Ciguatera Toxicity

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Practice Essentials

Ciguatera 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.



View Image

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:

Neurologic symptoms may include the following:

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

Cardiovascular findings may reflect the following:

Other general symptoms include the following:

See 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:

See Treatment and Medication for more detail.

For related poisoning articles, see Histamine Toxicity from Fish, Shellfish Toxicity, and Seafood Toxicity.

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 (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%.

Chemists 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.

CTX 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.

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. 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]  

Although more than 400 species of fish have been associated with ciguatera poisoning, the species most frequently implicated include the following:[4, 5]

Sexual 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.

Epidemiology

According 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]

Annually, 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]  

The 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.

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

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 and chronic fatigue syndrome have 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.

Ciguatera 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]  

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.

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.

History

Currently, ciguatera poisoning is a clinical diagnosis based upon a constellation of symptoms temporally related to ingestion of suspect fish products. Multiple individuals consuming the same fish and experiencing signs and symptoms consistent with ciguatera fish poisoning (CFP), strongly supports the diagnosis.[3]

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: gastrointestinal (GI), neurologic, and cardiovascular.

GI symptoms often appear first and can last 1-2 days. GI symptoms may include the following:

Neurologic symptoms usually are multiple, varied, and, at times, bizarre. In children, however, irritability may be the only presenting neurologic symptom. Neurologic symptoms may begin within a few hours to 3 days after the meal and can be persistent, lasting weeks to several months. They may be worsened by alcohol consumption, exercise, sexual intercourse, or changes in dietary behavior.

Neurologic symptoms may include the following:

Paradoxical temperature reversal is a classic reported finding. However, one study suggests that this perception is likely the result of the exaggerated and intense nerve depolarization and that gross temperature perception remains intact.[21]

Cardiovascular symptoms often resolve within 2-5 days and may reflect the following:

Other general symptoms include the following:

Physical Examination

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:

Approach Considerations

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.

Visual contrast sensitivity testing has been reported to be useful in confirming the diagnosis. The proposed mechanism suggests that neurotoxins such as ciguatera affect the ability to accurately discern shades of white, gray, and black.[22]

An assay has been developed that can qualitatively (and potentially quantitatively) measure ciguatoxin in fish and possibly human fluids.[23] At least one group in Japan has developed a monoclonal antibody immunoassay to detect the toxin in human tissues.[2]

The laboratories of the US Food and Drug Administration (FDA) can perform ciguatera toxin analyses on remnants of consumed fish submitted from the United States, Caribbean, and South Pacific. However, because the results of such analyses are not immediately available at the time of the patient’s initial presentation, initial care of the patient must proceed based on symptom progression, recent history of reef fish consumption, and exclusion of alternative diagnoses or explanations.[24]

Approach Considerations

Treatment is largely supportive and symptom driven. If performed within 3-4 hours of toxin ingestion, gastric decontamination with activated charcoal may help. Avoid administering ipecac syrup because of its potential to worsen fluid losses. Antiemetics may control nausea and vomiting.

Cool showers and antihistamines help relieve pruritus. If these measures do not provide relief, amitriptyline administration has proved effective and may also diminish severity of residual symptoms (eg, chronic pain syndromes).[25]

Mannitol infusion can help alleviate neurologic symptoms.[26] Start intravenous (IV) administration as soon as the diagnosis is confirmed. Patients given mannitol need adequate IV hydration; mannitol's diuretic effect requires strict observation of fluid intake and output. However, at least one prospective, controlled study found no difference between mannitol and normal saline in the treatment of ciguatera poisoning.[27]

Manage hypotension with volume replacement; pressor agents are rarely needed. Bradyarrhythmias respond well to atropine.

Gabapentin was found to be helpful in the resolution of symptoms in 2 patients diagnosed with ciguatera poisoning.[28] Intake of large amounts of vitamin B-12 has been reported to attenuate some of the symptoms.

Orogastric lavage is not recommended. It is not of proven benefit for ciguatera poisoning, and risks of this procedure are likely to outweigh benefits. Opiates and barbiturates may exacerbate symptoms and are not recommended.

One group in Japan has reported developing a strategy to use monoclonal antibodies to treat ciguatera toxicity.[29] Possibly an effective treatment will be available in the near future.

Long-Term Monitoring

During the recovery period, victims of ciguatera poisoning should avoid ingesting any of the following, which can cause an exacerbation of symptoms:

Prevention

Travelers to ciguatera-endemic areas should take the following precautions:

Instruct lactating mothers with ciguatoxin poisoning to avoid breastfeeding. The mother also may experience excessive nipple pain, and the infant may develop diarrhea. Advise patients that ciguatoxin can be transmitted through sexual intercourse.

No screening tests for the detection of ciguatera toxin in fish before they are distributed or consumed are available. Home products are available to detect ciguatoxin in fish at the time of preparation, but the reliability of these products in the hands of the consumer has not been validated.

Medication Summary

Medications used to treat ciguatera poisoning include the following:

Activated charcoal (Actidose-Aqua, EZ-Char, Kerr Insta-Char)

Clinical Context:  Activated charcoal is used for emergency treatment in poisoning caused by drugs and chemicals, and is the drug of choice when gastric decontamination is being considered. A network of pores adsorbs 100-1000 mg of drug per gram of charcoal. Activated charcoal prevents absorption by adsorbing the drug in the intestine; multidose charcoal may interrupt enterohepatic recirculation and enhance elimination by enterocapillary exsorption.

In theory, by constantly bathing the GI tract with charcoal, the intestinal lumen serves as a dialysis membrane for reverse absorption of the drug from the intestinal villous capillary blood into the intestine. Activated charcoal does not dissolve in water.

Class Summary

Gastrointestinal (GI) decontamination with oral activated charcoal is selectively used in the emergency treatment of poisoning caused by some drugs and chemicals. The network of pores present in activated charcoal adsorbs 100-1000 mg of drug per gram of charcoal. Activated charcoal does not dissolve in water.

Activated charcoal achieves its maximum effect when administered within 30 minutes after ingestion of a drug or toxin. However, decontamination with activated charcoal may be considered in any patient who presents within 4 hours after the ingestion.

Cyproheptadine

Clinical Context:  Cyproheptadine is a seratonin and histamine antagonist that competitively inhibits the H1 receptor, mediating bronchial constriction, smooth-muscle contraction, edema, hypotension, CNS depression, and cardiac arrhythmias. It prevents histamine release in blood vessels and is more effective in preventing histamine response than in reversing it; nevertheless, it is reported to ameliorate pruritus in ciguatera toxicity.

Diphenhydramine (Benadryl, Diphen, Altaryl, Anti-Hist)

Clinical Context:  Diphenhydramine is a histamine H1-receptor antagonist of effector cells in the respiratory tract, blood vessels, and GI smooth muscle. It has moderate to high anticholinergic and antiemetic properties. This agent is used for relief of symptoms caused by release of histamine in pruritus.

Hydroxyzine (Vistaril)

Clinical Context:  Hydroxyzine is H1-receptor antagonist with low to moderate antihistaminic properties; it inhibits respiratory, vascular, and GI smooth-muscle constriction. It has moderate to high anticholinergic and antiemetic properties. Antagonism of H1 receptors in the periphery mediates antipruritic effects.

Class Summary

These agents are used to reduce pruritus.

Amitriptyline

Clinical Context:  Amitriptyline has been reported to relieve pruritus and dysesthesias in patients with acute ciguatera toxicity, and to diminish the severity of residual symptoms (ie, chronic pain syndromes). This agent is most effective for chronic neurologic symptoms that often follow ciguatera poisoning. In this setting, amitriptyline may act by blocking fast sodium channels that have been activated by ciguatoxin.

Imipramine (Tofranil)

Clinical Context:  These agents have been suggested to act by inhibiting reuptake of noradrenaline at synapses in central descending pain modulating pathways located in the brainstem and spinal cord.

Doxepin (Silenor)

Clinical Context:  Doxepin increases the concentration of serotonin and norepinephrine in the CNS by inhibiting their reuptake by the presynaptic neuronal membrane. It inhibits histamine and acetylcholine activity and has proven useful in treatment of various forms of depression associated with chronic and neuropathic pain.

Nortriptyline (Pamelor)

Clinical Context:  Nortriptyline has demonstrated effectiveness in the treatment of chronic pain.

Desipramine (Norpramin)

Clinical Context:  This is the original TCA used for depression. These agents have been suggested to act by inhibiting the reuptake of noradrenaline at synapses in central descending pain modulating pathways located in the brainstem and spinal cord.

Class Summary

The anticholinergic and antihistaminic effects of these agents decrease pruritus. They are also used to treat associated neurologic pain.

Mannitol (Osmitrol, Resectisol, Aridol)

Clinical Context:  Mannitol is an osmotic diuretic that has become the mainstay of acute treatment in recent years. Mannitol has been reported to dramatically diminish or prevent neurologic symptoms associated with ciguatera poisoning. Mannitol is most effective when given early in course of treatment, but somewhat effective even after several days of symptoms. Neurologic symptoms often decrease within minutes of mannitol administration and may resolve completely within 2 days.

Class Summary

These agents are used empirically to treat neurologic symptoms associated with ciguatera poisoning. The toxic effect of ciguatoxin results from the opening of sodium channels in excitable tissues such as nerve and muscle. Mannitol produces osmotic inhibition of water transport in the proximal tubule and a subsequent decreased gradient for passive sodium absorption in the ascending limb of the loop of Henle.

Gabapentin (Neurontin)

Clinical Context:  Gabapentin is a membrane stabilizer, a structural analogue of inhibitory neurotransmitter gamma-amino butyric acid (GABA), which paradoxically is thought not to exert effect on GABA receptors. It appears to exert action via the alpha2delta1 and alpha2delta2 auxiliary subunits of voltage-gaited calcium channels. It is used to manage pain and provide sedation in neuropathic pain.

Pregabalin (Lyrica)

Clinical Context:  Pregabalin is a structural derivative of GABA; its mechanism of action unknown. Pregabalin binds with high affinity to the alpha2-delta site (a calcium channel subunit), and, in vitro, pregabalin reduces the calcium-dependent release of several neurotransmitters, possibly by modulating calcium channel function.

Class Summary

Used to manage pain and provide sedation in neuropathic pain.

Acetaminophen (Tylenol, Acephen, Cetafem, Valorin)

Clinical Context:  Acetaminophen is a clinically proven analgesic and antipyretic that produces analgesia by elevating the pain threshold and reduces fever through its action on the hypothalamic heat-regulating center. It equals aspirin in analgesic and antipyretic effectiveness and is unlikely to produce many of the adverse effects associated with aspirin and aspirin-containing products.

Class Summary

These agents are used to provide pain relief.

Ibuprofen (Advil, Caldolor, Addaprin, Motrin)

Clinical Context:  Ibuprofen is the drug of choice for patients with mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis. The intravenous form (Caldolor) is available only for hospital use and is indicated for pain or fever.

Ketoprofen

Clinical Context:  Ketoprofen is used for relief of mild to moderate pain and inflammation. Small dosages initially are indicated in small and elderly patients and in those with renal or liver disease. Doses over 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patient for response.

Naproxen (Aleve, Anaprox, Naprosyn)

Clinical Context:  Naproxen is used for relief of mild to moderate pain; it inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, which is responsible for prostaglandin synthesis. NSAIDs decrease intraglomerular pressure and decrease proteinuria.

Diclofenac (Voltaren, Cataflam XR, Zipsor, Cambia)

Clinical Context:  Diclofenac inhibits prostaglandin synthesis by decreasing cyclooxygenase activity, which, in turn, decreases the formation of prostaglandin precursors.

Class Summary

NAIDs are used for patients with mild to moderate pain. These agents inhibit inflammatory reactions and pain by decreasing prostaglandin synthesis.

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

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: BTG CroFab - Advisor and Consultant.

Chief Editor

Michael 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

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.

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Barracuda.

Barracuda.

Grouper.

Snapper.