in charts such as that above. Each colored pentagon represents the overall footprint based upon the five indicated metrics. As you can see, the footprint has gotten smaller year by year, especially in soil erosion (largely due to the adoption of reduced tillage practices). To their credit, the organization is looking to add additional metrics, such as for water quality and biodiversity (which would directly apply to pollinators). Image courtesy [[i]].
[i] Field to Market (2012 v2). Environmental and Socioeconomic Indicators for Measuring Outcomes of On-Farm Agricultural Production in the United States; Summary Report: Second Report (Version 2), December 2012. http://fieldtomarket.org/report/national-2/PNT_SummaryReport_A17.pdf
In reality, the problem is not any one company or product; rather, we need to step back and look at the entire agricultural system as a whole. Monsanto is clearly part of that system, but as far as corporate players go, perhaps more invested in sustainability than the norm. It might help to remember that it is the farmers themselves who made Monsanto wealthy--the company simply had the foresight to develop products that farmers wanted to buy.
Monsanto appears to genuinely want to be good a corporate citizen [3]. This is not merely lip service or "greenwashing"-the Gulf of Mexico Program recently announced that the Monsanto Company will receive a First Place 2013 Gulf Guardian Award for their Mississippi Watershed Project [4]. Monsanto's funding of the Honey Bee Health Summit, and its donations to Project Apis m. for the forage planting pilot project are of clear benefit to our industry--I suggest that we take advantage of their willingness to help us. The cynic may suggest that the Summit was about pitching a product to us, but that couldn't be further from the truth--Dr. Alex Inberg made quite clear that any such products were only in the earliest stages of development.
Let's Be Logical
I get plenty of alarmist emails forwarded to me every week parroting some "hate Monsanto" message. With each one, I check the facts behind the claim, and in most every case, have found them to be based upon exaggeration, misinterpretation, or distortion of the truth. When I informed a friend as to the truth behind a recent anti-Monsanto blast, she replied, "I just figured it was yet another crappy thing Monsanto was doing to try to kill us all." I must confess, I question the rationality of anyone who can think that a major agricultural company is truly trying to kill off its customer base (or all its employees)!
I realize that I am touching on emotional subjects, largely due to the fear factor drummed up by dedicated activists. I beg any reader that before sending me hate mail, that you first go to the trouble of carefully checking the facts for yourself-not someone else's interpretation, but go to the original sources!
The arguments by the anti-whatevers are often rife with fallacies in their logic. May I also suggest that you review these fallacies at [5], and put each argument by the anti's to the test. In the pesticide and GMO debate, I'm especially concerned about the overall effect of the logical fallacy called "The Middle Ground"-thinking that the midpoint between two extremes is likely close to the truth. The problem with that logic is that when one hears unsubstantiated extreme claims (such as that GMO's or glyphosate are the cause of every human health problem [6]), the natural (but illogical) tendency is give perhaps unmerited credence to such claims. This may lead us to erroneously conclude that our ignorant regulators are not watching out for our health. I do not purport to know where the truth actually lies, but I want to base my conclusions on hard evidence, and I assure you, all regulatory agencies look very carefully at all the evidence (check for yourself--their risk assessments are online, and you are free to comment [7, 8, 9]).
I do not wish to dwell on the GMO/human health issue, but let me put it this way: the vast majority of GM corn goes to animal feed. The livestock industry meticulously follows every detail of animal health. It's likely safe to assume that if GM corn were indeed unhealthful, the livestock industry would be the first to know! In any case, the scientific community is carefully investigating any potential health issues of GM crops, and since GM corn is such a tiny portion of most peoples' diets, I'm willing to trust our regulatory system on this one.
Take Home Sound Bites
I'm not going to name all the presenters, and information often came faster than we could scribble. Here are some notable "sound bites."
Colony Health
The clear common consensus was that the main causes of colony health problems are poor nutrition and the varroa/virus complex, sometimes exacerbated by pesticide issues.
I put nutrition first, since without food, other health issues are moot!
Provided that the colony is adequately fed, then the varroa/virus complex still remains the major problem for bees.
And if you place hives in an agricultural area, pesticides may enter the picture, either as outright kills, or as subtle sublethal effects.
Based upon 10,000 samples of beekeeper's hives by the Bee Informed Partnership, varroa is our number one problem.
In the year 2000 it was difficult to find viruses in colonies; now they are ubiquitous.
The consumer demands cheap, cosmetically-perfect food, so we will need to deal with pesticides.
You can't necessarily extrapolate from what happens in the lab to what will happen in the field.
We need to look at the total toxin burden to the colony.
We should amend FIFRA to register formulations rather than active ingredients.
Bees tend to do poorly on commodity crops.
The bee industry is having deep troubles at the same time that the rest of agriculture is experiencing increased returns.
We need to educate Big Ag.
Based upon the economic contribution of various livestock, the USDA should fund bee research right behind cows and swine, but above poultry.
The Varroa/Virus Complex
Based upon 10,000 samples of beekeeper's hives by the Bee Informed Partnership, varroa is our number one problem.
In the year 2000 it was difficult to find viruses in colonies; now they are ubiquitous
Pesticide Issues
The consumer demands cheap, cosmetically-perfect food, so we will need to deal with pesticides.
You can't necessarily extrapolate from what happens in the lab to what will happen in the field.
We need to look at the total toxin burden to the colony.
We should amend FIFRA to register formulations rather than active ingredients.
Agriculture and Nutrition
Bees tend to do poorly on commodity crops.
The bee industry is having deep troubles at the same time that the rest of agriculture is experiencing increased returns.
We need to educate Big Ag.
Based upon the economic contribution of various livestock, the USDA should fund bee research right behind cows and swine, but above poultry.
Toxins
The EPA is caught in a tough spot between the powerful agricultural lobbies, environmentalists, strident foodies, and beekeepers (who to the EPA's dismay, consistently fail to file adverse effects reports). When I asked EPA risk manager Tom Steeger how many pesticide incident reports he'd gotten so far this year at Beekill@epa.gov, he told me less than half a dozen.
Practical application: without incident reports, there is officially "no problem"! File that report if you experience a pesticide problem [10].
Understandably, some beekeepers are hesitant to "create waves" with local landowners. Dr. Steeger explains:
If they report to Beekill@epa.gov, they will be asked whether they reported to the state. They will also be asked if they would mind if the report is relayed to the state. If they do not wish to have the information relayed to the state, then it will not be relayed. While all incident data are useful, some are more useful than others. The most useful data are those reports that have been thoroughly investigated by the state.
I will elaborate upon pesticides and their sublethal effects next month.
Sentinel Apiaries
I asked major players at the Summit what we beekeepers could do toward getting bioindicator sentinel apiaries set up in agricultural areas across the country. Although all agreed that it would be a great idea, no one could come up with suggestions for funding such a program (the USGS is the most likely candidate).
Suggested idea: if carefully-managed stationary apiaries were set up across the country, we could firmly document which agricultural environments bees survive in, and in which they can't. Such bioindicator sentinel apiaries would help us to figure out which ag chemicals are causing the most problems.
Weighing The Costs And Benefits
Everyone these days seems to be worried about "toxins." And most people erroneously assume that "toxins" refer only to ag chemicals. Sure, the potential impacts of the sublethal effects of pesticides were discussed at the Summit, but a couple of interesting facts relevant to Monsanto's products have come to my attention. I'm no fan of widespread herbicide use, but while researching plant toxins, I came across a benefit of herbicides of which I was previously unaware [11]:
Another example of an agricultural change that has virtually eliminated many toxicity problems in the U.S. is the introduction and almost universal use of herbicides to control broad-leaved weeds in grain fields. In the past, before herbicides were used, grain fields were frequently heavily contaminated with many weeds, and both human and livestock toxicities occurred because of contamination of the grain with toxic weed seeds....There is a certain amount of irony associated with efforts in the U.S. to ban the use of herbicides. There is no known case of injury or death from residues on food, while prior to their use, public health and livestock problems existed because of natural toxins in grain. This situation still exists in many parts of the world.
Also of interest are the fungus-produced mycotoxins, which are among the most carcinogenic substances known to man, and clearly associated with human and animal disease. When insects feed on corn kernels under the husk, this opens the door for fungal growth, and the harvested grain may contain mycotoxins. Most countries set a regulatory "allowable level" in corn and other grains.
But since mycotoxins can't be completely avoided, the agencies must decide the levels of mycotoxins to be considered as "safe" in our diet. Not all agencies agree, so the allowable level varies substantially from country to country. For corn grain intended for human consumption, the U.S. allows at least twice the level as does the E.U. (another serving of mycotoxins anyone?).
What the heck has this got to do with Monsanto? Well, genetically engineered Bt corn, due to reducing insect damage, contains less mycotoxins. So here's some food for thought-should we be more concerned about the naturally-occurring plant and fungal toxins that are well known to cause human illness and cancer, or about glyphosate and Bt, neither of which have been clearly demonstrated to cause health problems? I'll let you think on it...
The Varroa/Virus Complex
Bee researchers voice a common message that regarding bee health issues, the varroa/virus complex is still the 800-pound gorilla. Monsanto is in a position to help on two fronts. First, the data from the aforementioned winter survival study in which I participated promises to help us much better understand the dynamics of what is actually taking place in our colonies over the winter. Monsanto agreed to allow me to share this data, and we are drooling in anticipation.
Secondly, Monsanto is investing serious funding into bringing the former Beeologics RNAi antiviral product to market, and is in the early stages of "non chemical" varroa and nosema treatments. We should be grateful that Monsanto is willing to take the gamble of working not only on an animal product, but doing so for such a relatively tiny market as ours.
Watch What You Say
I was glad for the chance to speak with stakeholders outside of the bee industry. Something that I had not previously thought of was how beekeepers had once again shot themselves in the foot. The U.S. commercial beekeeping industry is nowadays largely dependent upon almond pollination income to sustain itself. The fortunes of the bee industry and the almond industry are closely linked.
An almond grower at the Summit had me imagine a scenario in which a food manufacturer was trying to make the decision as to whether to include chopped almonds in a new product. And then that manufacturer hears some beekeeper on network TV suggesting that the almond industry was facing imminent collapse due to an upcoming shortage of bees. How do you think that sort of press plays to the almond industry?
The Two Worlds Of Beekeeping
What really struck me at the Summit was that hobby beekeepers are barely considered as stakeholders in the economic analyses of the bee industry. The reason was made clear by Gene Brandi, who did some quick math for our benefit. Gene pointed out that there are about 2.5 million managed hives of bees in the U.S. The average winter loss rate is running about 30%. That leaves about 1.7 million strong colonies for almond pollination. This winter the demand was for 1.6 million hives. And in the next few years, an additional 200,000 hives will be required for new orchards reaching bearing age. You do the math!
Few hobby beekeepers pollinate almonds, so as far as agriculture is concerned, the commercial migratory beekeepers are the only stakeholders of interest.
The Evolution Of Beekeeping
I found the above observation to be worth some thought. In my own career, I've evolved from being a hobby beekeeper to an (albeit small) commercial migratory beekeeper. During that time I've also witnessed some major evolution in the honey bee and in beekeeping practices.
Back in my early days as a beekeeper, bees were essentially semi-domesticated wild animals for which the beekeeper merely provided wooden nest boxes; it was generally up to the bees to take care of themselves, foraging in the wild for whatever they could find. At best, the beekeeper would feed a bit of syrup in spring or fall, and perhaps hand load the hives for a move to better pasture. There was a robust population of locally-adapted feral bees, often genetically distinct from the managed populations.
In cold winter areas, colonies were typically cyanided in fall, and all the honey harvested; the beekeeper took the winter off, and restarted with package bees in the spring. Honey production was the only reason to keep bees unless you were a package producer. The only disease that we worried about was AFB, but massive pesticide kills were commonplace. And California beekeepers asked almond growers for permission to move their hives to the orchards to take advantage of the nutritious bloom.
Then things started to change; not necessarily for the better. Secretary of Agriculture Earl Butz famously exhorted farmers to "get big or get out." Agricultural production grew more intense and the diversified family farm started down the path to extinction. Larger farms required more bees for pollination than the local population could provide, so beekeepers learned to use forklifts and semi trailers to move loads of hives.
Some California beekeepers twisted the arms of almond growers to start actually paying for pollination services--at 25C/ a hive to start with, finally reaching $8 by the time that I started moving bees to almonds. The semi-wild bee was replaced with selected breeds such as the Starline and Midnight. And then the bee got hit with some new parasites--chalkbrood, tracheal mite, and varroa. We suffered massive colony losses upon the arrival of the mites, and the feral population of bees disappeared. Canada closed the border, and the trend shifted toward the overwintering of colonies, or moving south for the winter.
Successful beekeeping now required additional skills and costs--and colony survival depended largely upon the degree of husbandry practiced by the beekeeper, whether hobby or commercial. We routinely treated colonies with antibiotics and miticides (although some of us started selecting for AFB- and mite-resistant stocks).
And then in the winter of 2004/2005 a perfect storm of poor forage, miticide failure, and the varroa/virus complex caused large-scale colony collapse. The almond growers were forced to bid their offered price for pollination rent from $45 up to $155 in one year. This changed everything! Midwestern honey producers tried something new--hauling their hives to California for the winter "gold rush." And as during the actual Gold Rush, many learned that gold mining was harder than it looked!
I did some math at that time, and brought to the attention of the editors that the bee industry had gone through a watershed event--in some years the industry as a whole now was making more income solely off almond pollination rentals than from total honey production nationwide (the low price of Chinese honey had much to do with this). Since almonds bloom in the dead of winter, and since colonies build up to swarm condition by early March, beekeepers who formerly took the winter off now no longer got a break! Beekeepers depended upon almond income to make ends meet, and modified their practices to this end.
At this point in time, the schism between hobby and commercial beekeeping has never been greater. The hobby beekeeper still wants to simply provide the box for bees to live in, while the commercial beekeeper invests formerly unthinkable amounts of money into each hive every season.
And this is where it gets really interesting-watching the genetics of the two populations of honey bees diverge. Most commercial beekeepers nowadays are truckers as much as beekeepers--modern day cowboys moving their herd from pasture to pasture (or from paying pollination to paying pollination). And their bees are bred for this model. The queen producers are selecting for a more and more "domesticated" bee--highly productive, with early build up, more resistant to miticides and pesticides, and largely dependent upon chemical parasite control and supplemental feeding.
Bottom line: the vast majority of managed colonies in the U.S. contain a population of bees that requires intensive husbandry, chemical control of parasites, and is dependent upon supplemental feeding, similarly to other livestock. This is not a criticism; it is simply a hard fact.
Concurrently, there is also a rebounding population of "wild type" feral and survivor colonies in many areas. These bees tend to be locally adapted, resilient, and have apparently worked out how to deal with the varroa/virus complex.
So let's consider the genetics of the small fraction of colonies managed by hobby beekeepers, most of whom have stationary apiaries. The BIP survey suggests that despite the fact that virtually 100% of commercial beekeepers treat their colonies for parasites, fully 70% of hobby beekeepers do not apply any treatments whatsoever! Not surprisingly, hobby beekeepers often suffer from a higher rate of winter losses [12]. But let's investigate this aspect more deeply.
I'm going to divide hobby beekeepers into two groups--those who start with commercial stocks of "domesticated" bees, and those who start with feral/survivor stock. One would expect that the "domesticated" commercial stocks would need the same sort of "help" from the beekeeper (miticides, antibiotics, supplemental feeding) that the package producers use in their own operations. It is not surprising then that when a newbee hobbyist goes "treatment free" with these bees, that the colony often succumbs. It is unreasonable to expect an animal bred for dependency upon human intervention to survive without assistance!
On the other hand, those beekeepers who are keeping a more "wild-type" survivor/feral stock find that these bees often survive quite well with little beekeeper intervention--even when kept in agricultural areas. I can't help but notice that there is a growing number of successful "natural" beekeepers. I suspect that their success has not so much to do with their management practices (or lack thereof), but is rather because they are keeping a more "natural" bee.
Practical application: it appears to me that our feral population of bees is finally rebounding from its decimation due to the invasion of varroa, and that the hobby beekeepers who are keeping feral/survivor stock are the first to be taking advantage of this event (this is not to discount the relatively few queen producers who are also breeding survivor stock). Could it be that we are finally seeing the tide coming back in, and that we will be able some day to go back to the "semi-wild bee in the box" model of beekeeping? I sure hope so!
But this now brings us to the important issue of forage.
The Forage Issue, Or Weeds, Bees Love 'Em
A major point at the Summit was the impact of changing agricultural practices upon commercial beekeeping. Crop plants provide only brief nutritional "boom or bust" events for bees, if at all. The short period of bloom may provide copious quantities of nectar and single-source pollen, but for the rest of the season they are a green desert so far as bees are concerned.
What is important to bees, other pollinators, and beneficial insects are the weeds, native plants, and brush between the rows, on the field margins and ditch banks, and in hedgerows and woods. It is these plants that provide the steady mix of diverse nectar and pollen upon which colony health is dependent. Such bee-friendly flora used to be a common feature in agricultural lands. But today's farms often appear "sterile"--all the pasture and biologically diverse "natural" areas have been cleared and herbicided right down to bare soil [13]. In some states, bee-friendly plants such as the sweet clovers are now considered to be noxious weeds [14]. And in California, "non crop vegetation" is discouraged in field margins around vegetable crops due to E. coli fears--leading to a conflict between food safety guidelines and environmental goals [15].
The major conversion in recent years of pasture/range/CRP lands to corn and soy has further eliminated the last good bee forage from large areas in the Midwest. Corn and soy are today largely grown using reduced tillage practices, which can have huge environmental benefits [16] when done with crop rotation and cover crops [17]. But in the short term, the reduction of tillage lends itself to the excessive use of herbicides to eliminate any sort of weed.
And this brings us back to Monsanto. I addressed the elephant in the living room at the Summit by pointing out that the flagship Roundup Ready®️ crops developed by Monsanto allow farmers to eliminate all extraneous vegetation from their land with impunity by using the herbicide glyphosate (formerly under Monsanto patent, and sold under the trade name Roundup®️). I questioned what Monsanto, in their desire to be a responsible corporate citizen, was doing to mitigate its indirect contribution to the loss of bee forage.
I must point out that these agri-deserts are certainly not the goal of Monsanto, but are rather due to the application of the recommendations of agricultural extension agents and the economic reality of farming. Monsanto and many other companies sell products demanded by agriculture--they can't really be blamed for the outcome, and if they weren't supplying those products, other companies readily would. In fact, the patents for Roundup Ready expire next year, so theoretically anyone will then be able to propagate Roundup Ready seed [18, 19].
To the company's credit, it has donated significant funds to Project Apis m. for a pilot program to plant bee forage on California ag lands. On a larger scale, the answer is less clear. Monsanto is clearly passionate about breeding cultivars that produce more food on less land. This is a net benefit to the environment, since it means that less natural habitat need be converted to cropland. But Monsanto really has no control over how farmers manage their lands--any landowner is free to plant from fencerow to fencerow, and kill any weed he so desires. And with high commodity prices, and government incentives to plant every available acre, they are doing so. In any case, we put the bug in Monsanto's ear that biodiversity on farmlands was a critical issue for the beekeeping industry.
Economics And Meeting The Demand For Almond Pollination
Our current model for supplying enough strong hives for the almond industry is dependent upon there being adequate summer pasture for our colonies. For the largest beekeepers, that has meant moving bees from California in winter to the Dakotas for summer, due to the previously vast swaths of pasture/range/CRP lands. But this bee-friendly, pesticide-free acreage is rapidly disappearing, and that is becoming a serious economic issue for beekeepers.
How serious? Let's do some math! Dr. Eric Mussen keeps track of the annual operating costs for a California commercial beekeeper to bring a strong hive to almonds--the current figure runs about $220. Even if that beekeeper gets $150 for almond rent, that hive still needs to earn another $70 before it breaks even (even more in a drought year). The beekeeper needs to do another couple of paid pollinations or make at least a 35-lb surplushoney crop before he turns any sort of profit. And that's only if he doesn't suffer from excessive winter losses (a number of beekeepers are not going to make it out of the red in 2013).
Almond grower Dan Cummings could easily tell me off the top of his head what percentages of his operating costs went to fertilizer, water, pollination services [20], etc. I was surprised that when I asked a few large-scale beekeepers a similar question regarding feed costs that they didn't know the answer offhand. One who later checked with his accountant found that 22% of his operating costs went to feed. This may help us to put into perspective the value of good forage.
Practical application: American agriculture used to rely upon the "free" pollination services provided by native insects and honey bees. Change in land use practices has now created a market for a pollination service industry. This industry initially relied upon natural forage to support its bees. But some of the same land use practices that created the need for migratory pollinators are now eliminating this natural forage, forcing the large commercial beekeepers to adopt the artificial feeding practices of the livestock industry. Change is the name of the game, and the Big Boys are having to adapt.
And how about that surplus honey crop? I was recently going over figures with various commercial California-based migratory beekeepers. Last season it was not unusual to feed 100 lbs of syrup per hive plus several pounds of protein supplement. The fed syrup far exceeded the weight of any honey crop! And the income to those beekeepers from almond pollination clearly exceeded any "profit" from the honey harvest. Commercial beekeeping is largely becoming a service industry to the almond growers.
And that pollination service industry is following in the footsteps of the livestock industry. Similar to our bees, livestock used to be provided a "nest area" and then left to forage as "semi-wild" animals. No longer-today's completely domesticated chickens and pigs never see the light of day nor green pasture--they live their entire lives in the carefully-controlled and very artificial environment of the concentrated animal feedlot operation. Cattle still forage naturally when young, but again are hustled off as soon as possible to confined dairy or feedlot facilities. The nutritional need of livestock are no longer obtained by them foraging in pasture and woodlots, but rather from them being brought formulated rations made from harvested monocultural corn, wheat, soy, and alfalfa (cut before it blooms).
And this seems to be the direction that commercial beekeeping is going. Traditional beekeeping practices may become as antiquated as the buggy whip. In order to service the almond industry, beekeepers who traditionally relied on "free" Midwestern forage are going to have to adapt. Some are already following the model of California beekeepers, who have long used supplemental feeding to get their bees through our normal summer drought. Unfortunately for the almond growers, they're just going to have to pay for the additional cost if they expect strong colonies in their orchards in February.
I hate to see it come to this. For over twenty years, I moved my hives from my home yards to almonds to summer pasture on irrigated alfalfa, and never had to feed a drop of sugar syrup or single pollen supplement patty. But now I keep them near home and carry feed to them when things dry up. It's neither natural nor romantic, but it works. Although today's pollen substitutes can't hold a candle to natural forage, they can be used to maintain (or even build) colony strength.
The hobbyist and sideliner: for the small-scale beekeeper who is less burdened with logistical issues, the situation is actually improving as we and the bees get a handle on managing the varroa/virus complex--small apiaries can nearly always eke out a living (or even produce big honey crops) in the woods and margins of ag lands or suburban areas.
The Nitty Gritty
There was a goodly amount of discussion at the Summit about the value of honey bees as pollinators to the agricultural industry, the economics of beekeeping, and suggestions that farmers should be encouraged to maintain more bee forage acreage for our benefit. I applaud those almond growers and other landowners who are experimenting with planting bee forage--this is clearly a step in the right direction. But do the math. Even the intense almond bloom can only support about two hives per acre for about three weeks of the year. So no matter how much forage fruit and nut growers plant, it won't get the bees through the summer--they will need to be moved elsewhere.
Pragmatic view: for the near future, the changing face of agriculture is going to change beekeeping practices more than beekeepers are going to change agricultural practices. We should continue to promote more environmentally-friendly agriculture, but in the meantime learn to deal with what we've got!
Let's consider whether our strategy of promoting pollinator habitat for its financial value to U.S. agriculture has merit. I'm going to set my smoker aside for a minute, and put on my objective (and perhaps cynical) analyst's hat. I'll go through my analysis step by step:
The consumer/voter wants cheap, abundant, cosmetically-perfect food.
We will only get such food if farmers make money growing it.
Any regulations that deny farmers the use of effective pesticides, or that force them to provide habitat for honey bees, will cost them money.
Politicians are scared to death of either rising food prices or opposition from the farm lobby.
There is strong political pressure to reduce direct payments to farmers.
There is no need for honey bees for the major commodity crops (corn, soy, wheat, rice, cotton) or vegetables. Only some fruit, nut, oil, and seed crops require bees. So Big Ag doesn't really have a financial incentive to care about bees.
Although honey bees may be worth $20 billion to U.S. agriculture, it is only the $4 billion almond industry that appears to be in any danger of a bee shortage. And even then, a good crop was set this year despite a severe shortage of strong colonies (good weather was likely a factor).
The supply of bee colonies to pollinate other pollinator-dependent crops is easily provided by the glut of hives following almond pollination.
Essentially, the country's pollination needs are being subsidized by the almond industry.
Beekeepers can offset the loss of natural forage by supplemental feeding.
Almond growers are making money, and if beekeepers need a few more dollars to feed their bees, the California almond growers (who grow 82% of the world's almonds) will simply pass that cost on to the consumer of this "luxury" product.
Conclusion: So, what's the problem?
Pragmatic point: to Big Ag, the pollinator issue is mainly a problem for the almond growers and the beekeepers to work out on their own. Our "you should do something about bee forage because of the economic value of honey bees to agriculture" is going to fall upon deaf ears. May I suggest that the bee industry instead adopt two talking points:
1. Pollinators (including honey bees) and other wildlife are threatened due to massive habitat conversion to agri-deserts. This is an environmental cause for action to promote and protect natural habitat in rural areas.
2. The Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) specifies that the registered uses of any pesticide "will not generally cause unreasonable adverse effects on the environment." We need to sway public and legislative opinion that the death of pollinators to pesticides is an "unreasonable adverse effect on the environment."
We Need A New "Silent Spring"
Luckily, our charismatic honey bees are becoming the poster child for our destruction of the natural environment, and everyone wants someone to help them. But talk is cheap, and it's going to be a hard sell to convince farmers to tithe a share of their productive acreage over to honey bees (unless they get something in return).
The plight of the honey bee in many areas today is less about pesticides (although those are clearly still an issue), but rather about them simply not being able to find enough to eat. Back when the diversified family farm was the rule, the accepted "inefficiency" of land use allowed plenty of wildlife (including pollinators) to coexist on the land. But in the name of progress we have "improved" agricultural technology to the point that we have eliminated all wildlife habitat from the model farm. The overwhelming financial incentive is for today's farmer to practice fencerow-to-fencerow scorched earth planting, leaving precious little remaining habitat for any form of life other than the crop.
What can we do to reverse this sad state of affairs for the displaced species? The driving force for change will need to come from the consumer and the voter. What we need is a groundswell of public support for more than just honey bees, but for wildlife habitat in general, particularly in rural areas (it may be surprising to some that bees often do much better in suburban areas than in the country). I suggest that we refocus our energies toward the specific issue of maintaining and recreating pollinator/wildlife habitat across the country (this focus still includes pesticides, since pollinators can't survive in poisoned habitat).
My dream is for another "Silent Spring" awakening of the American public. But the plight of the honey bee alone is not enough--we need to follow the lead of Western Europe and raise the environmental consciousness that natural habitat is disappearing at a rapid rate, and wildlife, birds, bats, and pollinators of all stripes are declining or going extinct. This is a Big Picture paradigm--for us to respect all species of life, big or small, and conserve their habitats.
Beekeepers are going to need to work with potential allies-a dicey proposition, since many of the environmental groups are dead set against honey bees (since honey bees are not native to this country). Luckily, the one thing that we have going for us is that whatever is good for wildlife habitat in general will also be good for honey bees.
Action Items And Resources
Stick to the two talking points mentioned above. The only way for an industry to get the attention of legislators is to present a unified message, and even better, to have other stakeholders presenting the same messages. Again:
1. The preservation and promotion of habitat is necessary for the survival of pollinators and wildlife, and
2. That the death of pollinators due to the registered use of any pesticide is an "unreasonable adverse effect on the environment." We need to start putting some teeth into the enforcement of existing pesticide regulations.
We beekeepers can help to direct the environmental stewardship sentiments of farmers and consumers (use the following linked references). The planting and maintenance of pollinator/wildlife habitat can resonate with farmers [21]. There is already a great model being promoted by the agribusiness giant Syngenta in Europe, in which love for the land (encouraged by subsidies) has gotten farmers to plant and maintain pollinator habitat [22]. A similar program is in place in California [23], and Project Apis m. is actively working to improve forage in the almond orchards [24]. Farmers can get assistance from various government programs [25, 26].
On the political front, we should continue to push for the specific protection and promotion of pollinators to be written into law [27]. Such a Congressional mandate would really help our cause!
Lastly, we should cultivate corporate sponsors willing to help us. Monsanto, Syngenta, Bayer, Costco, Haagen-Dazs, and others have funneled funding, public exposure, and expertise our way. Companies can actually wish to be good corporate citizens, and although they may not be perfect, the fact is that we live in an imperfect world. I'm willing to work with them when it benefits our beekeeping.
Disclaimer
I received payment from Monsanto this year for the rental of hives and the labor involved in running a research trial (as did two other nationally-prominent beekeepers). I can assure you that there is no financial incentive for us to run such trials, due to the hassle involved--we do it only for the benefit of the beekeeping industry. I am not constrained by any agreement to not speak my mind freely about Monsanto or any other corporation.
References
[1] Monsanto consistently makes Science Magazine's annual Top 20 Biotech and Pharmaceutical Industry Employers List. The magazine explains: "Besides innovation and research, survey respondents expect a leading company to be socially responsible, treat its employees with respect, and inspire their loyalty."
[2](Broken Link!) Field to Market (2012 v2). Environmental and Socioeconomic Indicators for Measuring Outcomes of On-Farm Agricultural Production in the United States; Summary Report: Second Report (Version 2), December 2012. (Broken Link!) http://fieldtomarket.org/report/national-2/PNT_SummaryReport_A17.pdf
[3] http://www.monsanto.com/whoweare/Pages/corporate-sustainability-report.aspx
[4] http://yosemite.epa.gov/opa/admpress.nsf/0/C38ABBC4C09BC77D85257B87006C2AF5
http://www.monsanto.com/improvingagriculture/Pages/mississippi-river-water-shed-project.aspx#.Ub8XiOe85AU
[5] https://yourlogicalfallacyis.com/
[6] Samsel , A and S Seneff (2013) Glyphosate's suppression of cytochrome P450 enzymes and amino acid biosynthesis by the gut microbiome: pathways to modern diseases. Entropy15(4): 1416-1463. http://www.mdpi.com/1099-4300/15/4/1416
[7] http://www.epa.gov/oppsrrd1/REDs/old_reds/glyphosate.pdf
[8] http://www.regulations.gov/#!documentDetail;D=EPA-HQ-OPP-2012-0132-0009
[9] http://www.regulations.gov/#!documentDetail;D=EPA-HQ-OPP-2012-0132-0005
[10] https://scientificbeekeeping.com/pesticide-incident-reporting/
[11] Cheeke, PR and LR Shull (1985) Natural Toxicants in Feeds and Poisonous Plants. Avi Publishing.
[12] http://beeinformed.org/2013/05/winter-loss-survey-2012-2013/
[13] http://www.cdfa.ca.gov/state_board/pdfs/Anderson_FSMA.pdf
[14] http://www.dnr.state.mn.us/invasives/terrestrialplants/herbaceous/whitesweetclover.html
[15] http://www.escholarship.org/uc/item/6f90g0dg#page-7
[16] (Broken Link!) http://ctic.paqinteractive.com/resourcedisplay/293/
[17] http://www.sare.org/Learning-Center/Books/Managing-Cover-Crops-Profitably-3rd-Edition
[18] http://www.seedworld.com/index.php?option=com_content&view=article&id=441%3Adec2011expirationdate&catid=71&Itemid=274
[19] http://www.monsanto.com/newsviews/Pages/roundup-ready-patent-expiration.aspx
[20] 12-14% of his operating costs
[21] http://www.hoosieragtoday.com/index.php/2013/06/18/farmers-work-with-nrcs-to-improve-pollinator-habitat/
[22] http://www.operationpollinator.com/
[23] Long, RF and JH Anderson (2010) Establishing hedgerows on farms in California. http://anrcatalog.ucdavis.edu/Items/8390.aspx
[24] http://projectapism.org/content/view/142/61/
[25] http://plants.usda.gov/pollinators/Using_Farm_Bill_Programs_for_Pollinator_Conservation.pdf
[26] http://plants.usda.gov/pollinators/Habitat_Development_for_Pollinators_NJ.pdf
[27] http://home.ezezine.com/1636/1636-2013.06.20.12.55.archive.html
Category: Miscellaneous articles, Topics
Tags: health summit, honey bee | honey bee Archives - Scientific Beekeeping | https://scientificbeekeeping.com/tag/honey-bee/ |
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