Ciguatera Toxicity in Emergency Medicine 

  • Author: Thomas C Arnold, MD, FAAEM, FACMT; Chief Editor: Asim Tarabar, MD   more...
 
Updated: May 21, 2010
 

Background

Ciguatera poisoning is the most common nonbacterial, fish-borne poisoning in the United States. It is caused by consumption of reef fish that feed on certain dinoflagellates (ie, algae) associated with coral reef systems. At least 5 types of ciguatoxin have been identified and are noted to accumulate in larger and older fish higher up the food chain.

Ciguatera poisoning has been a significant concern in tropical areas for centuries and generally is believed to be confined to coral reef fish in water between the latitudes of 35 degrees north and 35 degrees south. One study of the impact of climate changes on ciguatera producing organisms has suggested that elevations of sea surface temperatures may expand the band of concern above and below the 35th degree parallels.[1] Ironically, it also suggested that some areas may become too warm for the dinoflagellates to flourish. But, in the modern era of world travel and rapid transportation, many warm-water fish are available commercially in markets throughout the world, and cases of ciguatera poisoning may be seen in any location.

For related fish-borne poisoning articles, see Toxicity, Scombroid, Toxicity, Shellfish, and Toxicity, Seafood.

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Pathophysiology

Gambierdiscus toxicus is the dinoflagellate most notably responsible for production of ciguatoxin, although other species have been identified more recently. More than 400 species of fish have been implicated in ciguatera poisoning, starting with herbivores and then climbing up the food chain to the larger carnivorous fish.

Species of fish most frequently implicated include groupers, amberjack, red snappers, eel, sea bass, barracuda, and Spanish mackerel. Fish larger than 2 kg contain significant amounts of toxin and readily produce toxic effects when ingested. Although not completely reliable, an immunoassay and a mouse biologic assay are available for detection of ciguatoxin in affected fish. Ciguatoxin and other similar toxins are heat stable and lipid soluble; they are unaffected by temperature, gastric acid, or cooking method. Presence of toxin does not affect odor, color, or taste of the fish. Recently, chemists have been successful in synthesizing specific ciguatoxins, ensuring a practical supply will be available for future biological applications.[2]

Ciguatoxin produces toxic effects by activation of voltage-dependent sodium channels, resulting in hyperexcitability, decreased conduction, and prolonged refractoriness. Effects are most pronounced on neuronal, cardiac, and GI tissues.

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Epidemiology

Frequency

United States

Most ciguatera outbreaks in the United States occur in Hawaii and Florida, although tourists may develop symptoms after returning home. Global marketing of tropical fish has been responsible for sporadic cases reported across the United States mainland.

According to the 2008 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS), 168 single exposures to ciguatera were reported.[3]

International

Annually, an estimated 50,000 cases of ciguatera poisoning occur worldwide;[4, 5] however, this poisoning is difficult to track and is thought to be underreported. Ciguatera poisoning is endemic in Australia, the Caribbean, and the South Pacific islands. Recent studies have suggested that the incidence of this illness is continuing to increase. No doubt exists that ciguatera has had a substantial economic impact on many of the Third World countries where it is endemic.

Mortality/Morbidity

Ciguatera poisoning seldom is lethal. Typical mortality rate is 0.1%, although rates as high as 20% have been reported. Death usually is attributed to cardiovascular depression, respiratory paralysis, or hypovolemic shock.

The 2008 Annual Report of the American Association of Poison Control Centers' NPDS reported 46 minor outcomes, 54 moderate outcomes, 5 major outcomes and no deaths.[3]

Race

Several reports note that patients of similar ethnic backgrounds tend to share common symptom groupings.

Age

Children appear to be affected more severely and are involved more often in life-threatening cases.

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Contributor Information and Disclosures
Author

Thomas C Arnold, MD, FAAEM, FACMT  Professor and Chairman, Department of Emergency Medicine, Section of Clinical Toxicology, Louisiana State University School of Medicine in Shreveport; Medical Director, Louisiana Poison Control Center

Thomas 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, Louisiana State Medical Society, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Dana A Stearns, MD  Assistant Director of Undergraduate Education, Department of Emergency Medicine, Massachusetts General Hospital

Dana A Stearns, MD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians

Disclosure: Nothing to disclose.

John T VanDeVoort, PharmD  Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Michael J Burns, MD  Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center

Michael 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

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD  Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

References

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