Chapter 2 The Pre-Travel Consultation Counseling & Advice for Travelers
Food Poisoning from Marine Toxins
Seafood poisoning from marine toxins is an underrecognized 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
Ciguatera fish poisoning occurs after eating reef fish contaminated with toxins such as ciguatoxin or maitotoxin. These potent toxins originate from small marine organisms (dinoflagellates) that grow on and around coral reefs. Dinoflagellates are ingested by herbivorous fish. The toxins are then concentrated as they pass up the food chain to large carnivorous fish (usually >6 lb, 2.7 kg) and finally to humans. Toxins are concentrated in fish liver, intestinals, roe, and head.
Gambierdiscus toxicus, which produces ciguatoxin, may proliferate on dead coral reefs more quickly than other dinoflagellates. The risk of ciguatera is likely to increase as more coral reefs die 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.
Typical ciguatera poisoning results in a gastrointestinal illness and may also cause neurologic symptoms. Although very rare, cardiovascular collapse may result. The first symptoms usually appear 1–3 hours after eating contaminated fish and include nausea, vomiting, diarrhea, and abdominal pain.
Neurologic symptoms usually appear 3–72 hours after the meal and include paresthesias, pain in the teeth or the sensation that the teeth are loose, itching, metallic taste, blurred vision, or even transient blindness. Cold allodynia (dysesthesia when touching cold water or objects) is characteristic, though there can be acute sensitivity to both hot and cold. Neurologic symptoms usually last a few days to several weeks.
Chronic neuropsychiatric symptoms resembling chronic fatigue syndrome may be disabling, last several months or longer, and include malaise, depression, headaches, myalgias, and fatigue. Cardiac manifestations include bradycardia, other arrhythmias, and hypotension.
The overall death rate from ciguatera poisoning is approximately 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 fish that are known to carry ciguatera toxin. Commercial kits to test for ciguatera in fish are unreliable; however, reliable fish testing can be done by the US Food and Drug Administration (FDA). There is no easily available clinical test for ciguatera in humans.
Travelers can take the following precautions to prevent ciguatera fish poisoning:
- Avoid or limit consumption of the reef fish listed above.
- 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. Treatment is generally for specific symptoms and includes supportive care. Intravenous mannitol has been reported 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.
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 fish allergy.
Fish contaminated with histamine may have a peppery, sharp, salty, 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, refrigerated, or immediately frozen after it is caught (<38°F, <3.3°C). 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 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.
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
This is the most common and most severe form of shellfish poisoning. 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 averages 6% and is dependent on the availability of modern medical care, including mechanical ventilation. The death rate may be particularly high in children.
Neurotoxic Shellfish Poisoning
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 (Karenia brevis bloom) can induce bronchoconstriction and may cause acute, temporary respiratory discomfort in healthy people. People with asthma may experience more severe and prolonged effects.
Diarrheic Shellfish Poisoning
This produces chills, nausea, vomiting, abdominal cramps, and diarrhea. No deaths have been reported.
Amnesic Shellfish Poisoning
This is a rare form of shellfish poisoning that has been reported to produce gastroenteritis and neurologic symptoms that may be severe. There are little data on this type of poisoning.
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,” “brown tides,” etc. 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.
- 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.
- 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.
- Hungerford JM. Scombroid poisoning: a review. Toxicon. 2010 Aug 15;56(2):231–43.
- Isbister GK, Kiernan MC. Neurotoxic marine poisoning. Lancet Neurol. 2005 Apr;4(4):219–28.
- Palafox NA, Buenoconsejo-Lum LE. Ciguatera fish poisoning: review of clinical manifestations. J Toxicol Toxin Rev. 2001;20(2):141–60.
- 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.
- Sobel J, Painter J. Illnesses caused by marine toxins. Clin Infect Dis. 2005 Nov 1;41(9):1290–6.
- 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.
- Page created: August 01, 2013
- Page last updated: August 01, 2013
- Page last reviewed: August 01, 2013
- Content source: