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Chapter 2 The Pre-Travel Consultation Counseling & Advice for Travelers

Food Poisoning from Marine Toxins

Vernon E. Ansdell

Seafood poisoning from marine toxins is an under-recognized hazard for travelers, particularly in the tropics and subtropics. Furthermore, the risk is increasing because of factors such as climate change, coral reef damage, and spread of toxic algal blooms.


Ciguatera fish poisoning occurs after eating reef fish contaminated with toxins such as ciguatoxin or maitotoxin. These potent toxins originate from Gambierdiscus toxicus, a small marine organism (dinoflagellate) that grows on and around coral reefs. Dinoflagellates are ingested by herbivorous fish. The toxins produced by G. toxicus (gambiertoxins) are then modified and concentrated as they pass up the food chain to carnivorous fish and finally to humans. Ciguatoxins are concentrated in fish liver, intestines, roe, and heads.

G. toxicus may proliferate on dead coral reefs more effectively than other dinoflagellates. The risk of ciguatera is likely to increase as more coral reefs deteriorate because of climate change, ocean acidification, construction, and nutrient runoff.

Risk for Travelers

More than 50,000 cases of ciguatera poisoning occur globally every year. The incidence in travelers to highly endemic areas has been estimated as high as 3 per 100. Ciguatera is widespread in tropical and subtropical waters, usually between the latitudes of 35°N and 35°S; it is particularly common in the Pacific and Indian Oceans and the Caribbean Sea. The incidence and geographic distribution of ciguatera poisoning are increasing. Newly recognized areas of risk include the Canary Islands, the eastern Mediterranean, and the western Gulf of Mexico.

Fish that are most likely to cause ciguatera poisoning are carnivorous reef fish, including barracuda, grouper, moray eel, amberjack, sea bass, or sturgeon. Omnivorous and herbivorous fish such as parrot fish, surgeonfish, and red snapper can also be a risk.

Clinical Presentation

Typical ciguatera poisoning results in a gastrointestinal illness and may also cause neurologic symptoms. Although very rare, cardiovascular collapse may result. The first symptoms generally include nausea, vomiting, diarrhea, and abdominal pain, followed by neurologic symptoms such as paresthesias, pain in the teeth or the sensation that the teeth are loose, itching, metallic taste, blurred vision, or even transient blindness. Cold allodynia (abnormal sensation when touching cold water or objects) has historically been reported as characteristic, though new studies have found that there can be acute sensitivity to both hot and cold. Neurologic symptoms usually last a few days to several weeks.

The overall death rate from ciguatera poisoning is <0.1% but varies according to the toxin dose and availability of medical care to deal with complications. The diagnosis of ciguatera poisoning is based on the clinical signs and symptoms and a history of eating species of fish that are known to carry ciguatera toxin. Fish testing can be done by the Food and Drug Administration (FDA) in their laboratory at Dauphin Island. There is no easily available test for ciguatera toxins in human clinical specimens.


Travelers can take the following precautions to prevent ciguatera fish poisoning:

  • Avoid or limit consumption of the reef fish listed above, especially if the fish weighed >6 lb (2.7 kg).
  • Never eat high-risk fish such as barracuda or moray eel
  • Avoid the parts of the fish that concentrate ciguatera toxin: liver, intestines, roe, and head

Remember that ciguatera toxins do not affect the texture, taste, or smell of fish, and they are not destroyed by gastric acid, cooking, smoking, freezing, canning, salting, or pickling.


There is no specific antidote for ciguatoxin or maitotoxin poisonings. Treatment is generally for specific symptoms and includes supportive care. Intravenous mannitol has been reported in uncontrolled studies to reduce the severity and duration of neurologic symptoms, particularly if given within 48 hours of the appearance of symptoms.


Scombroid, one of the most common fish poisonings, occurs worldwide in both temperate and tropical waters. The illness occurs after eating improperly refrigerated or preserved fish containing high levels of histamine, and often resembles a moderate to severe allergic reaction.

Fish typically associated with scombroid have naturally high levels of histidine in the flesh and include tuna, mackerel, mahimahi (dolphin fish), sardine, anchovy, herring, bluefish, amberjack, and marlin. Histidine is converted to histamine by bacterial overgrowth in fish that has been improperly stored after capture. Histamine and other scombrotoxins are resistant to cooking, smoking, canning, or freezing.

Clinical Presentation

Symptoms of scombroid poisoning resemble an acute allergic reaction and usually appear 10–60 minutes after eating contaminated fish. They include flushing of the face and upper body (resembling sunburn), severe headache, palpitations, itching, blurred vision, abdominal cramps, and diarrhea. Untreated, symptoms usually resolve within 12 hours. Rarely, there may be respiratory compromise, malignant arrhythmias, and hypotension requiring hospitalization. Diagnosis is usually clinical. A clustering of cases helps exclude the possibility of true fish allergy.


Fish contaminated with histamine may have a peppery, sharp, salty, taste or “bubbly” feel but may also look, smell, and taste normal. The key to prevention is to make sure that the fish is properly iced or refrigerated at temperatures <38°F (<3.3°C), or immediately frozen after it is caught. Cooking, smoking, canning, or freezing will not destroy histamine in contaminated fish.


Scombroid poisoning usually responds well to antihistamines (H1-receptor blockers, although H2-receptor blockers may also be of benefit).


Several forms of shellfish poisoning may occur after ingesting filter-feeding bivalve mollusks (such as mussels, oysters, clams, scallops, and cockles) that contain potent toxins. The toxins originate in small marine organisms (dinoflagellates or diatoms) that are ingested and are concentrated by shellfish.

Risk for Travelers

Contaminated shellfish may be found in temperate and tropical waters, typically during or after dinoflagellate blooms called harmful algal blooms (HABs). One example of a HAB is the Florida red tide caused by Karenia brevis.

Clinical Presentation

Poisoning results in gastrointestinal and neurologic illness of varying severity. Symptoms typically appear 30–60 minutes after ingesting toxic shellfish but can be delayed for several hours. Diagnosis is usually one of exclusion and is usually made clinically in patients who recently ate shellfish.

Paralytic Shellfish Poisoning

Paralytic shellfish poisoning (PSP) is the most common and most severe form of shellfish poisoning. PSP is caused by eating shellfish contaminated with saxitoxins produced by dinoflagellates from Aelxandrium, Pyrodinium, and Gymnodinium genera. Symptoms usually appear 30–60 minutes after eating toxic shellfish and include numbness and tingling of the face, lips, tongue, arms, and legs. There may be headache, nausea, vomiting, and diarrhea. Severe cases are associated with ingestion of large doses of toxin and clinical features such as ataxia, dysphagia, mental status changes, flaccid paralysis, and respiratory failure. The case-fatality ratio is dependent on the availability of modern medical care, including mechanical ventilation. The death rate may be particularly high in children.

Neurotoxic Shellfish Poisoning

Neurotoxin shellfish poisoning is caused by eating shellfish contaminated with brevetoxins produced by the dinoflagellate K. brevis. Neurotoxic shellfish poisoning usually presents as gastroenteritis accompanied by minor neurologic symptoms resembling mild ciguatera poisoning or mild paralytic shellfish poisoning. Inhalation of aerosolized toxin in the sea spray associated with a Florida red tide (K. brevis bloom) can induce bronchoconstriction and may cause acute, temporary respiratory discomfort in healthy people. People with asthma may experience more severe and prolonged respiratory effects.

Diarrheic Shellfish Poisoning

Diarrheic shellfish poisoning (DSP) is caused by eating shellfish contaminated with a group of toxins that include polyether molecules (such as okadaic acid) produced by dinoflagellates from the genera Dinophysis and Prorocentrum lima. DSP produces chills, nausea, vomiting, abdominal cramps, and diarrhea. No deaths have been reported.

Amnesic Shellfish Poisoning

Amnesic shellfish poisoning (ASP) is a rare form of shellfish poisoning caused by eating shellfish, particularly blue mussels, contaminated with domoic acid produced by the diatom Nitzchia pungens. The first cases of ASP were reported after an outbreak associated with eating contaminated cultivated mussels. These cases were reported to have severe gastroenteric and neurologic symptoms. More recently, domoic acid exposure via the food web was implicated in die-off of marine mammals along the US Pacific Coast.


Shellfish poisoning can be prevented by avoiding potentially contaminated bivalve mollusks. This is particularly important in areas during or shortly after algal blooms, which may be locally referred to as “red tides” or “brown tides.” Travelers to developing countries should avoid eating all shellfish, because they carry a high risk of viral and bacterial infections. Marine shellfish toxins cannot be destroyed by cooking or freezing.


Treatment is symptomatic and supportive. Severe cases of paralytic shellfish poisoning may require mechanical ventilation.


  1. Ansdell V. Food-borne illness. In: Keystone JS, Freedman DO, Kozarsky PE, Connor BA, Nothdurft HD, editors. Travel Medicine. 3rd ed. Philadelphia: Saunders Elsevier; 2013. p. 425–32.
  2. Backer L, Fleming L, Rowan A, Baden D. Epidemiology and public health of human illnesses associated with harmful marine algae. In: Hallegraeff GM, Anderson DM, Cembella A, editors. Manual on Harmful Marine Microalgae. Paris: UNESCO; 2003. p. 723–49.
  3. Backer LC, Schurz-Rogers H, Fleming LE, Kirkpatrick B, Benson J. Marine phycotoxins in seafood. In: DÄ…browski WM, Sikorski ZE, editors. Toxins in Food. Boca Raton, FL: CRC Press; 2005. p. 144–74.
  4. Hungerford JM. Scombroid poisoning: a review. Toxicon. 2010 Aug 15;56(2):231–43.
  5. Isbister GK, Kiernan MC. Neurotoxic marine poisoning. Lancet Neurol. 2005 Apr;4(4):219–28.
  6. Palafox NA, Buenoconsejo-Lum LE. Ciguatera fish poisoning: review of clinical manifestations. J Toxicol Toxin Rev. 2001;20(2):141–60.
  7. Perl TM, Bedard L, Kosatsky T, Hockin JC, Todd EC, Remis RS. An outbreak of toxic encephalopathy caused by eating mussels contaminated with domoic acid. N Engl J Med. 1990 Jun 21;322(25):1775–80.
  8. Schnorf H, Taurarii M, Cundy T. Ciguatera fish poisoning: a double-blind randomized trial of mannitol therapy. Neurology. 2002 Mar 26;58(6):873–80.
  9. Sobel J, Painter J. Illnesses caused by marine toxins. Clin Infect Dis. 2005 Nov 1;41(9):1290–6.
  10. Stewart I, Lewis RJ, Eaglesham GK, Graham GC, Poole S, Craig SB. Emerging tropical diseases in Australia. Part 2. Ciguatera fish poisoning. Ann Trop Med Parasitol. 2010 Oct;104(7):557–71.