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Toxicity, Ciguatera

Author: Thomas Arnold, MD, Medical Director, Louisiana Poison Control Center, Associate Professor and Chairman, Department of Emergency Medicine, Section of Clinical Toxicology, Louisiana State University Health Sciences Center
Contributor Information and Disclosures

Updated: Jun 7, 2007

Introduction

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. 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.

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.

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.

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.

International

Annually, an estimated 50,000 cases of ciguatera poisoning occur worldwide; 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. 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.

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.

Clinical

History

Currently, ciguatera 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.

  • GI symptoms often are the first to appear, may last 1-2 days, and include the following:
    • Abdominal pain
    • Nausea
    • Vomiting
    • Diarrhea
  • Neurologic symptoms usually are multiple, varied, and, at times, bizarre. Symptoms may begin within a few hours to 3 days after the meal and can be persistent, lasting weeks to several months. Symptoms may include the following:
    • Lingual and circumoral paresthesias
    • Painful paresthesias of the extremities
    • Paradoxical temperature reversal (eg, cold objects feel hot and hot objects feel cold) (This is a classic reported finding; however, at least one study suggests that this perception is likely the result of the exaggerated and intense nerve depolarization and that gross temperature perception remains intact).
    • Dental pain (teeth feel loose)
    • Pruritus
    • Arthralgias
    • Myalgias
    • Weakness
    • Ataxia, vertigo
    • Respiratory paralysis
    • Coma
  • Cardiovascular symptoms are less common but can be severe. They usually resolve within 2-5 days. Patients may experience weakness and dizziness from bradycardia and hypotension.
  • Other features include dyspnea, sweating, salivation, chills, neck stiffness, and pruritus.

Physical

  • Dehydration from GI losses is a common finding.
  • Neurologic findings are extremely variable, from mild to life threatening.
  • Cardiovascular findings include bradycardia and hypotension. Signs of shock may be observed. Hypotension results from the following:
    • Fluid loss
    • Bradycardia
    • Peripheral vasodilation
    • Myocardial depression

Causes

Ingestion of sufficient quantities of fish with accumulated ciguatoxin produces this syndrome.

More on Toxicity, Ciguatera

Overview: Toxicity, Ciguatera
Differential Diagnoses & Workup: Toxicity, Ciguatera
Treatment & Medication: Toxicity, Ciguatera
Follow-up: Toxicity, Ciguatera
References

References

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Further Reading

Keywords

ciguatera poisoning, ciguatoxin, Gambierdiscus toxicus, grouper, amberjack, red snapper, eel, sea bass, barracuda, Spanish mackerel, ciguatera toxicity, fish-borne poisoning, reef fish poisoning

Contributor Information and Disclosures

Author

Thomas Arnold, MD, Medical Director, Louisiana Poison Control Center, Associate Professor and Chairman, Department of Emergency Medicine, Section of Clinical Toxicology, Louisiana State University Health Sciences Center
Thomas Arnold, MD 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.

Medical Editor

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.

Pharmacy Editor

John T VanDeVoort, PharmD, ABAT, Director of Pharmacy, Sacred Heart Hospital
John T VanDeVoort, PharmD, ABAT is a member of the following medical societies: American Academy of Clinical Toxicology and American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

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.

CME Editor

John Halamka, MD, Chief Information Officer, CareGroup Healthcare System, Assistant Professor of Medicine, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard Medical School
John Halamka, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

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