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Ciguatera Toxicity

  • Author: Thomas C Arnold, MD, FAAEM, FACMT; Chief Editor: Asim Tarabar, MD  more...
 
Updated: Dec 29, 2015
 

Practice Essentials

Ciguatera poisoning 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.

Barracuda. Barracuda.

See 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.

Signs and symptoms

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, which often appear first, may include the following:

  • Abdominal pain
  • Nausea
  • Vomiting
  • Diarrhea
  • Painful defecation

Neurologic 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; classic symptom)
  • Dental pain (teeth feel loose)
  • Pruritus
  • Arthralgias
  • Myalgias
  • Weakness
  • Ataxia, vertigo
  • Respiratory paralysis
  • Coma

In children, irritability may be the only presenting neurologic symptom.

Cardiovascular findings may reflect the following:

  • Bradycardia
  • Hypotension
  • Pulmonary edema

Other general symptoms include the following:

  • Dysuria
  • Chills
  • Sweating
  • Painful ejaculation
  • Metallic taste
  • Polymyositis

See Clinical Presentation for more detail.

Diagnosis

All 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.

See Workup for more detail.

Management

Treatment is largely supportive and symptom driven. Medications used to treat ciguatera poisoning include the following:

  • Activated charcoal
  • Antihistamines
  • Amitriptyline
  • Mannitol
  • Analgesics
  • Nonsteroidal anti-inflammatory drugs (NSAIDs)
  • Gabapentin

See Treatment and Medication for more detail.

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Background

Ciguatera poisoning is the most common nonbacterial fish-borne poisoning in the United States.[1, 2, 3] 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. All are noted to accumulate in larger and older fish higher up the food chain. See Pathophysiology.

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. However, 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.

Ciguatera toxin is heat-stable and is unaffected by temperature, gastric acid, or cooking. Contaminated fish have no specific odor, color, or taste, making identification of potential contamination extremely difficult.

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 after ingestion of the toxin or, rarely, as late as 24 hours afterward, but generally occurs within 6-12 hours. Symptoms increase in frequency and severity over the subsequent 4-6 hours. Reported symptoms are numerous but commonly affect 3 major organ systems: gastrointestinal (GI), neurologic, and cardiovascular. See Presentation.

Treatment is largely supportive and symptom driven. The osmotic diuretic mannitol has become the mainstay of acute treatment in recent years, as it has been reported to dramatically diminish or prevent neurologic symptoms. Amitriptyline has been reported to relieve pruritus and dysesthesias in patients with acute ciguatera toxicity, and to diminish the severity of residual symptoms. See Treatment and Medication.

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 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.

Ciguatoxin 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%.

Chemists have successfully synthesized specific ciguatoxins, ensuring that a practical supply will be available for future biological applications.[4] Although not completely reliable, an immunoassay and a mouse biologic assay are available for detection of ciguatoxin in affected fish.

Ciguatoxin 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.

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Etiology

Ingestion 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.

Although more than 400 species of fish have been associated with ciguatera poisoning, the species most frequently implicated include the following:[5, 6]

  • Grouper
  • Amberjack
  • Red snapper
  • Eel
  • Sea bass
  • Barracuda
  • Spanish mackerel

Sexual transmission of ciguatoxin has been reported.[7] For example, in one case report a man with ciguatera poisoning experienced painful ejaculation and his sexual partner subsequently experienced dyspareunia.[8] 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.

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Epidemiology

United States statistics

According to the 2014 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS),157 single exposures to ciguatera were reported.[9] Most ciguatera outbreaks occur in Hawaii and Florida.[10, 11] However, tourists who visit endemic areas (eg, the Caribbean) may not develop symptoms until after returning home.

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.[12]

International statistics

Annually, an estimated 50,000 cases of ciguatera poisoning occur worldwide.[7, 13, 14] 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.[12]

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.

In the US Virgin Islands, an estimated 300 cases per 10,000 population occur annually; a similar rate is found in the French West Indies. In St. Thomas, a household survey estimated that 4.4% of all households experienced ciguatera poisoning annually, which is at least 2640 persons per year or an annual incidence of 600 cases per year. In Puerto Rico, 7% of the residents have experienced at least one episode of ciguatera poisoning in their lifetime.

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.

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.[15] Ironically, it also suggested that some areas may become too warm for the dinoflagellates to flourish.

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Prognosis

The 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.[16] However, a person who has contracted ciguatera poisoning may develop an extreme sensitivity to any further ciguatera exposure.

Complications

Bradycardia, 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 has been reported. Chronic fatigue syndrome has been reported.

Premature 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.

Mortality/morbidity

Ciguatera poisoning is seldom lethal. The 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 2011 Annual Report of the American Association of Poison Control Centers' NPDS reported 36 minor outcomes, 69 moderate outcomes, 4 major outcomes, and 1 death.[9]

Morbidity 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.

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Patient Education

Patients 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.

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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 Health Sciences Center-Shreveport; Medical Director, Louisiana Poison 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, 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.

Acknowledgements

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.

Timothy 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

Timothy 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

Disclosure: Nothing to disclose.

Norvin Perez, MD Medical Director, Juneau Urgent and Family Care

Norvin Perez, MD is a member of the following medical societies: American College of Emergency Physicians and American Medical Association

Disclosure: Nothing to disclose.

Dana A Stearns, MD Assistant Director of Undergraduate Education, Department of Emergency Medicine, Massachusetts General Hospital; Assistant Professor of Surgery, Harvard Medical School

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

Disclosure: Nothing to disclose.

Jeffrey R Tucker, MD Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut School of Medicine, Connecticut Children's Medical Center

Disclosure: Merck Salary Employment

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and 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.

Roy M Vega, MD Assistant Professor of Pediatrics, Albert Einstein College of Medicine; Director, Pediatric Emergency Services, Department of Emergency Medicine, Bronx Lebanon Hospital Center

Roy M Vega, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

William T Zempsky, MD Associate Director, Assistant Professor, Department of Pediatrics, Division of Pediatric Emergency Medicine, University of Connecticut and Connecticut Children's Medical Center

William T Zempsky, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

References
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Barracuda.
Grouper.
Snapper.
 
 
 
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