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ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvODEzODY5LW92ZXJ2aWV3\nDrugs & Diseases > Emergency Medicine\nCiguatera Toxicity\nAuthor: Thomas C Arnold, MD, FAAEM, FACMT; Chief Editor: Michael A Miller, MD more...\nSections Ciguatera Toxicity\nAntidotes, Other\nAntihistamines, 1st Generation\nAntidepressants, TCAs\nDiuretics, Osmotic Agents\nAnticonvulsants, Other\nAnalgesics, Other\nCiguatera poisoning is the most common nonbacterial fish-borne poisoning in the United States. [1] It is caused by consumption of reef fish contaminated with ciguatoxin, which originates with certain dinoflagellates (ie, algae) associated with coral reef systems and accumulates up the food chain from small herbivorous fish to larger carnivorous fish, such as barracuda (see the image below) and grouper. Contaminated fish have no specific odor, color, or taste, making identification of potential contamination extremely difficult.\nBarracuda.\nSee 5 Cases of Food Poisoning: Can You Identify the Pathogen?, a Critical Images slideshow, to help identify various pathogens and symptoms related to foodborne disease.\nCiguatera poisoning is a clinical diagnosis based upon a constellation of symptoms temporally related to ingestion of suspect fish products. Onset of symptoms may be within 15 minutes or as late as 24 hours (rarely) after ingestion of the toxin. Generally, symptoms are noted within 6-12 hours after ingestion of tropical reef fish. Symptoms increase in frequency and severity over the subsequent 4-6 hours. Reported symptoms are numerous but commonly affect 3 major organ systems: GI, neurologic, and cardiovascular.\nGI symptoms, which often appear first, may include the following:\nPainful defecation\nNeurologic symptoms may include the following:\nLingual and circumoral paresthesias\nPainful paresthesias of the extremities\nParadoxical temperature reversal (eg, cold objects feel hot and hot objects feel cold; classic symptom)\nDental pain (teeth feel loose)\nArthralgias\nMyalgias\nAtaxia, vertigo\nRespiratory paralysis\nIn children, irritability may be the only presenting neurologic symptom.\nCardiovascular findings may reflect the following:\nOther general symptoms include the following:\nDysuria\nMetallic taste\nSee Presentation for more detail.\nAll routine laboratory tests are nonspecific for ciguatera poisoning, but the results may reflect volume depletion from fluid losses. Mild creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) elevations, if present, reflect muscle tissue breakdown.\nTreatment is largely supportive and symptom driven. Medications used to treat ciguatera poisoning include the following:\nNonsteroidal anti-inflammatory drugs (NSAIDs)\nFor related poisoning articles, see Histamine Toxicity from Fish, Shellfish Toxicity, and Seafood Toxicity.\nGambierdiscus toxicus is the dinoflagellate most notably responsible for production of ciguatoxin precursors, although other species have been identified more recently. These dinoflagellates, which live on the surfaces of seaweeds and denuded corals, are a primary nutritional source for small herbivorous fish. In turn, these small fish become prey for larger carnivorous fish that are subsequently consumed by humans.\nCiguatoxin (CTX) and other similar toxins are heat stable and lipid soluble; they are unaffected by temperature, gastric acid, or cooking method. The presence of the toxin does not affect the odor, color, or taste of the fish. In humans who eat contaminated fish, the reported attack rate is 73-100%.\nChemists have successfully synthesized specific ciguatoxins, ensuring that a practical supply will be available for future biological applications. [2] Although not completely reliable, an immunoassay and a mouse biologic assay are available for detection of ciguatoxin in affected fish.\nCTX produces toxic effects by activation of voltage-dependent sodium channels at the neuromuscular junction. Activation results in membrane hyperexcitability, spontaneous repetitive neurotransmitter release, blockage of synaptic transmission, and depletion of synaptic vesicles. Effects are most pronounced on neuronal, cardiac, and gastrointestinal tissues. Ciguatoxin causes an increase in parasympathetic tone and impairs sympathetic reflexes.\nIngestion of sufficient quantities of fish that contain accumulated ciguatoxin produces this syndrome. Fish larger than 2 kg can contain significant amounts of toxin and readily produce toxic effects when ingested. Ciguatera fish poisoning (CFP) is not due to the mishandling of fish and is not prevented by any particular storage, preparation, or cooking methods. [3]\nAlthough more than 400 species of fish have been associated with ciguatera poisoning, the species most frequently implicated include the following: [4, 5]\nRed snapper [6]\nEel [7]\nSexual transmission of ciguatoxin has been reported. [8] For example, in one case report a man with ciguatera poisoning experienced painful ejaculation and his sexual partner subsequently experienced dyspareunia. [9] Thus, ciguatoxin may be present in the semen of affected men and be capable of producing symptoms. Ciguatoxin may be transmitted to the fetus through the placenta or to infants through breast milk.\nAccording to the 2017 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS), 145 single exposures to ciguatera were reported. [10] Most ciguatera outbreaks occur in Hawaii and Florida. [11, 12] However, tourists who visit endemic areas (eg, the Caribbean) may not develop symptoms until after returning home. The incidence in travelers to highly endemic areas has been estimated as high as 3 per 100. [13] Additionally, because fish from tropical waters are now available globally, cases are reported across the US mainland. For example, from August 2010-July 2011, 28 cases of ciguatera poisoning were reported in New York City. [14]\nAnnually, an estimated 50,000 cases of ciguatera poisoning occur worldwide. [8, 15, 16] However, ciguatera poisoning is difficult to track and is thought to be underreported. It is estimated that only 10% of cases are reported to health authorities. [14] Ciguatera is widespread in tropical and subtropical waters, usually between between the latitudes of 35 degrees north and 35 degrees south; it is particularly common in the Pacific and Indian Oceans and the Caribbean Sea. The highest incidences of ciguatera poisoning have been reported in the US Virgin Islands (1200 per 100,000), French Polynesia (1400 per 100,000) and Cook Islands (1760 per 100,000). [17]\nThe incidence and geographic distribution of ciguatera poisoning are increasing due to climate change. [18] Newly recognized areas of risk include the Canary Islands, the eastern Mediterranean, and the western Gulf of Mexico. [13] G toxicus, which produces ciguatera toxin, tends to proliferate on dead coral reefs. The risk of ciguatera is likely to increase as more coral reefs die or are jeopardized as a result of environmental factors, construction, and nutrient run-off. [17] One study of the impact of climate changes on ciguatera-producing organisms has suggested that elevation of sea surface temperatures may expand the band of concern above and below the 35th degree parallels. [19] Ironically, it also suggested that some areas may become too warm for the dinoflagellates to flourish.\nThe prognosis is excellent. A small longitudinal cohort study from Miami revealed that all 12 patients were back to baseline on all neuropsychological studies by 6 months. [20] However, a person who has contracted ciguatera poisoning may develop an extreme sensitivity to any further ciguatera exposure.\nBradycardia, hypotension, and T-wave abnormalities may occur in relation to the amount of ingested ciguatoxin. Cardiovascular symptoms often occur within 2-5 days of ingestion and usually resolve within 5 days. Pulmonary edema and chronic fatigue syndrome have been reported.\nPremature labor and spontaneous abortion have been reported in mothers with ciguatera poisoning, as have effects on the fetus and newborn child through placental and breast milk transmission.\nCiguatera poisoning is seldom lethal. The mortality rate is < 0.1% but varies according to the toxin dose and availability of medical care to manage complications. [13] Rates as high as 20% have been reported. The 2017 Annual Report of the American Association of Poison Control Centers' NPDS reported 32 minor outcomes, 27 moderate outcomes, 3 major outcomes, and no deaths. [10] Death usually is attributed to cardiovascular depression, respiratory paralysis, or hypovolemic shock. Risk factors identified in fatalities include consumption of large amounts of viscera and head, G toxicus, and consumption of reef fish collected after storms. [17]\nMorbidity from ciguatera poisoning may be high, and symptoms may be prolonged. Children appear to be affected more severely and are involved more often in life-threatening cases. Most morbidity is neurologic. Neurologic symptoms resolve after 1-2 weeks, but pain, paresthesia, pruritus, and weakness may persist for several weeks. Symptoms increase following ingestion of animal proteins. Chronic symptoms may occur and may result in permanent nerve damage.\nPatients who have experienced ciguatera poisoning should be advised that they may develop an extreme sensitivity to any further exposure to ciguatera. They should be instructed to refrain from eating fish from areas where ciguatera poisoning is endemic. Toxin concentration in the head, viscera, and roe suggest avoiding consumption of these parts. Commercial products are sold to detect ciguatoxin in fish during home preparation, but the reliability of these consumer products has not been validated.\n[Guideline] Dickey RW, Plakas SM. Ciguatera: a public health perspective. Toxicon. 2010 Aug 15. 56(2):123-36. [Medline].\nTsumuraya T, Fujii I, Hirama M. Production of monoclonal antibodies for sandwich immunoassay detection of Pacific ciguatoxins. Toxicon. 2010 Oct. 56(5):797-803. [Medline].\nFriedman MA, Fernandez M, Backer LC, et al. An Updated Review of Ciguatera Fish Poisoning: Clinical, Epidemiological, Environmental, and Public Health Management. Mar Drugs. 2017 Mar 14. 15 (3):[Medline]. [Full Text].\nHsieh CH, Hwang KL, Lee MM, Lan CH, Lin WF, Hwang DF. Species identification of ciguatoxin-carrying grouper implicated in food poisoning. J Food Prot. 2009 Nov. 72(11):2375-9. [Medline].\nCenters for Disease Control and Prevention. Ciguatera fish poisoning--Texas, 1998, and South Carolina, 2004. MMWR Morb Mortal Wkly Rep. 2006 Sep 1. 55(34):935-7. [Medline].\nHa DV, Uesugi A, Uchida H, Ky PX, Minh DQ, Watanabe R, et al. Identification of Causative Ciguatoxins in Red Snappers Lutjanus bohar Implicated in Ciguatera Fish Poisonings in Vietnam. Toxins (Basel). 2018 Oct 20. 10 (10):[Medline]. [Full Text].\nChan TYK. Regional Variations in the Risk and Severity of Ciguatera Caused by Eating Moray Eels. Toxins (Basel). 2017 Jun 26. 9 (7):[Medline]. [Full Text].\nCenters for Disease Control and Prevention. Cluster of ciguatera fish poisoning--North Carolina, 2007. MMWR Morb Mortal Wkly Rep. 2009 Mar 27. 58(11):283-5. [Medline].\nLange WR, Lipkin KM, Yang GC. Can ciguatera be a sexually transmitted disease?. J Toxicol Clin Toxicol. 1989. 27(3):193-7. [Medline].\nGummin DD, Mowry JB, Spyker DA, Brooks DE, Osterthaler KM, Banner W. 2017 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 35th Annual Report. Clin Toxicol (Phila). 2018 Dec 21. 55 (10):1-203. [Medline]. [Full Text].\nTester PA, Feldman RL, Nau AW, Kibler SR, Wayne Litaker R. Ciguatera fish poisoning and sea surface temperatures in the Caribbean Sea and the West Indies. Toxicon. 2010 Oct. 56(5):698-710. [Medline].\nRadke EG, Reich A, Morris JG Jr. Epidemiology of Ciguatera in Florida. Am J Trop Med Hyg. 2015 Aug. 93 (2):425-32. [Medline].\nAnsdell, VE. Food Poisoning from Marine Toxins. Gary W. Brunette, Editor in Chief. CDC Yellow Book 2018: Health Information for International Travelers. New York: Oxford University Press; May 31, 2017. 77-80. [Full Text].\nCiguatera fish poisoning - New York City, 2010-2011. MMWR Morb Mortal Wkly Rep. 2013 Feb 1. 62(4):61-5. [Medline].\nTing JY, Brown AF. Ciguatera poisoning: a global issue with common management problems. Eur J Emerg Med. 2001 Dec. 8(4):295-300. [Medline].\nChan TY. Ciguatera fish poisoning in East Asia and southeast Asia. Mar Drugs. 2015 Jun 2. 13 (6):3466-78. [Medline].\nChan TY. Characteristic Features and Contributory Factors in Fatal Ciguatera Fish Poisoning--Implications for Prevention and Public Education. Am J Trop Med Hyg. 2016 Apr. 94 (4):704-9. [Medline].\nBotana LM. Toxicological Perspective on Climate Change: Aquatic Toxins. Chem Res Toxicol. 2016 Apr 18. 29 (4):619-25. [Medline]. [Full Text].\nLlewellyn LE. Revisiting the association between sea surface temperature and the epidemiology of fish poisoning in the South Pacific: reassessing the link between ciguatera and climate change. Toxicon. 2010 Oct. 56(5):691-7. [Medline].\nFriedman MA, Arena P, Levin B, Fleming L, Fernandez M, Weisman R, et al. Neuropsychological study of ciguatera fish poisoning: a longitudinal case-control study. Arch Clin Neuropsychol. 2007 May. 22(4):545-53. [Medline].\nCameron J, Capra MF. The basis of the paradoxical disturbance of temperature perception in ciguatera poisoning. J Toxicol Clin Toxicol. 1993. 31 (4):571-9. [Medline].\nShoemaker RC, House D, Ryan JC. Defining the neurotoxin derived illness chronic ciguatera using markers of chronic systemic inflammatory disturbances: a case/control study. Neurotoxicol Teratol. 2010 Nov-Dec. 32(6):633-9. [Medline].\nBaden DG, Melinek R, Sechet V, Trainer VL, Schultz DR, Rein KS, et al. Modified immunoassays for polyether toxins: implications of biological matrixes, metabolic states, and epitope recognition. J AOAC Int. 1995 Mar-Apr. 78(2):499-508. [Medline].\nFriedman MA, Fleming LE, Fernandez M, Bienfang P, Schrank K, Dickey R, et al. Ciguatera fish poisoning: treatment, prevention and management. Mar Drugs. 2008. 6(3):456-79. [Medline]. [Full Text].\nTraylor J, Gossman WG. Toxicity, Ciguatera. 2018 Jan. [Medline]. [Full Text].\nEastaugh JA. Delayed use of intravenous mannitol in ciguatera (fish poisoning). Ann Emerg Med. 1996 Jul. 28(1):105-6. [Medline].\nSchnorf H, Taurarii M, Cundy T. Ciguatera fish poisoning: a double-blind randomized trial of mannitol therapy. Neurology. 2002 Mar 26. 58(6):873-80. [Medline].\nPerez CM, Vasquez PA, Perret CF. Treatment of ciguatera poisoning with gabapentin. N Engl J Med. 2001 Mar 1. 344(9):692-3. [Medline].\nInoue M, Lee N, Tsumuraya T, Fujii I, Hirama M. Use of monoclonal antibodies as an effective strategy for treatment of ciguatera poisoning. Toxicon. 2009 Jun. 53(7-8):802-5. [Medline].\nGrouper.\nSnapper.\nThomas C Arnold, MD, FAAEM, FACMT Professor and Chairman, Department of Emergency Medicine, Section of Clinical Toxicology, Louisiana State University Health Sciences Center-Shreveport; Medical Director, Louisiana Poison Center\nThomas C Arnold, MD, FAAEM, FACMT is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology\nDisclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: BTG CroFab - Advisor and Consultant.\nMichael A Miller, MD Clinical Professor of Emergency Medicine, Medical Toxicologist, Department of Emergency Medicine, Texas A&M Health Sciences Center; CHRISTUS Spohn Emergency Medicine Residency Program\nMichael A Miller, MD is a member of the following medical societies: American College of Medical Toxicology\nMichael J Burns, MD Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center\nMichael J Burns, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine\nTimothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin\nTimothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society\nNorvin Perez, MD Medical Director, Juneau Urgent and Family Care\nNorvin Perez, MD is a member of the following medical societies: American College of Emergency Physicians and American Medical Association\nDana A Stearns, MD Assistant Director of Undergraduate Education, Department of Emergency Medicine, Massachusetts General Hospital; Assistant Professor of Surgery, Harvard Medical School\nDana A Stearns, MD is a member of the following medical societies: American College of Emergency Physicians\nJeffrey R Tucker, MD Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut School of Medicine, Connecticut Children's Medical Center\nDisclosure: Merck Salary Employment\nJohn T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals\nJohn T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists\nRoy M Vega, MD Assistant Professor of Pediatrics, Albert Einstein College of Medicine; Director, Pediatric Emergency Services, Department of Emergency Medicine, Bronx Lebanon Hospital Center\nRoy M Vega, MD is a member of the following medical societies: American Academy of Pediatrics\nWilliam T Zempsky, MD Associate Director, Assistant Professor, Department of Pediatrics, Division of Pediatric Emergency Medicine, University of Connecticut and Connecticut Children's Medical Center\nWilliam T Zempsky, MD is a member of the following medical societies: American Academy of Pediatrics\nencoded search term (Ciguatera Toxicity) and Ciguatera Toxicity\nSeafood Toxicity\nBotulinum Toxin\nBotulinum Toxin in Pain Management\nBotulinum Toxin Injections in Plastic Surgery\nPathophysiology and Etiology of Lead Toxicity\nBotulinum Toxin for Laryngeal Dystonia\nLocal Anesthetic Toxicity\nDietary Supplement Causes Widespread Selenium Poisoning\nAtopic Dermatitis: Five Promising Targeted Therapies\n'Tis the Season for Gout\nAccording to Emergency Physicians\nUS Air Ambulances: Expensive, Risky, and Regulation-Averse\nDoc Gets New Heart, Loses Residency in 5 Weeks\nEmergency Reversal of Anticoagulation\nSepsis in Pregnancy: Recognition and Resuscitation\nFast Five Quiz: Drug Overdoses\nDiseases & Conditions Seafood Toxicity\nDiseases & Conditions Ethylene Glycol Toxicity\n2002 325451-overview Procedures\nProcedures Botulinum Toxin\nProcedures Botulinum Toxin in Pain Management"