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ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMjIwOTY3LW92ZXJ2aWV3\nDrugs & Diseases > Infectious Diseases\nAuthor: Sandra G Gompf, MD, FACP, FIDSA; Chief Editor: Michael Stuart Bronze, MD more...\nSections Rabies\nPreexposure Prophylaxis or Immunization\nPostexposure Approach to Animal Bites and other Exposures\nPostexposure Prophylaxis or Immunization Before Symptom Onset\nMedical Treatment After Symptom Onset\nDeterrence and Prevention\nPassive Immunizing Agents\nRabies Vaccines (United States)\nRabies is caused by a neurotropic virus of the family Rhabdoviridae, genus Lyssavirus, subgroup rabies virus.\nThe virus is commonly transmitted via saliva that contaminates bites, scratches, and wounds, and, recently, via mucosal exposure. [1] Rabies transmission via transplanted neurologic tissues (corneas) and solid organs has also been documented. [2, 3, 4] One case of rabies was reported in China after exposure of an open wound to the blood of a person bitten by a dog; the exposed person succumbed to rabies after seeking no medical care, while the bitten individual received postexposure prophylaxis and did not develop rabies. [5]\nAnimal species that present the highest transmission risk to humans include canines (dogs, foxes, coyotes), cats, raccoons, and bats. In the case of bats, exposure may go unrecognized by a sleeping individual; thus, postexposure prophylaxis (PEP) is recommended whenever a bat is discovered in the room of a sleeping or incapacitated person. [6]\nThe lowest-risk species is the opossum, in which the virus does not replicate because of its low body temperature.\nHuman-to-human rabies virus transmission via saliva is theoretically possible. While it has not been documented, a mucosal, scratch, or bite exposure to saliva or blood of a person (or any other mammal) suspected of having rabies would be managed in a manner similar to that of any other exposure, with rabies PEP.\nStandard precautions are recommended in the care of patients with rabies in healthcare settings, including use of personal protective equipment during activities that may pose a risk of salivary contamination of mucosa or break in the skin. [7]\nRabies PEP should begin as soon as possible following an exposure, but no specific time frame has been defined, nor is it ever \"too late\" for PEP. Rabies is almost invariably fatal once symptoms begin, regardless of treatment, while PEP is safe and nearly 100% effective if administered before onset. Although the incubation period of rabies is typically 1-3 months, this may be hastened to a few days if inoculation occurs on the head and neck or may be prolonged if inoculation occurs on a site more distant from the central nervous system. It may also be delayed by very many years. (See Presentation).\nThe fatal madness of rabies has been described throughout recorded history, and its association with rabid canines is well known. For centuries, dog bites were treated prophylactically with cautery, with predictable and unfortunate results. In the 19th century, Pasteur developed a vaccine that successfully prevented rabies after inoculation and launched a new era of hope in the management of this uniformly fatal disease. (See Treatment and Medications.)\nRabies is a viral disease that affects the central nervous system (CNS). The genus Lyssavirus contains more than 80 viruses. Classic rabies, the focus of this article, is the prototypical human Lyssavirus pathogen. (See Etiology.)\nThere are 10 viruses in the rabies serogroup, most of which only rarely cause human disease. The genus Lyssavirus, rabies serogroup, includes the classic rabies virus, Mokola virus, Duvenhage virus, Obodhiang virus, Kotonkan virus, Rochambeau virus, European bat Lyssavirus types 1 and 2, and Australian bat Lyssavirus. (See Etiology.) Five antigenic variants of rabies strains are recognized in the United States (see the image below).\nDistribution of the 5 strains of rabies virus and the associated wildlife in the United States.\nThe rabies virus is a bullet-shaped virion with a single-stranded ribonucleic acid (RNA) nucleocapsid core and lipoprotein envelope. Its nucleocapsid material consists of Negri bodies, which are observed in the cytoplasm of infected neurons (see the image below). The virus is transmitted in saliva or in aerosolized secretions from infected animals, typically via a bite. The virus is not hardy and is quickly inactivated by drying, ultraviolet rays, x-rays, trypsin, detergents, and ether. (See Etiology.)\nHematoxylin and eosin stain of Negri body in a rabies-infected neuron. Courtesy of the US Centers for Disease Control and Prevention.\nRabies is a highly neurotropic virus that evades immune surveillance by its sequestration in the nervous system. Upon inoculation, it enters the peripheral nerves. A prolonged incubation follows, the length of which depends on the size of the inoculum and its proximity to the CNS. Amplification occurs until bare nucleocapsids spill into the myoneural junction and enter motor and sensory axons. At this point, prophylactic therapy becomes futile, and rabies can be expected to follow its fatal course, with a mortality rate of 100%.\nThe rabies virus travels along these axons at a rate of 12-24 mm/d to enter the spinal ganglion. Its multiplication in the ganglion is heralded by the onset of pain or paresthesia at the site of the inoculum, which is the first clinical symptom and a hallmark finding. From here, the rabies virus spreads quickly, at a rate of 200-400 mm/d, into the CNS, and spread is marked by rapidly progressive encephalitis. Thereafter, the virus spreads to the periphery and salivary glands.\nFrom the standpoint of diagnosis and therapeutic opportunities, it is important to understand that rabies does not cause cytotoxicity. Neuronal morphology and lifespan is normal throughout the course of the disease. Death occurs from global neurologic and organ dysfunction. The virion acts in the synaptic space, where homology in amino acid sequences between neurotransmitter receptors for acetylcholine, GABA, and glycine may afford a mechanism for viral binding of these receptors. Thus, its action is neurotoxic, rather than direct damage.\nFurther, as disease progresses, virus may no longer be viable or replicating in tissue, although Negri bodies are present. If the virus could be contained or the binding action reversed, a cure might indeed be possible.\nRabies is recognized as global zoonosis yet remains remarkably neglected, despite unmatched lethality. It remains a threat underappreciated by healthcare practitioners in many endemic areas, often owing to lack of rapid diagnostic tools, postmortem evaluation, and public health reporting. Further, few resources have been devoted to its mechanisms of disease and potential therapeutic targets; the therapeutic approach remains a crude guess at best, based on anecdotal experiences shared across the globe. Most attention has focused on preventive strategies, which are fortunately highly effective where implemented.\nThe prevalence of rabies varies by location depending on animal-control effectiveness and immunization programs. The largest number of human deaths annually was recorded during the first half of the 20th century, with an average of 50 documented cases per year. Most were related to rabid-dog exposure. After 1940, when canine rabies vaccination programs began, the average number of documented cases declined to 2 per year. From 2001-2005, 15 cases of human rabies were reported in the United States.\nHuman rabies reflects the prevalence of animal infection and the extent of contact this population has with humans. Less than 5% of cases in developed nations occur in domesticated dogs; however, unvaccinated dogs serve as the main reservoir worldwide. Undomesticated canines, such as coyotes, wolves, jackals, and foxes, are most prone to rabies and serve as reservoirs. These reservoirs allow rabies to remain an indefinite public health concern, and ongoing public health measures are critical to its control. Animal-control and vaccination strategies currently supersede postexposure prophylaxis in preventing the spread of rabies. Through such programs, rabies has been eliminated in some parts of the United States, as well as several nations.\nTerrestrial rabies in the United States is most common in raccoons on the eastern coast and in skunks, foxes, coyotes, and dogs on the Texas-Mexico border. Canine rabies, and to a lesser extent, bat rabies are significant problems in Mexico and around the world. (Opossums are rarely infected and are not considered a likely risk for exposure.)\nThe only rodent in the United States that can carry rabies long enough to transmit it to humans is the groundhog. Other small rodents (eg, squirrels, chipmunks, rats, mice) and lagomorphs (eg, rabbits, hares) usually die before being able to transmit rabies virus to humans, and human disease has not been documented from these mammals.\nDomestic animals usually succumb to the virus strain predominant in their geographic region. Other cases have been associated with dog or animal bites in travelers returning from abroad, especially in countries where wild canine rabies is endemic. In other countries, canines are the most common source of rabies. Other animals, such as mongooses, jackals, ferrets, and domestic farm animals, may be common sources. Human-to-human transmission has only occurred with corneal and other organ transplants. [2, 3] Transmission of virus in saliva through mucous membranes, open wounds, or scratches is possible but rarely documented.\nRabies continues to adapt to new hosts and evolve transmissibility in previously “dead-end” hosts. In Arizona 2001, a mutated bat strain was confirmed to have developed both pathogenicity and transmissibility in both foxes and skunks, which previously were not seriously affected or contagious upon infection. Human encroachments into natural areas, as in suburban development, have been associated with the spread of rabies strains in the past. [8]\nIn addition, changes in epidemiology are expected to follow global climate change and are most likely to be detected in areas of climate extremes. This is being illustrated in Alaska, as increased viral transmission shifts from red fox to arctic fox populations following warming trends. Increased surveillance is needed to improve predictive models of epidemiology and human risk. [9]\nBat (avian) rabies appears to be widespread in the 49 continental states, and since 1980, most endemic rabies cases in humans in the United States have been associated with bat strains. [10]\nBat bites, if noticed by the patient, are generally thought to be trivial injuries because of the small size of most temperate-zone species (eg, silver-haired bats, eastern pipistrelles). In addition, bat bites can go completely unrecognized by the patient; consequently, appropriate postexposure prophylaxis is not administered.\nOne third of rabies cases occur in children, and most have no known exposure to a rabid animal. Because children may not be able to recall contact with a bat, if a bat is found in a room where a child has been sleeping, the bat should be captured and submitted for examination to the county or state health authorities. In 60% of cases, testing of the bat can avoid the need for rabies immunization. [11]\nAt least 30 of the more than 39 species of bats in the United States have been reported as rabid at some time.\nRaccoons have been recognized a reservoir for rabies in the southeastern United States since the 1950s. [12] Currently, the risk of raccoon transmission exists in all of the eastern coastal states and Alabama, Pennsylvania, Vermont, West Virginia, and Ohio.\nThree areas are associated with skunk-borne rabies: the north-central United States, the south-central United States, and California. As recently as 2001, a new skunk-borne variant arose from a bat strain and has since been quickly spreading.\nCats are the most common domestic animals reported by US health departments as being rabid, owing to the high number of unvaccinated strays with possible contacts with bats and other mammals. [13, 14]\nDogs and cats along the Mexican border\nLimited resources and minimal public health infrastructure in the bordering communities have hindered efforts to maintain animal control through dog-vaccination programs. Viral studies of human cases reported from US border states implicate an urban canine rabies strain and a link to coyote rabies in southern Texas. [15]\nLower-risk animal species in the United States\nAny mammal is potentially at risk for rabies, some more than others. Lower-risk animal species in the United States include dogs, cats, and ferrets in areas not near a border. No person in the United States has ever contracted rabies from a dog, cat, or ferret held in quarantine for 10 days. American opossums are especially at low risk, because the species’ low body temperature hinders replication.\nAnimal rabies vaccine\nThe vaccinia-rabies glycoprotein virus used in rabies vaccine–laden baits for wild animals is a self-replicating agent. This oral animal vaccine may cause adverse effects in some humans exposed to it through animal bits, particularly in hosts with altered immunocompetence and persons in whom smallpox vaccination is contraindicated (eg, pregnant women, patients with an exfoliative skin condition). [16]\nTransplantation patients\nThe innate state of immunosuppression in this population often provides a favorable environment for viral replication. Recipients of neurally derived tissues are at highest risk; however, any tissue poses a risk. In 2004, kidneys and liver were inadvertently transplanted from a donor from Texas with rabies that had gone undiagnosed; the recipients developed clinical rabies within 30 days, resulting in 100% mortality. [17]\nRabies is more prevalent in the developing world than in industrialized countries. The World Health Organization (WHO) estimates that rabies is responsible for 35,000-50,000 deaths annually worldwide and that gross underreporting is likely. An estimated 10 million people receive postexposure prophylaxis each year after being exposed to animals with suspected rabies. Unvaccinated dogs are the major reservoir for rabies.\nGlobal reservoirs of rabies virus are as follows [18, 19] :\nEurope - Foxes, bats\nMiddle East - Wolves, dogs\nAsia - Dogs\nAfrica - Dogs, mongooses, antelopes\nNorth America - Foxes, skunks, raccoons, insectivorous bats\nSouth America - Dogs, vampire bats\nSex-related demographics\nEncounters with rabid animal vectors may be increased in males, who may have greater contact in certain geographic areas. Evidence to support this is found in data on dog bites, which are observed more frequently in males than in females.\nRabies virus infection is remarkable for the lack of evident pathology in the face of dramatic neurological symptoms. Minimal inflammation and neuronal cytopathy may be observed even postmortem. Similarly, viremia does not occur or play a role in spread to the CNS.\nPathophysiology has been best characterized in canine rabies variants. Canine rabies in humans requires deep-muscle inoculation. Endogenous muscle micro-RNA bind to viral transcripts and limit both replication and viral protein production, such that the virus is able to evade detection by antigen-presenting cells. Once enough virus replicates (or with a high-level inoculum or direct nerve injury), it binds motor neuron junctions at postsynaptic nicotinic acetylcholine receptors, which initiates uptake into the motor endplate. From here, the virus rapidly propagates across motor axons and chemical synapses in retrograde fashion toward the ganglia and nerve roots, at which point the prodromal symptoms of neuralgia and hypoesthesia may begin, in addition to fever and flulike illness.\nOnce reaching the CNS, it spreads throughout via the more ubiquitous nicotinic acetylcholine receptors of the brain. Of note, anterograde spread of rabies virus may then occur via sensory and autonomic pathways from the CNS to viscera, explaining many of the symptoms of progressive disease. Throughout propagation of the virus along motor pathways, the virus elicits little inflammation, and the motor neurons continue their otherwise normal functions of neurotransmission. Increasing signs of inflammation develop as CNS and visceral spread occurs, although a significant paucity of findings remains, other than mild nonspecific MRI T2 enhancements. Spinal fluid remains largely acellular, even in the presence of detectable rabies virus.\nPropagation to the CNS via peripheral sensory or autonomic synapses does not seem to occur with canine variants, and only about 30% of cases result in peripheral sensory neuralgia. However, 70% of cases with bat variants result in neuropathic pain in the region of inoculation, as well as Horner syndrome and other findings; thus, these alternate pathways may occur in bat rabies variants. [20, 21]\nDespite aggressive and intensive care management, the prognosis of rabies remains exceedingly poor. The very few cases of survival have involved bat variants.\nThe general public should be aware of the risk of rabies with wild and feral domestic canine breeds, cats, raccoons, and, in particular, bats, which often appear to be innocuous or produce small injuries that may be dismissed. Bats found in a room with a sleeping child or incapacitated individual should prompt rabies prophylaxis. Animals with rabies may act unusually docile or be found out and about in daylight when otherwise nocturnal, or the animal may be unusually aggressive. Thus, the concept of \"unprovoked\" versus \"provoked\" injury is not useful in determining rabies risk. Children should be taught not to pet or handle wild animals. A bat on the ground or easily caught should be considered rabid.\nPrompt washing of potentially rabies-exposed wounds or mucosa with soap and water is important and may significantly reduce viral inoculum.\nTravelers to areas endemic for rabies and who may participate in activities that may increase the exposure risk (eg, exploring caves or ruins, exposure to wild or feral animals) should seek rabies preexposure prophylaxis or be aware of sites to access reliable postexposure prophylaxis in the area. CDC Travel offers comprehensive guidance based on type of travel, region, and activity for the public and healthcare professionals.\nZhao H, Zhang J, Cheng C, Zhou YH. Rabies Acquired through Mucosal Exposure, China, 2013. Emerg Infect Dis. 2019 May. 25 (5):1028-1029. [Medline]. [Full Text].\nCenters for Disease Control and Prevention. Investigation of rabies infections in organ donor and transplant recipients--Alabama, Arkansas, Oklahoma, and Texas, 2004. MMWR Morb Mortal Wkly Rep. 2004 Jul 9. 53(26):586-9. [Medline].\nSrinivasan A, Burton EC, Kuehnert MJ, et al. Transmission of rabies virus from an organ donor to four transplant recipients. N Engl J Med. 2005 Mar 17. 352(11):1103-11. [Medline].\nCenters for Disease Control and Prevention. CDC confirms rabies death in organ transplant recipient. CDC Newsroom. March 15, 2013. Available at https://www.cdc.gov/media/releases/2013/s0315_rabies_organs.html.\nZhu JY, Pan J, Lu YQ. A case report on indirect transmission of human rabies. J Zhejiang Univ Sci B. 2015 Nov. 16 (11):969-70. [Medline]. [Full Text].\nShankar SK, Mahadevan A, Sapico SD, Ghodkirekar MS, Pinto RG, Madhusudana SN. Rabies viral encephalitis with probable 25 year incubation period!. Ann Indian Acad Neurol. 2012 Jul. 15 (3):221-3. [Medline]. [Full Text].\nCDC. Guideline for Isolation Precautions: Preventing Transmission of Infectious Agents in Healthcare Settings (2007). Centers for Disease Control and Prevention. Available at https://www.cdc.gov/infectioncontrol/guidelines/isolation/precautions.html#IIIa. Nov 25, 2015; Accessed: May 28, 2019.\nBlanton JD, Palmer D, Christian KA, Rupprecht CE. Rabies surveillance in the United States during 2007. J Am Vet Med Assoc. 2008 Sep 15. 233(6):884-97. [Medline].\nKim BI, Blanton JD, Gilbert A, et al. A Conceptual Model for the Impact of Climate Change on Fox Rabies in Alaska, 1980-2010. Zoonoses Public Health. 2013 Mar 4. [Medline].\nMessenger SL, Smith JS, Rupprecht CE. Emerging epidemiology of bat-associated cryptic cases of rabies in humans in the United States. Clin Infect Dis. 2002 Sep 15. 35(6):738-47. [Medline].\nWilloughby RE Jr, Hammarin AL. Prophylaxis against rabies in children exposed to bats. Pediatr Infect Dis J. 2005 Dec. 24(12):1109-10. [Medline].\nMcLean RG. Rabies in raccoons in the Southeastern United States. J Infect Dis. 1971 Jun. 123(6):680-1. [Medline].\nNational Association of State Public Health Veterinarians. 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Available at https://apps.who.int/iris/bitstream/handle/10665/259855/WHO-CDS-NTD-NZD-2018.04-eng.pdf?sequence=1. 2017; Accessed: 1 Jun 2019.\nHemachudha T, Ugolini G, Wacharapluesadee S, Sungkarat W, Shuangshoti S, Laothamatas J. Human rabies: neuropathogenesis, diagnosis, and management. Lancet Neurol. 2013 May. 12 (5):498-513. [Medline]. [Full Text].\nUgolini G. Rabies virus as a transneuronal tracer of neuronal connections. Adv Virus Res. 2011. 79:165-202. [Medline]. [Full Text].\nSmith JS, Fishbein DB, Rupprecht CE, Clark K. Unexplained rabies in three immigrants in the United States. A virologic investigation. N Engl J Med. 1991 Jan 24. 324 (4):205-11. [Medline]. [Full Text].\nGrattan-Smith PJ, O'Regan WJ, Ellis PS, O'Flaherty SJ, McIntyre PB, Barnes CJ. Rabies. A second Australian case, with a long incubation period. Med J Aust. 1992 May 4. 156 (9):651-4. [Medline]. [Full Text].\nJohnson N, Fooks AR, McColl K. Reexamination of Human Rabies Case with Long Incubation, Australia. 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[Medline].\nMoran GJ, Talan DA, Mower W, et al. Appropriateness of rabies postexposure prophylaxis treatment for animal exposures. Emergency ID Net Study Group. JAMA. 2000 Aug 23-30. 284(8):1001-7. [Medline].\nProsniak M, Faber M, Hanlon CA, Rupprecht CE, Hooper DC, Dietzschold B. Development of a cocktail of recombinant-expressed human rabies virus-neutralizing monoclonal antibodies for postexposure prophylaxis of rabies. J Infect Dis. 2003 Jul 1. 188(1):53-6. [Medline].\nWilson JM, Hettiarachchi J, Wijesuriya LM. Presenting features and diagnosis of rabies. Lancet. 1975 Dec 6. 2(7945):1139-40. [Medline].\nA Human Monoclonal Antibody to Rabies Virus Provides Protective Neutralizing Activity: Results of a Phase 1 Study, 50th Annual Meeting, Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC). Boston, MA, 2010:\nWHO. Rabies. World Health Organization. Available at http://www.who.int/mediacentre/factsheets/fs099/en/. 21 May 2019; Accessed: 1 Jun 2019.\nSenthilkumaran S, Jena NN, Gore SB, Manikam R, Thirumalaikolundusubramanian P. Factors for early death in rabies- the bitter truth. Indian J Crit Care Med. 2015 Sep. 19 (9):566-7. [Medline].\nTaylor E, Banyard AC, Bourhy H, Cliquet F, Ertl H, Fehlner-Gardiner C, et al. Avoiding preventable deaths: The scourge of counterfeit rabies vaccines. Vaccine. 2019 Apr 17. 37 (17):2285-2287. [Medline]. [Full Text].\nQuiambao BP, Ambas C, Diego S, Bosch Castells V, Korejwo J, Petit C, et al. Intradermal post-exposure rabies vaccination with purified Vero cell rabies vaccine: Comparison of a one-week, 4-site regimen versus updated Thai Red Cross regimen in a randomized non-inferiority trial in the Philippines. Vaccine. 2019 Apr 10. 37 (16):2268-2277. [Medline]. [Full Text].\nGuo Y, Duan M, Wang X, Gao J, Guan Z, Zhang M. Early events in rabies virus infection-Attachment, entry, and intracellular trafficking. Virus Res. 2019 Apr 2. 263:217-225. [Medline]. [Full Text].\nTable 1. Risk Categories for Active Preexposure Immunization and Rabies Titer Monitoring\nImmunization Regimen\nRabies research laboratory or biologics production workers\nPrimary course; booster when serum antibody is less than 1:5 dilution based on RFFIT results\nEvery 6 months\nRabies diagnostic laboratory workers, spelunkers, veterinarians and staff, animal control and wildlife workers in rabies-enzootic areas, travelers to areas of enzootic rabies for more than 30 days\nPrimary course; booster every 2 years or when serum antibody is less than 1:5 dilution based on RFFIT results\nEvery 2 years if not regularly boosted\nInfrequent\nVeterinarians and staff/students, animal control and wildlife workers in areas of low rabies risk\nPrimary course; no booster\nUS population at large\nSandra G Gompf, MD, FACP, FIDSA Associate Professor of Infectious Diseases and International Medicine, University of South Florida College of Medicine; Chief, Infectious Diseases Section, Director, Occupational Health and Infection Control Programs, James A Haley Veterans Hospital\nSandra G Gompf, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America\nTri M Pham, MD Consulting Physician, Division of Infectious Diseases, Watson Clinic, Lakeland\nTri M Pham, MD is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America\nCharurut Somboonwit, MD, FACP Associate Professor of Internal Medicine, Division of Infectious Disease and International Medicine, University of South Florida College of Medicine; Clinical Research and Communicable Diseases Director, USF Health and Hillsborough Health Department\nCharurut Somboonwit, MD, FACP is a member of the following medical societies: American College of Physicians, American Medical Association, Infectious Diseases Society of America\nAlbert L Vincent, PhD Associate Professor, Division of Infectious Diseases and International Health, Department of Internal Medicine, University of South Florida College of Medicine; Scientific and Research Advisor to the Division of Epidemiology, Hillsborough County Health Department\nDisclosure: Partner received none from none for none.\nLeslie L Barton, MD Professor Emerita of Pediatrics, University of Arizona College of Medicine\nLeslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics, Association of Pediatric Program Directors, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society\nRichard B Brown, MD, FACP Chief, Division of Infectious Diseases, Baystate Medical Center; Professor, Department of Internal Medicine, Tufts University School of Medicine\nRichard B Brown, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, and Massachusetts Medical Society\nWendy Carter, DO, Division of Infectious and Tropical Medicine, University of South Florida College of Medicine\nWendy Carter, DO is a member of the following medical societies: American College of Physicians, American Medical Association, American Osteopathic Association, and Infectious Diseases Society of America\nLucinda Elko, MD, Division of Infectious and Tropical Medicine, University of South Florida College of Medicine\nLucinda Elko, MD is a member of the following medical societies: Alpha Omega Alpha\nDonna J Fisher, MD Assistant Professor of Pediatrics, Tufts University School of Medicine; Interim Chief, Division of Pediatric Infectious Diseases, Baystate Children's Hospital\nDonna J Fisher, MD is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Society for Healthcare Epidemiology of America\nAnibal Jose Maldonado, MD, Fellow, Division of Infectious Diseases and International Medicine, University of South Florida\nAnibal Jose Maldonado, MD is a member of the following medical societies: American College of Physicians, American Medical Association, and Infectious Diseases Society of America\nRussell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine\nRussell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association\nencoded search term (Rabies) and Rabies\nEmergency Treatment of Rabies\nVaccinations/Immunizations During Pregnancy\nPediatric Vaccines: Global Brands and Country Availability\nAnimal Bites in Emergency Medicine\nAnimal Bites to the Head and Neck\nTrends in Human Rabies Deaths and Exposures — United States, 1938–2018\nPrize Photos Reveal Medicine's Humanity\nBats Now Pose Greatest Risk for Rabiesin the US\n2010 hdcv-imovax-rabies-vaccine-343168 Drugs\nDrugs rabies vaccine\n2010 hyperrab-s-d-kedrab-rabies-immune-globulin-human-righ-343142 Drugs\nDrugs rabies immune globulin, human (rig)\nNews Bats Now Pose Greatest Risk for Rabiesin the US\nJournal Article Trends in Human Rabies Deaths and Exposures — United States, 1938–2018"