Poisoning from ingested marine toxins is an underrecognized hazard for travelers, particularly in the tropics and subtropics. Furthermore, the risk is increasing because of climate change, coral reef damage, and spread of toxic algal blooms (Map 2-30).
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 are then modified and concentrated as they pass up the marine 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 poisoning is likely to increase as coral reefs deteriorate because of climate change, ocean acidification, offshore construction, and nutrient runoff.
Up to 50,000 cases of ciguatera poisoning get reported annually worldwide. Because the disease is underrecognized and underreported, this is likely a significant underestimate. 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. Medical practitioners must be aware that cases of ciguatera fish poisoning acquired by travelers in endemic areas may present in nonendemic (temperate) areas. In addition, cases of ciguatera fish poisoning are seen with increasing frequency in nonendemic areas as a result of the increasing global trade in seafood products.
Fish that are most likely to cause ciguatera poisoning are large carnivorous reef fish, such as 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.
Ciguatera poisoning may cause gastrointestinal, cardiovascular, neurologic, and neuropsychiatric illness. The first symptoms usually develop within 3–6 hours after eating contaminated fish but may be delayed for up to 30 hours. Adverse health effects referable to the above-named organ systems include:
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 characteristic signs and symptoms and a history of eating fish species known to carry ciguatera toxin. Fish testing can be done by the US Food and Drug Administration (FDA) in their laboratory at Dauphin Island. There is no readily available test for ciguatera toxins in human clinical specimens.
Travelers can take the following precautions to prevent ciguatera fish poisoning:
Ciguatera toxins do not affect the texture, taste, or smell of fish, nor are they destroyed by gastric acid, cooking, smoking, freezing, canning, salting, or pickling.
There is no specific antidote for ciguatoxin or maitotoxin poisonings. Symptomatic treatment may include gabapentin or pregabalin (neuropathic symptoms), amitriptyline (chronic paresthesias, depression, and pruritus), fluoxetine (chronic fatigue), and nifedipine or acetaminophen (headaches). 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. It should only be given to hemodynamically stable, well-hydrated patients.
After recovering from ciguatera poisoning, patients may want to avoid consuming fish, nuts, alcohol, or caffeine for at least 6 months, as they may cause a relapse in symptoms.
Scombroid occurs worldwide in both temperate and tropical waters. One of the most common fish poisonings, it 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, mahi mahi (dolphin fish), sardine, anchovy, herring, bluefish, amberjack, and marlin. Histidine is converted to histamine by bacterial overgrowth in fish improperly stored after capture. Histamine and other scombrotoxins are resistant to cooking, smoking, canning, or freezing.
Scombroid poisoning resembles an acute allergic reaction, usually appearing 10–60 minutes after eating contaminated fish. Symptoms 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 but may last up to 48 hours. Rarely, there may be respiratory compromise, malignant arrhythmias, and hypotension requiring hospitalization. There are no long-term sequelae. Diagnosis is usually clinical. 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 will usually 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 being 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 provide some benefit).
Several forms of poisoning may occur after ingesting toxin-containing shellfish, including filter-feeding bivalve mollusks (mussels, oysters, clams, scallops, and cockles), gastropod mollusks (abalone, whelks, and moon snails), or crustaceans (Dungeness crab, shrimp, and lobster). Toxins originate in small marine organisms (dinoflagellates or diatoms) that are ingested and are concentrated by shellfish.
Contaminated (toxic) shellfish may be found in temperate and tropical waters, typically during or after phytoplankton blooms, also 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 typically is made clinically in patients who have recently eaten shellfish.
Paralytic shellfish poisoning (PSP) is the most common and most severe form of shellfish poisoning. PSP is caused by eating shellfish contaminated with saxitoxins. These potent neurotoxins are produced by various dinoflagellates. A wide range of shellfish may cause PSP, but most cases occur after eating mussels or clams.
PSP occurs worldwide but is most common in temperate waters, especially off the Pacific and Atlantic Coasts of North America, including Alaska. The Philippines, China, Chile, Scotland, Ireland, New Zealand, and Australia have all reported cases.
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 (NSP) is caused by eating shellfish contaminated with brevetoxins produced by the dinoflagellate K. brevis . Predominately an illness of the Western Hemisphere (southeastern coast of the United States, the Gulf of Mexico, and the Caribbean), there are also reports of the disease from New Zealand.
NSP usually presents as a gastroenteritis accompanied by neurologic symptoms resembling mild ciguatera or paralytic shellfish poisoning, 30 minutes to 3 hours after a shellfish meal. A syndrome known as aerosolized red tide respiratory irritation (ARTRI) occurs when aerosolized brevetoxins are inhaled in sea spray. This has been reported in association with a red tide (K. brevis HAB) in Florida. It 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 (DSP) is caused by eating shellfish contaminated with toxins such as okadaic acid. It occurs worldwide, with outbreaks reported from China, Japan, Scandinavia, France, Belgium, Spain, Chile, Uruguay, Ireland, the United States, and Canada.
Most cases result from eating toxic bivalve mollusks such as mussels and scallops. Symptoms usually occur within 2 hours of eating contaminated shellfish and include chills, diarrhea, nausea, vomiting, and abdominal pain. Symptoms usually resolve within 2–3 days. No deaths have been reported.
Amnesic shellfish poisoning (ASP) is a rare form of shellfish poisoning caused by eating shellfish contaminated with domoic acid, produced by the diatom Pseudonitzchia spp. Outbreaks of ASP have been reported in Canada, Scotland, Ireland, France, Belgium, Spain, Portugal, New Zealand, Australia, and Chile. Implicated shellfish include mussels, scallops, razor clams, and other crustaceans.
In most cases, gastrointestinal symptoms such as diarrhea, vomiting, and abdominal pain develop within 24 hours of eating toxic shellfish, followed by headache, memory loss, and cognitive impairment. In severe cases there may be hypotension, arrhythmias, ophthalmoplegia, coma, and death. Survivors may have severe anterograde, short-term memory deficits.
Shellfish poisoning can be prevented by avoiding potentially contaminated shellfish. This is particularly important in areas during or shortly after algal blooms, which may be locally referred to as “red tides” or “brown tides.” Shellfish also carry a significant risk of infection from various viral and bacterial infections, for example hepatitis A virus, norovirus, Vibrio vulnificus, Vibrio parahaemolyticus , and several Salmonella and Shigella species. Ideally, travelers to developing countries should avoid eating all shellfish. 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.
Vernon E. Ansdell