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Seafood Poisoning
49 Seafood Poisoning Vernon Ansdell
KEY POINTS • Travelers to the Caribbean and Indo-Pacific Ocean regions should be aware of the risk of ciguatera poisoning and avoid consumption of large carnivorous reef fish such as grouper, snapper, amberjack, and barracuda. The toxin survives normal cooking procedures.
• Paralytic shellfish poisoning occurs after ingestion of contaminated bivalve mollusks such as clams, mussels, oysters, and scallops. The toxin survives normal cooking procedures.
INTRODUCTION
The toxins that cause ciguatera poisoning originate from dinoflagellates such as Gambierdiscus toxicus, which are found on marine algae usually attached to dead coral reefs. Dinoflagellates are ingested by herbivorous fish and the toxins are concentrated as they pass up the food chain to large (usually >6 lb) carnivorous fish and finally to humans. CTX, maitotoxin, and scaritoxin are among the most lethal natural substances known and may be concentrated up to 50–100 times in parts of the fish such as the liver, gastrointestinal tract, roe, and head. The toxins do not affect the appearance, texture, smell, or taste of the affected fish and are not destroyed by gastric acid, cooking, or other fish-processing methods such as canning, drying, freezing, smoking, salting, or pickling. CTX has recently been completely characterized and synthesized,5 which may lead to advances in the understanding of its mechanism of action and potential therapies. Pacific Ocean, Caribbean, and Indian ocean CTX appear to be structurally different.6–9 Over 400 species of fish have been implicated in ciguatera poisoning. They are mainly carnivorous reef fish, such as grouper, snapper, barracuda, jack, sturgeon, sea bass, and moray eel. Certain herbivorous or omnivorous reef fish, such as surgeonfish and parrotfish, may also be responsible. Open ocean pelagic fishes such as tuna and mahi-mahi have not been associated with ciguatera poisoning. A wide range of symptoms has been reported, including generalized symptoms of profound weakness, chills, sweating, arthralgia, myalgia, and a metallic taste in the mouth. Typically, there is an acute gastrointestinal illness followed by neurologic symptoms and, rarely, cardiovascular collapse. The onset of symptoms is usually within 1–3 hours of eating contaminated fish, but may occur within 15–30 minutes or be delayed for up to 30 hours. Most symptoms resolve within 1–4 weeks. Gastrointestinal symptoms occur in most cases and include diarrhea, nausea, vomiting, and abdominal pain. They usually occur 1–3 hours after eating affected fish and may last for 1–2 days. Neurologic symptoms tend to occur later and may be delayed for up to 72 hours and last for several months or even years. Neurologic symptoms include cold allodynia (dysesthesia when touching cold water or objects). This is very characteristic of ciguatera poisoning but is not pathognomonic, as it may also occur in neurotoxic shellfish poisoning (NSP). Other neurologic
Seafood poisoning in travelers has become increasingly common in recent years. Multiple factors are probably involved including increased travel to areas where seafood poisonings are common, more adventurous eating habits, global climate change, coral reef damage, and spread of toxic algal blooms. In addition, more cases are being recognized in traditionally nonendemic areas as a result of increased importation of seafood from endemic areas.
CIGUATERA Ciguatera-like illnesses were known in ancient Egypt. Some of the earliest recorded cases in travelers were in the crews sailing with European explorers such as Christopher Columbus and James Cook1 (Box 49.1). Captain Bligh and his followers apparently developed ciguatera poisoning after the historic mutiny aboard HMS Bounty, and it has been speculated that Alexander the Great refused to let his troops eat fish because of concerns regarding ciguatera poisoning. Estimates suggest there are 50,000–500,000 new cases of ciguatera poisoning worldwide every year, making it one of the most common causes of marine poisoning from a food toxin (Table 49.1). It is widespread in tropical and subtropical waters between latitudes 35° north and 35° south, and is particularly common in the Pacific and Indian oceans and the Caribbean Sea (Fig. 49.1). Recent evidence suggests increasing worldwide incidence of ciguatera poisoning, especially in the Pacific. Newly recognized areas of risk include the Canary Islands, the western Gulf of Mexico, and the eastern Mediterranean. Most cases follow the ingestion of coral reef fish containing potent toxins such as ciguatoxin (CTX), maitotoxin, and scaritoxin that originate in dinoflagellates found in coral reefs. Average annual incidence rates for ciguatera fish poisoning vary from 5 to 50/100,000 in major endemic areas, with rates up to 1500/100,000 or even higher in some areas of the South Pacific during certain years.2–5 Of particular relevance to scuba divers is the fact that many of the symptoms of ciguatera poisoning may closely mimic those of decompression sickness.
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CHAPTER 49 Seafood Poisoning Abstract
Keywords
Poisoning from ingestion of toxin-contaminated fish and shellfish results in severe, potentially life-threatening illnesses in travelers and residents in many countries worldwide. Various factors have resulted in an increase in poisonings recently, including increased seafood consumption, increased growth in world travel and trade, and global climate change. In general, seafood toxins are not detected by taste, smell, or appearance of contaminated seafood and they are not destroyed by cooking, freezing, marinating, smoking, or brining. Symptoms of seafood poisoning typically develop within minutes to hours following ingestion of toxic food. A very careful food and travel history is critical to making a prompt and accurate diagnosis of seafood poisoning. In most cases the diagnosis of seafood poisoning is made clinically and treatment is symptomatic and supportive since there is no specific antidote. Scombroid (histamine fish poisoning) is an important exception since it responds promptly to treatment with antihistamines. Potentially life-threatening seafood poisonings include pufferfish poisoning, paralytic shellfish poisoning, amnesic shellfish poisoning, and ciguatera poisoning. Life-saving treatment may involve treatment in intensive care that is not available in many developing countries. Travelers need to be aware of this important information.
Amnesic shellfish poisoning Ciguatera fish poisoning Diarrheic shellfish poisoning Neurotoxin shellfish poisoning Paralytic shellfish poisoning Pufferfish poisoning Scombroid (Histamine fish poisoning)
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symptoms include paresthesia involving the arms, legs, perioral area, tongue, and throat. Up to one-third of patients report pain in the teeth or a sensation that the teeth are numb or loose. Visual symptoms include blurred vision and transient blindness. Chronic neuropsychiatric symptoms may be very disabling and include malaise, depression, headache, myalgia, and fatigue.10 Cardiac manifestations include bradycardia (possibly due to cholinesterase inhibition), tachycardia, and other arrhythmias. Hypotension in the absence of hypovolemia may be due to the hypotensive properties of maitotoxin. Persistent symptomatic hypotension has been described
BOX 49.1 Excerpt From the Journals of
Captain James Cook’s Voyage in the South Pacific in 1774 The Night before we came out of Port, two Red fish about the Size of large Bream and not unlike them were caught with hook and line of which Most of the officers and Some of the Petty officers dined the next day. In the Evening everyone who had eat of these fish were seiz’d with Violant pains in the head and Limbs, so as to be unable to stand, together with a kind of Scorching heat all over the Skin, there remained no doubt but that it was occasioned by the fish being of a Poisoness nature and communicated its bad effects to everyone who had the ill luck to eat of it even to the Dogs and Hogs, one of the latter died in about Sixteen hours after and a young dog soon after shared the same fate: and it was a week or ten days before all the gentlemen recovered.
and is probably due to an increase in parasympathetic tone and impaired sympathetic reflexes. Hypertension has also been described. The cardiac effects of ciguatera poisoning may be serious, but usually resolve within 5 days of onset. Pruritus, particularly involving the palms and soles, occurs 2–5 days after ingestion of contaminated fish and has been reported in 5%–89% of cases. It seems to be more common in the Pacific than the Caribbean and is particularly common in New Caledonia, where ciguatera poisoning is called la gratte, meaning “the itch.” Deaths result from respiratory or cardiac failure and are most common in patients who have eaten parts of the fish known to contain high levels of toxin, such as the liver, intestines, or roe. The case fatality rate is usually 0.1%–1%, depending on geographic location. Deaths are more common in countries with limited intensive care capabilities. Several factors have been shown to influence the severity of ciguatera poisoning. These include the amount of fish eaten and the consumption of parts known to contain high levels of toxin, such as the head, liver, intestine, and roe, or soup made from those parts. Previous exposure to ciguatera also increases the severity of poisoning, probably as a result of accumulation of toxin or immune sensitization. Diagnosis of ciguatera poisoning is usually made on clinical grounds. If a portion of the fish is still available, it should be frozen and, if possible, submitted to a laboratory that can test for the presence of toxin. Radioimmunoassays or enzyme-linked immunosorbent assays have been developed to investigate ciguatera poisoning A test kit for rapid detection of ciguatera toxin is no longer commercially available.
35ºN
35ºS
= regions with high ciguatera prevalence = regions with moderate ciguatera prevalence = regions with potential for causing ciguatera poisoning
FIG. 49.1 Worldwide distribution of ciguatera. Pink indicates coral reef regions located between 35° north and 35° south latitudes; lilac indicates disease-endemic areas of ciguatera; red circle indicates Canary Islands (latitude 28°06′N, longitude 15°24′W. (Reprinted from Smithsonian Contributions to the Marine Sciences, Number 38, “Ciguatera Fish Poisoning in the Caribbean,” by Tester et al. Permission of Smithsonian Institution.)
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CHAPTER 49 Seafood Poisoning TABLE 49.1 Summary of Seafood Toxins Seafood Vehicle
Geographic Distribution
Inadequately chilled histidine-rich fish (e.g., mahi-mahi, tuna, mackerel, skipjack) Large carnivorous tropical and subtropical reef fish (e.g., barracuda, grouper, moray eel, snapper, jack, sea bass) Pufferfish, porcupine fish, and (rarely) ocean sunfish
Worldwide
Flushing, headache, nausea, vomiting, diarrhea, wheezing, urticarial
10–60 minutes
Tropical and subtropical waters between 35° N and 35° S. Commonest in the Pacific and Indian oceans and Caribbean Sea
Gastroenteritis followed by neurologic symptoms (e.g., dysesthesia, cold allodynia, pruritus, weakness). Rarely, bradycardia and hypotension
GI symptoms: 1–3 hours Neurologic symptoms: 3–72 hours
Worldwide. Commonest in Japan, Indo-Pacific Ocean
10 minutes– 4 hours
Dinoflagellates, Alexandrium spp. and others
Bivalve mollusks
Brevetoxins
Dinoflagellates. Karenia brevis
Bivalve mollusks
Worldwide. Commonest in temperate coastal waters, especially US Northeast, Pacific Northwest, Alaska Rare. Gulf of Mexico, Caribbean Sea, Florida, North Carolina, and New Zealand
Perioral paresthesias, nausea, dizziness followed by weakness, numbness, ascending paralysis, slurred speech, incoordination, respiratory failure, circulatory collapse Paresthesias of face and limbs, gastroenteritis. Severe cases: dysphagia, dysphonia, ataxia, weakness, respiratory failure
15 minutes– 8 hours
Diarrheic shellfish poisoning
Okadaic acid and others
Dinoflagellates. Dinophysis species
Bivalve mollusks
Gastroenteritis and neurologic symptoms (e.g., paresthesias, cold allodynia, vertigo, ataxia; rarely paralysis, coma, and seizures). Bronchoconstriction, rhinorrhea, and conjunctivitis in the presence of aerosol (aerosolized red tide respiratory irritation) Gastroenteritis
Amnesic shellfish poisoning
Domoic acid
Diatoms. Pseudonitzschia spp.
Mussels, razor clams, crustaceans
Syndrome
Toxin
Origin of Toxin
Scombroid
Histamine
Ciguatera
Ciguatoxin Maitotoxin
Histidine converted to histamine by bacteria with high histidine decarboxylase activity Dinoflagellates. Gambierdiscus toxicus and others
Pufferfish poisoning
Tetrodotoxin
Bacterial action
Paralytic shellfish poisoning
Saxitoxin
Neurotoxic shellfish poisoning
Medical management is mainly symptomatic and supportive. If patients are seen within 3 hours of ingestion of contaminated fish, emetics such as ipecac or gastric lavage followed by activated charcoal may be indicated. In theory, antiemetics and antidiarrheals should be avoided because they may prolong toxin contact time. Bradycardia responds to atropine. Intravenous fluids are indicated if there is volume depletion and hypotension. Hypotension in the absence of volume depletion is treated with vasopressors such as dopamine or dobutamine. Intravenous calcium gluconate 10% can be used to treat the inhibited calcium uptake caused by ciguatoxins. Treatment of prolonged orthostatic hypotension may require sodium and fluid replacement, fludrocortisone
Japan, Europe, Canada, Indonesia, New Zealand, South America Extremely rare. Northeast Canada, US Northeast and West, Europe, Australia, New Zealand
Typical Symptoms
Gastroenteritis followed by neurologic symptoms (e.g., retrograde and antegrade amnesia, cognitive impairment, autonomic dysfunction, headache, ophthalmoplegia, seizures, coma)
Typical Onset
30 minutes– 4 hours
30 minutes– 12 hours
GI symptoms: <24 hours Neurologic symptoms: <48 hours
acetate, and lower-extremity support stockings. Lidocaine or mexiletine have been used to treat ventricular arrhythmias. Treatment options for specific symptoms include cyproheptadine or hydroxyzine for pruritus, acetaminophen or nifedipine for headache,9 and nonsteroidal antiinflammatory drugs (NSAIDs) for musculoskeletal pains. Amitriptyline appears to be effective in treating depression associated with ciguatera poisoning and may also be effective in treating other neuropsychiatric symptoms, such as dysesthesias.11,12 Systemic exertion intolerance disease (also known as chronic fatigue syndrome) associated with ciguatera poisoning may respond to treatment with fluoxetine.13 Two patients with painful peripheral neuropathy and cold dysesthesia improved after treatment
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with pregabalin.14 There is limited evidence that cholestyramine, an ion exchange resin, may relieve some of the symptoms of chronic ciguatera poisoning by binding ciguatoxins in the intestine.15 Intravenous mannitol (1 g/kg over 30 minutes) has been reported to reduce the severity and duration of neurologic symptoms, particularly if given within the first 24 hours of poisoning.16 A double-blind randomized controlled trial found no significant difference between intravenous mannitol and intravenous saline.17 Clinical opinion is divided on the use of mannitol in ciguatera poisoning, but many experts often recommend using it in the acute phase.18 If used, it should be given with caution and only after ensuring adequate hydration. A potential mechanism of action has not been established. Recent case reports suggest that gabapentin (Neurontin), a drug occasionally used to treat neuropathic pain, may be useful in relieving symptoms late in the illness.19 Disturbances to reef systems and the subsequent proliferation of toxic dinoflagellates are an important impact on the incidence of ciguatera poisoning, although there is often a 6–24-month time lag. Reef systems may be disrupted by natural disasters such as hurricanes, tidal waves, heavy rains, and earthquakes, or manmade activities such as underwater nuclear explosions, coastal construction projects, dredging, shipwrecks, or golf-course run-off. There are concerns that ciguatera poisoning may increase as more coral reefs die as a result of global warming, nutrient run-off, and construction. Travelers to endemic areas, particularly the Caribbean and Indo-Pacific regions, should be warned about the risk of ciguatera poisoning and should avoid or limit consumption of reef fish, particularly carnivorous fish weighing >6 lb.2,20,21 The risk of ciguatera fish poisoning in local populations on some endemic Pacific Island populations has been estimated at 2% per year. Particularly high-risk fish such as tropical moray eels or barracuda should never be eaten. Travelers should be reminded that it is important to avoid parts of the fish known to contain large amounts of toxin, such as the head, liver, intestine, and roe, or soup made from these parts, and not to consume large reef fish weighing >6 lb. Any patient with a history of ciguatera poisoning should avoid overexertion with dehydration and consumption of reef fish, fish sauces, shellfish, alcoholic beverages, caffeine, nuts, and nut oils for at least 6 months, as they may provoke recurrent symptoms. Some experts also recommend avoidance of any fish (salt and freshwater), chicken, and pork. In a survival situation, organ meat should be fed to susceptible animals such as dogs, cats, or mongooses. If the animals show no sign of illness, then the flesh of the fish is probably safe for human consumption.
SCOMBROID (HISTAMINE FISH POISONING) Scombroid is one of the most common fish poisonings and occurs worldwide in both temperate and tropical waters. The illness often resembles a moderate to severe allergic reaction and occurs after eating improperly refrigerated or preserved fish containing high levels of histamine. Fish that cause scombroid include dark- or red-muscled fish belonging to the family Scombridae, such as albacore, bluefin and yellowfin tuna, mackerel, saury, skipjack, and bonito. Various nonscombroid fish may also be responsible, including mahi-mahi (dolphinfish) (Fig. 49.2), sardine, pilchard, anchovy, herring, bluefish, amberjack, and black marlin.22–24 Cases of fish poisoning closely resembling scombroid were described by Captain Edmund Fanning while sailing in the North Atlantic in 1797 (Box 49.2). Fish that cause scombroid have high levels of the amino acid histidine in the flesh. As a result of improper handling and storage after catch, histidine is converted to histamine and other scombrotoxins by bacteria with high histidine decarboxylase activity. These bacteria occur as normal
FIG. 49.2 Mahi-mahi (dolphinfish), a common cause of scombroid poisoning. Prompt refrigeration, using ice as shown here, will prevent poisoning. (Photograph courtesy David Ansdell.)
BOX 49.2 Excerpt From the Journals of
Captain Edmund Fanning’s Voyage in the North Atlantic 1797
“During this period we caught, with hook and grains, as many of the Spanish mackerel, or bonetos, as were wished for; shoals of these fish, as well as the dolphin, being all around us; … On eating of the dolphin and mackerel, almost all on board were affected with a severe pain in the head, which shortly after was much inflamed; the eyes became red, and these distressing symptoms were attended with violent vomiting. Those who were thus affected, were evidently poisoned; the head and some of the limbs began also to swell, which swelling increased, until they had attained a most disagreeable form, having at the same time, a reddish cast over the head and limbs thus swollen … whenever the fish, on being taken out of the water, was immediately cooked, and then eaten, no evil or unpleasant sensation was experienced; …”
surface flora or secondary contaminants and include Morganella morganii, Klebsiella pneumoniae, Escherichia coli, Aerobacter aerogenes, and Plesiomonas shigelloides. Conversion of histidine to histamine and other scombrotoxins occurs optimally at 20°C–30°C, and scombroid typically occurs in fish that have not been promptly refrigerated or frozen after capture. Histamine and other scombrotoxins are resistant to freezing, cooking, smoking, or canning. Symptoms of scombroid poisoning usually appear abruptly 10–60 minutes after eating contaminated fish, although they may appear within a few minutes of ingestion or be delayed for several hours. Untreated, symptoms typically last an average of 4 hours but occasionally may persist for up to 24 hours. Symptoms often resemble an acute immunoglobulin E (IgE)–mediated allergic reaction and are frequently misdiagnosed as an allergy to fish. Affected fish often have a peppery, sharp, metallic, or bitter taste, but may be normal in taste and appearance. There are several characteristic symptoms of scombroid poisoning. Flushing of the skin resembling sunburn with a well-demarcated edge confined to the face and upper body may be present (Fig. 49.3). Pruritus is common, and there may be urticaria or angioneurotic edema. A throbbing headache is often present. Gastrointestinal symptoms include nausea, vomiting, abdominal cramps, and diarrhea. Other clinical features may include perioral paresthesias, burning of the mouth and gums, conjunctival suffusion, palpitations, blurred vision, and diaphoresis.
CHAPTER 49 Seafood Poisoning
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BOX 49.3 Excerpt From the Journals of
Captain James Cook’s Voyage in the South Pacific in 1774 This afternoon a fish being struck by one of the natives near the watering place, the Captain’s clerk purchased it, and sent it to him after his return on board. It was of a new species, something like a sun-fish, with a large, long, ugly head. Having no suspicion of its being of a poisonous nature, they ordered it to be dressed for supper; but, very luckily, the operation of drawing and describing took up so much time that it was too late, so that only the liver and roe were dressed, of which the two Mr. Fortsters and the Captain did but taste. About three o’clock in the morning they all found themselves seized with an extraordinary weakness and numbness all over their limbs. The Captain had almost lost the sense of feeling; nor could he distinguish between light and heavy bodies, of such as he had strength to move; a quart pot full of water and a feather being the same in his hand. They each took an emetic, and after that a sweet, which gave them much relief. In the morning, one of the pigs which had eaten the entrails was found dead.
PUFFERFISH (FUGU) POISONING
FIG. 49.3 Widespread rash on the upper chest area. (From Jantschitsch C, Kinaciyan T, Manafi M, et al. Severe scombroid fish poisoning: an underrecognized dermatologic emergency. J Am Acad Dermatol 2011;65(1):246–7, Fig. 1c.)
Scombroid is usually a benign, self-limited illness; rarely, however, it may produce a more serious illness with potentially life-threatening complications such as respiratory compromise, malignant arrhythmias, and hypotension requiring hospitalization.22–26 There are no long-term sequelae. Serious illness seems to be more likely in the elderly and asthmatics. Patients who are already taking isoniazid may have a severe reaction because the drug inhibits histamine metabolism. Deaths are extremely rare. As expected, persons already taking antihistamines tend to have fewer symptoms. Diagnosis is usually made on clinical grounds. There may be a clustering of cases, which helps to exclude the possibility of fish allergy. The diagnosis can be confirmed by measuring histamine levels in any leftover fish. Treatment with H1 antagonists (e.g., diphenhydramine) given orally or parenterally provides symptomatic relief. Newer, second-generation, nonsedating H1 antagonists (e.g., loratadine) have not yet been proved to be as effective. H2 antagonists (e.g., cimetidine) given orally or parenterally may shorten the course of illness and have been particularly useful in controlling headache.27 A combination of H1 and H2 antagonists may be particularly valuable, but rarely may cause hypotension. Steroids have not been shown to be of any benefit. In severe scombroid poisoning intravenous fluids, inhaled bronchodilators, oxygen, and pressor agents may be indicated. Gastric lavage or catharsis may be worthwhile if large quantities of contaminated fish have been consumed within the previous few hours. The most important preventive measure is to chill the fish promptly after capture and maintain adequate refrigeration until the fish is prepared for consumption. Fish kept at ≤15°C–20°C prior to cooking should be safe for consumption. Canned fish may be a source of scombroid if the fish is not adequately refrigerated after capture and before canning or if an opened can is not refrigerated promptly.
Pufferfish poisoning has been recognized since ancient Egyptian times. One of the earliest recorded outbreaks of pufferfish poisoning in travelers may have involved Captain Cook and members of his crew, who became ill after eating pufferfish liver while sailing in the South Pacific during their second voyage around the world in 1774 (Box 49.3). Pufferfish or fugu poisoning occurs after ingestion of fish containing tetrodotoxin, a potent neurotoxin. Potentially toxic fish are distributed widely throughout the world and include pufferfish, porcupine fish, and ocean sunfish.2 The toxin is usually concentrated in the ovaries, liver, intestines, and skin of the fish. It is likely that tetrodotoxin is synthesized by bacteria such as Actinomyces, Alteromonas, Aeromonas, Pseudomonas, and Vibrio spp. that are associated with pufferfish.28,29 Most cases of pufferfish poisoning occur in Japan, where pufferfish or fugu is eaten as a very expensive and prized delicacy. The fugu is filleted, thinly sliced, and then arranged in traditional patterns such as a crane. The fugu experience is characterized by tingling of the lips and tongue, a sensation of generalized warmth and flushing, and a feeling of euphoria and exhilaration. Over the 78-year period from 1886 to 1963, there were 6386 cases of fugu poisoning in Japan, with an approximately 59% mortality. Increased awareness of fugu poisoning and strict regulation and training of licensed fugu chefs has resulted in far fewer cases and lower mortality in recent years. For example, in the 10-year period from 1967 to 1976 there were 1105 cases and 372 deaths (34% mortality), and from 1983 to 1992 there were only 449 cases and 49 deaths (11% mortality).29 Nowadays, all cooks and restaurants handling fugu must be licensed, and most cases of pufferfish poisoning occur in inexperienced fishermen who prepare their own food. In 1996, three cases of fugu poisoning occurred in San Diego in chefs who ate prepackaged, ready-to-eat fugu illegally imported from Japan.30 Tetrodotoxin is a heat-stable, water-soluble, nonprotein toxin that is 50 times more potent than strychnine. It acts by binding to sodium channels and blocking axonal nerve transmission, and results in ascending paralysis and respiratory failure. In addition to pufferfish, porcupine fish, and ocean sunfish, tetrodotoxin has been found in other marine animals, such as starfishes, flatworms, various crabs, and mollusks. Venom from the salivary glands of the blue ringed octopus contains tetrodotoxin and bites may be fatal. Levels of toxin are usually highest in the ovaries, liver, intestine, and skin. The toxin does not alter the taste or appearance of the fish, and it is not destroyed or inactivated by cooking, canning, freezing, or smoking.
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The onset of symptoms of pufferfish poisoning may occur within 10 minutes of ingestion of toxic fish or be delayed for ≥4 hours. Severe cases are usually associated with ingestion of large amounts of toxin and early onset of symptoms. Initial symptoms include perioral paresthesias and numbness, nausea, and dizziness. Later, there may be more generalized paraesthesia and numbness, dysarthria, ataxia, ascending paralysis, and a variety of other symptoms, such as headache, hypersalivation, diaphoresis, vomiting, abdominal pain, and diarrhea. In the most severe cases there is widespread paralysis, respiratory failure, bradycardia and other arrhythmias, and hypotension. Most deaths are due to respiratory failure and occur within the first 6 hours. In patients who survive the first 24 hours the prognosis is usually excellent. Diagnosis is made on clinical grounds. There is no specific antidote for tetrodotoxin and treatment is aimed at limiting absorption of toxin and treating the adverse effects. Absorption of toxin can be limited by gastric lavage, which is indicated if patients are seen within 3 hours of ingestion of toxic fish. Emetic agents such as ipecac should probably be avoided because of the risk of aspiration. In severe cases, intravenous fluids, vasopressors, endotracheal intubation, and ventilatory support may be indicated. Bradycardia may respond to atropine. As a general rule, all cases of pufferfish poisoning should be admitted to hospital for observation. Moderate or severe poisonings should be admitted to an intensive care unit.31 It is impossible to guarantee that fish are free from toxins, and travelers should be advised to avoid any potentially toxic fish even when prepared by trained chefs in licensed restaurants. In life-threatening (survival) situations, travelers should take advantage of the water-soluble properties of the toxin. Viscera and skin must not be eaten under any circumstances, but the muscle of the fish can be shredded into small pieces, kneaded, and soaked in water for at least 4 hours in an attempt to remove toxin prior to consumption.
PARALYTIC SHELLFISH POISONING Paralytic shellfish poisoning (PSP) has been recognized for over 200 years. The first documented outbreak in travelers was in 1793 and was reported in Captain George Vancouver’s A Voyage of Discovery to the North Pacific Ocean and Round the World. On June 15, 1793, during his exploration of British Columbia, Vancouver described in his diary classic cases of PSP in five crew members who had eaten locally harvested mussels for breakfast. One of the crew members, John Carter, died 5.5 hours later. The others survived. Vancouver subsequently named the area where the mussels were harvested Poison Cove. PSP is the most common and most serious form of shellfish poisoning and occurs after eating contaminated bivalve mollusks (clams, cockles, mussels, oysters, and scallops), crustaceans (Dungeness crabs, shrimp, and lobsters) containing saxitoxin, and other potent neurotoxins produced by dinoflagellates (e.g., Alexandrium sp.). Saxitoxin, like CTX and tetrodotoxin, causes paralysis by blocking sodium channels in nerve cell membranes. It is 50 times more potent than curare. Saxitoxin and other toxins that cause PSP are heat stable and are not destroyed by normal cooking procedures, marinating, or freezing. As in other forms of shellfish poisoning, outbreaks of PSP often follow dinoflagellate blooms. In the past, most cases of PSP occurred in cold, temperate waters above latitude 30° north and below latitude 30° south. Recently, however, outbreaks in tropical and subtropical waters have become more frequent, with cases reported from countries such as Guatemala, El Salvador, Mexico, Thailand, Singapore, Malaysia, Papua New Guinea, India, and the Solomon Islands. Because the main toxins that produce pufferfish poisoning (tetrodotoxin) and PSP (saxitoxin) are very similar, the clinical effects are almost indistinguishable. Symptoms of PSP usually occur within 30–60
minutes of eating toxic shellfish but can be delayed for 3 hours or longer. Early symptoms include paresthesias of the face, lips, and tongue, and later the arms and legs. Affected persons may complain of lightheadedness or a floating sensation. Other symptoms may include headache, increased salivation, nausea, vomiting, and diarrhea. Hypertension may be an important finding. Severe cases are usually associated with ingestion of large doses of toxin and clinical features, such as ataxia, dysphagia, and mental status changes. Flaccid paralysis occurs in the most severe cases, with respiratory insufficiency as a result of paralysis of the diaphragm and chest wall muscles. Deaths are typically caused by respiratory failure and tend to occur within 12 hours of eating toxic shellfish. For patients who survive past 12 hours, the prognosis is good. Recovery usually occurs within a week but may occasionally be prolonged for several weeks.32,33 Case fatality rate averages 6% but may be as high as 44%. Mortality is higher in children, who seem to be particularly sensitive to the effects of the toxin. Travelers to low- and middle-income countries who are tempted to eat shellfish should be reminded that the highest mortality from PSP occurs in areas with poor access to good-quality medical care. Diagnosis is usually made on clinical grounds, although in special circumstances it can be confirmed by a standard mouse bioassay method. There are no antidotes for PSP, but saxitoxin and other toxins that cause PSP bind well to charcoal and, if safe, oral charcoal should be given. Sufferers should be observed for at least 24 hours for respiratory insufficiency. Mechanical ventilation may be necessary. PSP can be prevented by avoiding potentially contaminated shellfish. This is particularly important in children, who are at greater risk of fatal illness. It is important to emphasize that the presence of the toxin does not affect the appearance, smell, or taste of the shellfish, and cooking will not destroy the toxin. Because of the lack of sophisticated medical facilities for resuscitation and mechanical ventilation, it is prudent for all travelers to developing countries to completely avoid potentially toxic shellfish.
NEUROTOXIC SHELLFISH POISONING NSP occurs after eating bivalve mollusks (e.g., oysters, clams, scallops, and mussels) contaminated by heat-stable brevetoxins produced by the marine dinoflagellate Karenia brevis. K. brevis is an important cause of red tides and has been responsible for the deaths of large numbers of fish, seabirds, and even marine mammals, such as manatees. NSP was first described on the west coast of Florida in 1844. Since then, it has been reported from the Gulf of Mexico, the east coast of Florida, the Caribbean, the North Carolina coast, and New Zealand. It is expected to be reported from other areas of the world in the future.34 NSP usually presents as gastroenteritis, accompanied by neurologic symptoms, and often resembles mild PSP or ciguatera poisoning. No deaths have been reported in humans. Inhalation of aerosolized brevetoxins from the sea spray associated with a red tide may cause an acute respiratory illness often referred to as aerosolized red tide respiratory irritation (ARTRI). Symptoms of NSP may develop within 15 minutes of ingestion of contaminated shellfish or be delayed for up to 18 hours. Gastrointestinal symptoms include abdominal pain, nausea, vomiting, and diarrhea. There may be myalgias and dizziness. Neurologic symptoms include circumoral paresthesias, paresthesias of the arms and legs, temperature reversal, vertigo, and ataxia. Symptoms may last for several hours or a few days. Symptoms of ARTRI occur almost immediately after exposure and include a nonproductive cough, wheezing, conjunctivitis, and rhinorrhea. Asthmatics are particularly susceptible, and there is some
CHAPTER 49 Seafood Poisoning anecdotal evidence of long-term pulmonary symptoms following ARTRI in the elderly or those with preexisting lung disease.35,36 Treatment of NSP and ARTRI is symptomatic and supportive. Wheezing usually responds to inhaled bronchodilators. Preventive measures include avoiding shellfish associated with red tides and limiting coastline exposure to red tides and aerosolized brevetoxins. Particle masks can be used to prevent inhalation of aerosolized toxins.
DIARRHEIC SHELLFISH POISONING Diarrheic shellfish poisoning (DSP) results from ingestion of contaminated bivalve mollusks (clams, mussels, and scallops) containing okadaic acid and other toxins produced by various marine dinoflagellates. Historically, DSP was reported predominantly from Japan and European countries, such as the Netherlands, Italy, and Spain. As a result of increased global spread of toxic dinoflagellates, outbreaks have recently been reported from Canada, South America, Australia, New Zealand, and Indonesia. As in other shellfish poisonings, outbreaks tend to follow red tides or dinoflagellate blooms. Okadaic acid triggers sodium release by intestinal cells and produces diarrhea. Symptoms usually appear 30 minutes to 6 hours after ingestion of contaminated shellfish, although onset may be delayed for up to 12 hours. Typically, symptoms last for up to 4 days and include diarrhea, abdominal cramps, nausea, vomiting, weakness, and chills. The severity of symptoms is usually related to the amount of toxin ingested. No fatalities have been reported. Diagnosis is usually made on clinical grounds and treatment is symptomatic and supportive.
AMNESIC SHELLFISH POISONING Amnesic shellfish poisoning (ASP) is a recently described toxic encephalopathy. It was first identified in 1987 after an outbreak involving over 100 Canadians who had eaten mussels contaminated by domoic acid harvested off Prince Edward Island. Domoic acid is a heat-stable toxin produced by diatoms, such as Nitzschia pungens. High levels of toxin have been demonstrated in shellfish in areas such as the Pacific Northwest, the Gulf of Mexico, and off the west coast of Scotland, although no clinical cases have been reported from those areas. In the Prince Edward Island outbreak, symptoms of ASP developed within 15 minutes to 38 hours (median 6 hours) of ingestion of contaminated mussels.37 Acute gastrointestinal symptoms were very common and included nausea, vomiting, abdominal cramps, and diarrhea. Neurologic features occurred in over one-third of patients and included headaches, short-term memory loss, confusion, disorientation, dizziness, seizures, and comas. Several patients developed long-term cognitive dysfunction. There were four deaths, all in patients >70 years of age.37,38 Treatment for ASP is symptomatic and supportive.39 Potentially contaminated shellfish, particularly those associated with red tides, should never be eaten.
CONCLUSION Toxin contaminated fish and shellfish are an important but generally avoidable form of poisoning in travelers. Illness may be severe and potentially life threatening. Seafood toxins are not usually detected by taste, smell, or appearance of contaminated food and cannot be destroyed by cooking, smoking, freezing, marinating, or brining. With the exception of scombroid (histamine fish poisoning) there is no effective antidote and treatment is symptomatic and supportive. Many factors are responsible for the increase in cases of seafood poisoning in travelers and effective pretravel counseling is essential. Sensible precautions will prevent most cases. Seafood poisoning is an
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important consideration in symptomatic returned travelers and a high index of suspicion is necessary to avoid misdiagnosis. A careful food history is always important. Specific diagnostic tests are not readily available.
REFERENCES 1. Doherty M. Captain Cook on poison fish. Neurology 2005;65:1788–91. 2. Friedman MA, Fernandez M, Backer LC, et al. An updated review of ciguatera fish poisoning: clinical, epidemiological, environmental, and public health management. Mar Drugs 2017;15:72. 3. Lehane L, Lewis RJ. Ciguatera: recent advances but the risk remains. Int J Food Microbiol 2000;61:91–125. 4. Stewart I, Lewis RJ, Eaglesham GK, et al. Emerging tropical diseases in Australia. Part 2. Ciguatera fish poisoning. Ann Trop Med Parasitol 2010;104(7):557–71. 5. Chan TYK. Ciguatera fish poisoning in East Asia and Southeast Asia. Mar Drugs 2015;13:3466–78. 6. Skinner MP, Brewer TD, Johnstone R, et al. Ciguatera fish poisoning in the Pacific Islands (1998 to 2008). PLoS Negl Trop Dis 2011;5:e1416. 7. Lewis RJ. The changing face of ciguatera. Toxicon 2001;39:97–106. 8. Glaziou P, Legrand AM. The epidemiology of ciguatera fish poisoning. Toxicon 1994;32:863–73. 9. Hamilton B, Hurbungs M, Vernoux JP, et al. Isolation and characterisation of Indian Ocean ciguatoxin. Toxicon 2002;40:685–93. 10. Bagnis R, Kuberski T, Langier S. Clinical observations on 3009 cases of ciguatera fish poisoning in the South Pacific. Am J Trop Med Hyg 1979;28:1067. 11. Calvert GM, Hryhorczuk DO, Leikin JB. Treatment of ciguatera fish poisoning with amitriptyline and nifedipine. J Toxicol Clin Toxicol 1987;25:423–8. 12. Davis RT, Villar LA. Symptomatic improvement with amitriptyline in ciguatera fish poisoning. N Engl J Med 1986;315:65. 13. Berlin RM, King SL, Blythe DG. Symptomatic improvement of chronic fatigue with fluoxetine in ciguatera fish poisoning. Med J Aust 1992;157:567. 14. Brett J, Murnion B. Pregabalin to treat ciguatera fish poisoning. Clin Toxicol (Phila) 2015;53:568. 15. Palafox NA, Buenconsejo-Lum LE. Ciguatera fish poisoning: review of clinical manifestations. J Toxicol–Toxin Reviews 2001;20(2):141–60. 16. Palafox NA, Buenconsejo-Lum L, Riklon S, et al. Successful treatment of ciguatera fish poisoning with intravenous mannitol. JAMA 1988;259:2740. 17. Schnorf H, Taurarii M, Cundy T. Ciguatera fish poisoning: a double-blind randomized trial of mannitol therapy. Neurol 2002;58:873–80. 18. Isbister GK, Kiernan MC. Neurotoxic marine poisoning. Lancet Neurol 2005;4:219–28. 19. Perez CM, Vasquez PA, Perret CF. Treatment of ciguatera poisoning with gabapentin. N Engl J Med 2001;344:692–3. 20. Develoux M. A case of ciguatera fish poisoning in a French traveler. Eurosurveillance 2008;6:1–2. 21. Arnett MV, Lim JT. Ciguatera fish poisoning: impact for military health care provider. Mili Med 2007;172(9):1012–15. 22. Hungerford JM. Scombroid poisoning: a review. Toxicon 2010;56: 231–43. 23. Feng C, Teuber S, Gershwin ME. Histamine (scombroid) fish poisoning. Clin Rev Allergy Immunol 2016;50(10):64–9. 24. Lavon O, Lurie Y, Bentur Y. Scombroid fish poisoning in Israel, 2005–2007. IMAJ 2008;789–92. 25. Waldo OA, Snipelisky DF, Dawson LD. 46-year-old man with abdominal pain and hypotension. Mayo Clin Proc 2015;90(1):135–8. 26. Anastasius M, Yiannikas J. Scombroid fish poisoning illness and coronary artery vasospasm. Australas Med J 2015;8(3):96–9. 27. Blakesley ML. Scombroid poisoning; prompt resolution of symptoms with cimetidine. Ann Emerg Med 1983;12:104. 28. Lago J, Rodriguez LP, Blanco L, et al. Tetrodotoxin, an extremely potent marine neurotoxin: distribution, toxicity, origin and therapeutic uses. Mar Drugs 2015;13:6384–406.
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29. Kaku N, Meier J. Clinical toxicology of fugu poisoning. In: Meier J, White J, editors. Handbook of Clinical Toxicology of Animal Venoms and Poisons. 1st ed. Boca Raton: CRC Press; 1995. p. 75–83. 30. Centers for Disease Control. Tetrodotoxin poisoning associated with eating pufferfish transported from Japan-California 1996. MMWR 1996;45:389–91. 31. Sobel J, Painter J. Illness caused by marine toxins. Clin Infect Dis 2005;41:1290–6. 32. Gessner BD, Middaugh JP. Paralytic shellfish poisoning in Alaska: a 20-year retrospective analysis. Am J Epidemiol 1995;141:766. 33. Hurley W, Wolterstorff C, MacDonald R, et al. Paralytic shellfish poisoning: a case series. West J Emerg Med 2014;15(4):378–81. 34. Morris PD, Campbell DS, Taylor TJ, et al. Clinical and epidemiological features of neurotoxic shellfish poisoning in North Carolina. Am J Public Health 1991;81:471–4.
35. Milian A, Nierenberg K, Fleming LE. Reported respiratory symptom intensity in asthmatics during exposure to aerosolized red tide toxins. J Asthma 2007;44:583. 36. Fleming LE, Kirkpatrick B, Backer LC. Aerosolized red-tide toxins (bevetoxins) and asthma. Chest 2007;131:187. 37. Peri TM, Bedard L, Kosatsky T, et al. An outbreak of toxic encephalopathy caused by eating mussels contaminated with domoic acid. N Engl J Med 1990;322:1775–80. 38. Teitelbaum JS, Zatorre RJ, Carpenter S, et al. Neurologic sequelae of domoic acid intoxication due to the ingestion of contaminated mussels. N Engl J Med 1990;322:1781–7. 39. Schroeder G, Bates SS, Spallino J. Amnesic shellfish poisoning: emergency medical management. J Marine Sci Res Dev 2015;6:179–82.
KEY POINTS • Travelers to the Caribbean and Indo-Pacific Ocean regions should be aware of the risk of ciguatera poisoning and avoid consumption of large carnivorous reef fish such as grouper, snapper, amberjack, and barracuda. The toxin survives normal cooking procedures.
• Paralytic shellfish poisoning occurs after ingestion of contaminated bivalve mollusks such as clams, mussels, oysters, and scallops. The toxin survives normal cooking procedures.
INTRODUCTION
The toxins that cause ciguatera poisoning originate from dinoflagellates such as Gambierdiscus toxicus, which are found on marine algae usually attached to dead coral reefs. Dinoflagellates are ingested by herbivorous fish and the toxins are concentrated as they pass up the food chain to large (usually >6 lb) carnivorous fish and finally to humans. CTX, maitotoxin, and scaritoxin are among the most lethal natural substances known and may be concentrated up to 50–100 times in parts of the fish such as the liver, gastrointestinal tract, roe, and head. The toxins do not affect the appearance, texture, smell, or taste of the affected fish and are not destroyed by gastric acid, cooking, or other fish-processing methods such as canning, drying, freezing, smoking, salting, or pickling. CTX has recently been completely characterized and synthesized,5 which may lead to advances in the understanding of its mechanism of action and potential therapies. Pacific Ocean, Caribbean, and Indian ocean CTX appear to be structurally different.6–9 Over 400 species of fish have been implicated in ciguatera poisoning. They are mainly carnivorous reef fish, such as grouper, snapper, barracuda, jack, sturgeon, sea bass, and moray eel. Certain herbivorous or omnivorous reef fish, such as surgeonfish and parrotfish, may also be responsible. Open ocean pelagic fishes such as tuna and mahi-mahi have not been associated with ciguatera poisoning. A wide range of symptoms has been reported, including generalized symptoms of profound weakness, chills, sweating, arthralgia, myalgia, and a metallic taste in the mouth. Typically, there is an acute gastrointestinal illness followed by neurologic symptoms and, rarely, cardiovascular collapse. The onset of symptoms is usually within 1–3 hours of eating contaminated fish, but may occur within 15–30 minutes or be delayed for up to 30 hours. Most symptoms resolve within 1–4 weeks. Gastrointestinal symptoms occur in most cases and include diarrhea, nausea, vomiting, and abdominal pain. They usually occur 1–3 hours after eating affected fish and may last for 1–2 days. Neurologic symptoms tend to occur later and may be delayed for up to 72 hours and last for several months or even years. Neurologic symptoms include cold allodynia (dysesthesia when touching cold water or objects). This is very characteristic of ciguatera poisoning but is not pathognomonic, as it may also occur in neurotoxic shellfish poisoning (NSP). Other neurologic
Seafood poisoning in travelers has become increasingly common in recent years. Multiple factors are probably involved including increased travel to areas where seafood poisonings are common, more adventurous eating habits, global climate change, coral reef damage, and spread of toxic algal blooms. In addition, more cases are being recognized in traditionally nonendemic areas as a result of increased importation of seafood from endemic areas.
CIGUATERA Ciguatera-like illnesses were known in ancient Egypt. Some of the earliest recorded cases in travelers were in the crews sailing with European explorers such as Christopher Columbus and James Cook1 (Box 49.1). Captain Bligh and his followers apparently developed ciguatera poisoning after the historic mutiny aboard HMS Bounty, and it has been speculated that Alexander the Great refused to let his troops eat fish because of concerns regarding ciguatera poisoning. Estimates suggest there are 50,000–500,000 new cases of ciguatera poisoning worldwide every year, making it one of the most common causes of marine poisoning from a food toxin (Table 49.1). It is widespread in tropical and subtropical waters between latitudes 35° north and 35° south, and is particularly common in the Pacific and Indian oceans and the Caribbean Sea (Fig. 49.1). Recent evidence suggests increasing worldwide incidence of ciguatera poisoning, especially in the Pacific. Newly recognized areas of risk include the Canary Islands, the western Gulf of Mexico, and the eastern Mediterranean. Most cases follow the ingestion of coral reef fish containing potent toxins such as ciguatoxin (CTX), maitotoxin, and scaritoxin that originate in dinoflagellates found in coral reefs. Average annual incidence rates for ciguatera fish poisoning vary from 5 to 50/100,000 in major endemic areas, with rates up to 1500/100,000 or even higher in some areas of the South Pacific during certain years.2–5 Of particular relevance to scuba divers is the fact that many of the symptoms of ciguatera poisoning may closely mimic those of decompression sickness.
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CHAPTER 49 Seafood Poisoning Abstract
Keywords
Poisoning from ingestion of toxin-contaminated fish and shellfish results in severe, potentially life-threatening illnesses in travelers and residents in many countries worldwide. Various factors have resulted in an increase in poisonings recently, including increased seafood consumption, increased growth in world travel and trade, and global climate change. In general, seafood toxins are not detected by taste, smell, or appearance of contaminated seafood and they are not destroyed by cooking, freezing, marinating, smoking, or brining. Symptoms of seafood poisoning typically develop within minutes to hours following ingestion of toxic food. A very careful food and travel history is critical to making a prompt and accurate diagnosis of seafood poisoning. In most cases the diagnosis of seafood poisoning is made clinically and treatment is symptomatic and supportive since there is no specific antidote. Scombroid (histamine fish poisoning) is an important exception since it responds promptly to treatment with antihistamines. Potentially life-threatening seafood poisonings include pufferfish poisoning, paralytic shellfish poisoning, amnesic shellfish poisoning, and ciguatera poisoning. Life-saving treatment may involve treatment in intensive care that is not available in many developing countries. Travelers need to be aware of this important information.
Amnesic shellfish poisoning Ciguatera fish poisoning Diarrheic shellfish poisoning Neurotoxin shellfish poisoning Paralytic shellfish poisoning Pufferfish poisoning Scombroid (Histamine fish poisoning)
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symptoms include paresthesia involving the arms, legs, perioral area, tongue, and throat. Up to one-third of patients report pain in the teeth or a sensation that the teeth are numb or loose. Visual symptoms include blurred vision and transient blindness. Chronic neuropsychiatric symptoms may be very disabling and include malaise, depression, headache, myalgia, and fatigue.10 Cardiac manifestations include bradycardia (possibly due to cholinesterase inhibition), tachycardia, and other arrhythmias. Hypotension in the absence of hypovolemia may be due to the hypotensive properties of maitotoxin. Persistent symptomatic hypotension has been described
BOX 49.1 Excerpt From the Journals of
Captain James Cook’s Voyage in the South Pacific in 1774 The Night before we came out of Port, two Red fish about the Size of large Bream and not unlike them were caught with hook and line of which Most of the officers and Some of the Petty officers dined the next day. In the Evening everyone who had eat of these fish were seiz’d with Violant pains in the head and Limbs, so as to be unable to stand, together with a kind of Scorching heat all over the Skin, there remained no doubt but that it was occasioned by the fish being of a Poisoness nature and communicated its bad effects to everyone who had the ill luck to eat of it even to the Dogs and Hogs, one of the latter died in about Sixteen hours after and a young dog soon after shared the same fate: and it was a week or ten days before all the gentlemen recovered.
and is probably due to an increase in parasympathetic tone and impaired sympathetic reflexes. Hypertension has also been described. The cardiac effects of ciguatera poisoning may be serious, but usually resolve within 5 days of onset. Pruritus, particularly involving the palms and soles, occurs 2–5 days after ingestion of contaminated fish and has been reported in 5%–89% of cases. It seems to be more common in the Pacific than the Caribbean and is particularly common in New Caledonia, where ciguatera poisoning is called la gratte, meaning “the itch.” Deaths result from respiratory or cardiac failure and are most common in patients who have eaten parts of the fish known to contain high levels of toxin, such as the liver, intestines, or roe. The case fatality rate is usually 0.1%–1%, depending on geographic location. Deaths are more common in countries with limited intensive care capabilities. Several factors have been shown to influence the severity of ciguatera poisoning. These include the amount of fish eaten and the consumption of parts known to contain high levels of toxin, such as the head, liver, intestine, and roe, or soup made from those parts. Previous exposure to ciguatera also increases the severity of poisoning, probably as a result of accumulation of toxin or immune sensitization. Diagnosis of ciguatera poisoning is usually made on clinical grounds. If a portion of the fish is still available, it should be frozen and, if possible, submitted to a laboratory that can test for the presence of toxin. Radioimmunoassays or enzyme-linked immunosorbent assays have been developed to investigate ciguatera poisoning A test kit for rapid detection of ciguatera toxin is no longer commercially available.
35ºN
35ºS
= regions with high ciguatera prevalence = regions with moderate ciguatera prevalence = regions with potential for causing ciguatera poisoning
FIG. 49.1 Worldwide distribution of ciguatera. Pink indicates coral reef regions located between 35° north and 35° south latitudes; lilac indicates disease-endemic areas of ciguatera; red circle indicates Canary Islands (latitude 28°06′N, longitude 15°24′W. (Reprinted from Smithsonian Contributions to the Marine Sciences, Number 38, “Ciguatera Fish Poisoning in the Caribbean,” by Tester et al. Permission of Smithsonian Institution.)
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CHAPTER 49 Seafood Poisoning TABLE 49.1 Summary of Seafood Toxins Seafood Vehicle
Geographic Distribution
Inadequately chilled histidine-rich fish (e.g., mahi-mahi, tuna, mackerel, skipjack) Large carnivorous tropical and subtropical reef fish (e.g., barracuda, grouper, moray eel, snapper, jack, sea bass) Pufferfish, porcupine fish, and (rarely) ocean sunfish
Worldwide
Flushing, headache, nausea, vomiting, diarrhea, wheezing, urticarial
10–60 minutes
Tropical and subtropical waters between 35° N and 35° S. Commonest in the Pacific and Indian oceans and Caribbean Sea
Gastroenteritis followed by neurologic symptoms (e.g., dysesthesia, cold allodynia, pruritus, weakness). Rarely, bradycardia and hypotension
GI symptoms: 1–3 hours Neurologic symptoms: 3–72 hours
Worldwide. Commonest in Japan, Indo-Pacific Ocean
10 minutes– 4 hours
Dinoflagellates, Alexandrium spp. and others
Bivalve mollusks
Brevetoxins
Dinoflagellates. Karenia brevis
Bivalve mollusks
Worldwide. Commonest in temperate coastal waters, especially US Northeast, Pacific Northwest, Alaska Rare. Gulf of Mexico, Caribbean Sea, Florida, North Carolina, and New Zealand
Perioral paresthesias, nausea, dizziness followed by weakness, numbness, ascending paralysis, slurred speech, incoordination, respiratory failure, circulatory collapse Paresthesias of face and limbs, gastroenteritis. Severe cases: dysphagia, dysphonia, ataxia, weakness, respiratory failure
15 minutes– 8 hours
Diarrheic shellfish poisoning
Okadaic acid and others
Dinoflagellates. Dinophysis species
Bivalve mollusks
Gastroenteritis and neurologic symptoms (e.g., paresthesias, cold allodynia, vertigo, ataxia; rarely paralysis, coma, and seizures). Bronchoconstriction, rhinorrhea, and conjunctivitis in the presence of aerosol (aerosolized red tide respiratory irritation) Gastroenteritis
Amnesic shellfish poisoning
Domoic acid
Diatoms. Pseudonitzschia spp.
Mussels, razor clams, crustaceans
Syndrome
Toxin
Origin of Toxin
Scombroid
Histamine
Ciguatera
Ciguatoxin Maitotoxin
Histidine converted to histamine by bacteria with high histidine decarboxylase activity Dinoflagellates. Gambierdiscus toxicus and others
Pufferfish poisoning
Tetrodotoxin
Bacterial action
Paralytic shellfish poisoning
Saxitoxin
Neurotoxic shellfish poisoning
Medical management is mainly symptomatic and supportive. If patients are seen within 3 hours of ingestion of contaminated fish, emetics such as ipecac or gastric lavage followed by activated charcoal may be indicated. In theory, antiemetics and antidiarrheals should be avoided because they may prolong toxin contact time. Bradycardia responds to atropine. Intravenous fluids are indicated if there is volume depletion and hypotension. Hypotension in the absence of volume depletion is treated with vasopressors such as dopamine or dobutamine. Intravenous calcium gluconate 10% can be used to treat the inhibited calcium uptake caused by ciguatoxins. Treatment of prolonged orthostatic hypotension may require sodium and fluid replacement, fludrocortisone
Japan, Europe, Canada, Indonesia, New Zealand, South America Extremely rare. Northeast Canada, US Northeast and West, Europe, Australia, New Zealand
Typical Symptoms
Gastroenteritis followed by neurologic symptoms (e.g., retrograde and antegrade amnesia, cognitive impairment, autonomic dysfunction, headache, ophthalmoplegia, seizures, coma)
Typical Onset
30 minutes– 4 hours
30 minutes– 12 hours
GI symptoms: <24 hours Neurologic symptoms: <48 hours
acetate, and lower-extremity support stockings. Lidocaine or mexiletine have been used to treat ventricular arrhythmias. Treatment options for specific symptoms include cyproheptadine or hydroxyzine for pruritus, acetaminophen or nifedipine for headache,9 and nonsteroidal antiinflammatory drugs (NSAIDs) for musculoskeletal pains. Amitriptyline appears to be effective in treating depression associated with ciguatera poisoning and may also be effective in treating other neuropsychiatric symptoms, such as dysesthesias.11,12 Systemic exertion intolerance disease (also known as chronic fatigue syndrome) associated with ciguatera poisoning may respond to treatment with fluoxetine.13 Two patients with painful peripheral neuropathy and cold dysesthesia improved after treatment
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with pregabalin.14 There is limited evidence that cholestyramine, an ion exchange resin, may relieve some of the symptoms of chronic ciguatera poisoning by binding ciguatoxins in the intestine.15 Intravenous mannitol (1 g/kg over 30 minutes) has been reported to reduce the severity and duration of neurologic symptoms, particularly if given within the first 24 hours of poisoning.16 A double-blind randomized controlled trial found no significant difference between intravenous mannitol and intravenous saline.17 Clinical opinion is divided on the use of mannitol in ciguatera poisoning, but many experts often recommend using it in the acute phase.18 If used, it should be given with caution and only after ensuring adequate hydration. A potential mechanism of action has not been established. Recent case reports suggest that gabapentin (Neurontin), a drug occasionally used to treat neuropathic pain, may be useful in relieving symptoms late in the illness.19 Disturbances to reef systems and the subsequent proliferation of toxic dinoflagellates are an important impact on the incidence of ciguatera poisoning, although there is often a 6–24-month time lag. Reef systems may be disrupted by natural disasters such as hurricanes, tidal waves, heavy rains, and earthquakes, or manmade activities such as underwater nuclear explosions, coastal construction projects, dredging, shipwrecks, or golf-course run-off. There are concerns that ciguatera poisoning may increase as more coral reefs die as a result of global warming, nutrient run-off, and construction. Travelers to endemic areas, particularly the Caribbean and Indo-Pacific regions, should be warned about the risk of ciguatera poisoning and should avoid or limit consumption of reef fish, particularly carnivorous fish weighing >6 lb.2,20,21 The risk of ciguatera fish poisoning in local populations on some endemic Pacific Island populations has been estimated at 2% per year. Particularly high-risk fish such as tropical moray eels or barracuda should never be eaten. Travelers should be reminded that it is important to avoid parts of the fish known to contain large amounts of toxin, such as the head, liver, intestine, and roe, or soup made from these parts, and not to consume large reef fish weighing >6 lb. Any patient with a history of ciguatera poisoning should avoid overexertion with dehydration and consumption of reef fish, fish sauces, shellfish, alcoholic beverages, caffeine, nuts, and nut oils for at least 6 months, as they may provoke recurrent symptoms. Some experts also recommend avoidance of any fish (salt and freshwater), chicken, and pork. In a survival situation, organ meat should be fed to susceptible animals such as dogs, cats, or mongooses. If the animals show no sign of illness, then the flesh of the fish is probably safe for human consumption.
SCOMBROID (HISTAMINE FISH POISONING) Scombroid is one of the most common fish poisonings and occurs worldwide in both temperate and tropical waters. The illness often resembles a moderate to severe allergic reaction and occurs after eating improperly refrigerated or preserved fish containing high levels of histamine. Fish that cause scombroid include dark- or red-muscled fish belonging to the family Scombridae, such as albacore, bluefin and yellowfin tuna, mackerel, saury, skipjack, and bonito. Various nonscombroid fish may also be responsible, including mahi-mahi (dolphinfish) (Fig. 49.2), sardine, pilchard, anchovy, herring, bluefish, amberjack, and black marlin.22–24 Cases of fish poisoning closely resembling scombroid were described by Captain Edmund Fanning while sailing in the North Atlantic in 1797 (Box 49.2). Fish that cause scombroid have high levels of the amino acid histidine in the flesh. As a result of improper handling and storage after catch, histidine is converted to histamine and other scombrotoxins by bacteria with high histidine decarboxylase activity. These bacteria occur as normal
FIG. 49.2 Mahi-mahi (dolphinfish), a common cause of scombroid poisoning. Prompt refrigeration, using ice as shown here, will prevent poisoning. (Photograph courtesy David Ansdell.)
BOX 49.2 Excerpt From the Journals of
Captain Edmund Fanning’s Voyage in the North Atlantic 1797
“During this period we caught, with hook and grains, as many of the Spanish mackerel, or bonetos, as were wished for; shoals of these fish, as well as the dolphin, being all around us; … On eating of the dolphin and mackerel, almost all on board were affected with a severe pain in the head, which shortly after was much inflamed; the eyes became red, and these distressing symptoms were attended with violent vomiting. Those who were thus affected, were evidently poisoned; the head and some of the limbs began also to swell, which swelling increased, until they had attained a most disagreeable form, having at the same time, a reddish cast over the head and limbs thus swollen … whenever the fish, on being taken out of the water, was immediately cooked, and then eaten, no evil or unpleasant sensation was experienced; …”
surface flora or secondary contaminants and include Morganella morganii, Klebsiella pneumoniae, Escherichia coli, Aerobacter aerogenes, and Plesiomonas shigelloides. Conversion of histidine to histamine and other scombrotoxins occurs optimally at 20°C–30°C, and scombroid typically occurs in fish that have not been promptly refrigerated or frozen after capture. Histamine and other scombrotoxins are resistant to freezing, cooking, smoking, or canning. Symptoms of scombroid poisoning usually appear abruptly 10–60 minutes after eating contaminated fish, although they may appear within a few minutes of ingestion or be delayed for several hours. Untreated, symptoms typically last an average of 4 hours but occasionally may persist for up to 24 hours. Symptoms often resemble an acute immunoglobulin E (IgE)–mediated allergic reaction and are frequently misdiagnosed as an allergy to fish. Affected fish often have a peppery, sharp, metallic, or bitter taste, but may be normal in taste and appearance. There are several characteristic symptoms of scombroid poisoning. Flushing of the skin resembling sunburn with a well-demarcated edge confined to the face and upper body may be present (Fig. 49.3). Pruritus is common, and there may be urticaria or angioneurotic edema. A throbbing headache is often present. Gastrointestinal symptoms include nausea, vomiting, abdominal cramps, and diarrhea. Other clinical features may include perioral paresthesias, burning of the mouth and gums, conjunctival suffusion, palpitations, blurred vision, and diaphoresis.
CHAPTER 49 Seafood Poisoning
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BOX 49.3 Excerpt From the Journals of
Captain James Cook’s Voyage in the South Pacific in 1774 This afternoon a fish being struck by one of the natives near the watering place, the Captain’s clerk purchased it, and sent it to him after his return on board. It was of a new species, something like a sun-fish, with a large, long, ugly head. Having no suspicion of its being of a poisonous nature, they ordered it to be dressed for supper; but, very luckily, the operation of drawing and describing took up so much time that it was too late, so that only the liver and roe were dressed, of which the two Mr. Fortsters and the Captain did but taste. About three o’clock in the morning they all found themselves seized with an extraordinary weakness and numbness all over their limbs. The Captain had almost lost the sense of feeling; nor could he distinguish between light and heavy bodies, of such as he had strength to move; a quart pot full of water and a feather being the same in his hand. They each took an emetic, and after that a sweet, which gave them much relief. In the morning, one of the pigs which had eaten the entrails was found dead.
PUFFERFISH (FUGU) POISONING
FIG. 49.3 Widespread rash on the upper chest area. (From Jantschitsch C, Kinaciyan T, Manafi M, et al. Severe scombroid fish poisoning: an underrecognized dermatologic emergency. J Am Acad Dermatol 2011;65(1):246–7, Fig. 1c.)
Scombroid is usually a benign, self-limited illness; rarely, however, it may produce a more serious illness with potentially life-threatening complications such as respiratory compromise, malignant arrhythmias, and hypotension requiring hospitalization.22–26 There are no long-term sequelae. Serious illness seems to be more likely in the elderly and asthmatics. Patients who are already taking isoniazid may have a severe reaction because the drug inhibits histamine metabolism. Deaths are extremely rare. As expected, persons already taking antihistamines tend to have fewer symptoms. Diagnosis is usually made on clinical grounds. There may be a clustering of cases, which helps to exclude the possibility of fish allergy. The diagnosis can be confirmed by measuring histamine levels in any leftover fish. Treatment with H1 antagonists (e.g., diphenhydramine) given orally or parenterally provides symptomatic relief. Newer, second-generation, nonsedating H1 antagonists (e.g., loratadine) have not yet been proved to be as effective. H2 antagonists (e.g., cimetidine) given orally or parenterally may shorten the course of illness and have been particularly useful in controlling headache.27 A combination of H1 and H2 antagonists may be particularly valuable, but rarely may cause hypotension. Steroids have not been shown to be of any benefit. In severe scombroid poisoning intravenous fluids, inhaled bronchodilators, oxygen, and pressor agents may be indicated. Gastric lavage or catharsis may be worthwhile if large quantities of contaminated fish have been consumed within the previous few hours. The most important preventive measure is to chill the fish promptly after capture and maintain adequate refrigeration until the fish is prepared for consumption. Fish kept at ≤15°C–20°C prior to cooking should be safe for consumption. Canned fish may be a source of scombroid if the fish is not adequately refrigerated after capture and before canning or if an opened can is not refrigerated promptly.
Pufferfish poisoning has been recognized since ancient Egyptian times. One of the earliest recorded outbreaks of pufferfish poisoning in travelers may have involved Captain Cook and members of his crew, who became ill after eating pufferfish liver while sailing in the South Pacific during their second voyage around the world in 1774 (Box 49.3). Pufferfish or fugu poisoning occurs after ingestion of fish containing tetrodotoxin, a potent neurotoxin. Potentially toxic fish are distributed widely throughout the world and include pufferfish, porcupine fish, and ocean sunfish.2 The toxin is usually concentrated in the ovaries, liver, intestines, and skin of the fish. It is likely that tetrodotoxin is synthesized by bacteria such as Actinomyces, Alteromonas, Aeromonas, Pseudomonas, and Vibrio spp. that are associated with pufferfish.28,29 Most cases of pufferfish poisoning occur in Japan, where pufferfish or fugu is eaten as a very expensive and prized delicacy. The fugu is filleted, thinly sliced, and then arranged in traditional patterns such as a crane. The fugu experience is characterized by tingling of the lips and tongue, a sensation of generalized warmth and flushing, and a feeling of euphoria and exhilaration. Over the 78-year period from 1886 to 1963, there were 6386 cases of fugu poisoning in Japan, with an approximately 59% mortality. Increased awareness of fugu poisoning and strict regulation and training of licensed fugu chefs has resulted in far fewer cases and lower mortality in recent years. For example, in the 10-year period from 1967 to 1976 there were 1105 cases and 372 deaths (34% mortality), and from 1983 to 1992 there were only 449 cases and 49 deaths (11% mortality).29 Nowadays, all cooks and restaurants handling fugu must be licensed, and most cases of pufferfish poisoning occur in inexperienced fishermen who prepare their own food. In 1996, three cases of fugu poisoning occurred in San Diego in chefs who ate prepackaged, ready-to-eat fugu illegally imported from Japan.30 Tetrodotoxin is a heat-stable, water-soluble, nonprotein toxin that is 50 times more potent than strychnine. It acts by binding to sodium channels and blocking axonal nerve transmission, and results in ascending paralysis and respiratory failure. In addition to pufferfish, porcupine fish, and ocean sunfish, tetrodotoxin has been found in other marine animals, such as starfishes, flatworms, various crabs, and mollusks. Venom from the salivary glands of the blue ringed octopus contains tetrodotoxin and bites may be fatal. Levels of toxin are usually highest in the ovaries, liver, intestine, and skin. The toxin does not alter the taste or appearance of the fish, and it is not destroyed or inactivated by cooking, canning, freezing, or smoking.
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The onset of symptoms of pufferfish poisoning may occur within 10 minutes of ingestion of toxic fish or be delayed for ≥4 hours. Severe cases are usually associated with ingestion of large amounts of toxin and early onset of symptoms. Initial symptoms include perioral paresthesias and numbness, nausea, and dizziness. Later, there may be more generalized paraesthesia and numbness, dysarthria, ataxia, ascending paralysis, and a variety of other symptoms, such as headache, hypersalivation, diaphoresis, vomiting, abdominal pain, and diarrhea. In the most severe cases there is widespread paralysis, respiratory failure, bradycardia and other arrhythmias, and hypotension. Most deaths are due to respiratory failure and occur within the first 6 hours. In patients who survive the first 24 hours the prognosis is usually excellent. Diagnosis is made on clinical grounds. There is no specific antidote for tetrodotoxin and treatment is aimed at limiting absorption of toxin and treating the adverse effects. Absorption of toxin can be limited by gastric lavage, which is indicated if patients are seen within 3 hours of ingestion of toxic fish. Emetic agents such as ipecac should probably be avoided because of the risk of aspiration. In severe cases, intravenous fluids, vasopressors, endotracheal intubation, and ventilatory support may be indicated. Bradycardia may respond to atropine. As a general rule, all cases of pufferfish poisoning should be admitted to hospital for observation. Moderate or severe poisonings should be admitted to an intensive care unit.31 It is impossible to guarantee that fish are free from toxins, and travelers should be advised to avoid any potentially toxic fish even when prepared by trained chefs in licensed restaurants. In life-threatening (survival) situations, travelers should take advantage of the water-soluble properties of the toxin. Viscera and skin must not be eaten under any circumstances, but the muscle of the fish can be shredded into small pieces, kneaded, and soaked in water for at least 4 hours in an attempt to remove toxin prior to consumption.
PARALYTIC SHELLFISH POISONING Paralytic shellfish poisoning (PSP) has been recognized for over 200 years. The first documented outbreak in travelers was in 1793 and was reported in Captain George Vancouver’s A Voyage of Discovery to the North Pacific Ocean and Round the World. On June 15, 1793, during his exploration of British Columbia, Vancouver described in his diary classic cases of PSP in five crew members who had eaten locally harvested mussels for breakfast. One of the crew members, John Carter, died 5.5 hours later. The others survived. Vancouver subsequently named the area where the mussels were harvested Poison Cove. PSP is the most common and most serious form of shellfish poisoning and occurs after eating contaminated bivalve mollusks (clams, cockles, mussels, oysters, and scallops), crustaceans (Dungeness crabs, shrimp, and lobsters) containing saxitoxin, and other potent neurotoxins produced by dinoflagellates (e.g., Alexandrium sp.). Saxitoxin, like CTX and tetrodotoxin, causes paralysis by blocking sodium channels in nerve cell membranes. It is 50 times more potent than curare. Saxitoxin and other toxins that cause PSP are heat stable and are not destroyed by normal cooking procedures, marinating, or freezing. As in other forms of shellfish poisoning, outbreaks of PSP often follow dinoflagellate blooms. In the past, most cases of PSP occurred in cold, temperate waters above latitude 30° north and below latitude 30° south. Recently, however, outbreaks in tropical and subtropical waters have become more frequent, with cases reported from countries such as Guatemala, El Salvador, Mexico, Thailand, Singapore, Malaysia, Papua New Guinea, India, and the Solomon Islands. Because the main toxins that produce pufferfish poisoning (tetrodotoxin) and PSP (saxitoxin) are very similar, the clinical effects are almost indistinguishable. Symptoms of PSP usually occur within 30–60
minutes of eating toxic shellfish but can be delayed for 3 hours or longer. Early symptoms include paresthesias of the face, lips, and tongue, and later the arms and legs. Affected persons may complain of lightheadedness or a floating sensation. Other symptoms may include headache, increased salivation, nausea, vomiting, and diarrhea. Hypertension may be an important finding. Severe cases are usually associated with ingestion of large doses of toxin and clinical features, such as ataxia, dysphagia, and mental status changes. Flaccid paralysis occurs in the most severe cases, with respiratory insufficiency as a result of paralysis of the diaphragm and chest wall muscles. Deaths are typically caused by respiratory failure and tend to occur within 12 hours of eating toxic shellfish. For patients who survive past 12 hours, the prognosis is good. Recovery usually occurs within a week but may occasionally be prolonged for several weeks.32,33 Case fatality rate averages 6% but may be as high as 44%. Mortality is higher in children, who seem to be particularly sensitive to the effects of the toxin. Travelers to low- and middle-income countries who are tempted to eat shellfish should be reminded that the highest mortality from PSP occurs in areas with poor access to good-quality medical care. Diagnosis is usually made on clinical grounds, although in special circumstances it can be confirmed by a standard mouse bioassay method. There are no antidotes for PSP, but saxitoxin and other toxins that cause PSP bind well to charcoal and, if safe, oral charcoal should be given. Sufferers should be observed for at least 24 hours for respiratory insufficiency. Mechanical ventilation may be necessary. PSP can be prevented by avoiding potentially contaminated shellfish. This is particularly important in children, who are at greater risk of fatal illness. It is important to emphasize that the presence of the toxin does not affect the appearance, smell, or taste of the shellfish, and cooking will not destroy the toxin. Because of the lack of sophisticated medical facilities for resuscitation and mechanical ventilation, it is prudent for all travelers to developing countries to completely avoid potentially toxic shellfish.
NEUROTOXIC SHELLFISH POISONING NSP occurs after eating bivalve mollusks (e.g., oysters, clams, scallops, and mussels) contaminated by heat-stable brevetoxins produced by the marine dinoflagellate Karenia brevis. K. brevis is an important cause of red tides and has been responsible for the deaths of large numbers of fish, seabirds, and even marine mammals, such as manatees. NSP was first described on the west coast of Florida in 1844. Since then, it has been reported from the Gulf of Mexico, the east coast of Florida, the Caribbean, the North Carolina coast, and New Zealand. It is expected to be reported from other areas of the world in the future.34 NSP usually presents as gastroenteritis, accompanied by neurologic symptoms, and often resembles mild PSP or ciguatera poisoning. No deaths have been reported in humans. Inhalation of aerosolized brevetoxins from the sea spray associated with a red tide may cause an acute respiratory illness often referred to as aerosolized red tide respiratory irritation (ARTRI). Symptoms of NSP may develop within 15 minutes of ingestion of contaminated shellfish or be delayed for up to 18 hours. Gastrointestinal symptoms include abdominal pain, nausea, vomiting, and diarrhea. There may be myalgias and dizziness. Neurologic symptoms include circumoral paresthesias, paresthesias of the arms and legs, temperature reversal, vertigo, and ataxia. Symptoms may last for several hours or a few days. Symptoms of ARTRI occur almost immediately after exposure and include a nonproductive cough, wheezing, conjunctivitis, and rhinorrhea. Asthmatics are particularly susceptible, and there is some
CHAPTER 49 Seafood Poisoning anecdotal evidence of long-term pulmonary symptoms following ARTRI in the elderly or those with preexisting lung disease.35,36 Treatment of NSP and ARTRI is symptomatic and supportive. Wheezing usually responds to inhaled bronchodilators. Preventive measures include avoiding shellfish associated with red tides and limiting coastline exposure to red tides and aerosolized brevetoxins. Particle masks can be used to prevent inhalation of aerosolized toxins.
DIARRHEIC SHELLFISH POISONING Diarrheic shellfish poisoning (DSP) results from ingestion of contaminated bivalve mollusks (clams, mussels, and scallops) containing okadaic acid and other toxins produced by various marine dinoflagellates. Historically, DSP was reported predominantly from Japan and European countries, such as the Netherlands, Italy, and Spain. As a result of increased global spread of toxic dinoflagellates, outbreaks have recently been reported from Canada, South America, Australia, New Zealand, and Indonesia. As in other shellfish poisonings, outbreaks tend to follow red tides or dinoflagellate blooms. Okadaic acid triggers sodium release by intestinal cells and produces diarrhea. Symptoms usually appear 30 minutes to 6 hours after ingestion of contaminated shellfish, although onset may be delayed for up to 12 hours. Typically, symptoms last for up to 4 days and include diarrhea, abdominal cramps, nausea, vomiting, weakness, and chills. The severity of symptoms is usually related to the amount of toxin ingested. No fatalities have been reported. Diagnosis is usually made on clinical grounds and treatment is symptomatic and supportive.
AMNESIC SHELLFISH POISONING Amnesic shellfish poisoning (ASP) is a recently described toxic encephalopathy. It was first identified in 1987 after an outbreak involving over 100 Canadians who had eaten mussels contaminated by domoic acid harvested off Prince Edward Island. Domoic acid is a heat-stable toxin produced by diatoms, such as Nitzschia pungens. High levels of toxin have been demonstrated in shellfish in areas such as the Pacific Northwest, the Gulf of Mexico, and off the west coast of Scotland, although no clinical cases have been reported from those areas. In the Prince Edward Island outbreak, symptoms of ASP developed within 15 minutes to 38 hours (median 6 hours) of ingestion of contaminated mussels.37 Acute gastrointestinal symptoms were very common and included nausea, vomiting, abdominal cramps, and diarrhea. Neurologic features occurred in over one-third of patients and included headaches, short-term memory loss, confusion, disorientation, dizziness, seizures, and comas. Several patients developed long-term cognitive dysfunction. There were four deaths, all in patients >70 years of age.37,38 Treatment for ASP is symptomatic and supportive.39 Potentially contaminated shellfish, particularly those associated with red tides, should never be eaten.
CONCLUSION Toxin contaminated fish and shellfish are an important but generally avoidable form of poisoning in travelers. Illness may be severe and potentially life threatening. Seafood toxins are not usually detected by taste, smell, or appearance of contaminated food and cannot be destroyed by cooking, smoking, freezing, marinating, or brining. With the exception of scombroid (histamine fish poisoning) there is no effective antidote and treatment is symptomatic and supportive. Many factors are responsible for the increase in cases of seafood poisoning in travelers and effective pretravel counseling is essential. Sensible precautions will prevent most cases. Seafood poisoning is an
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important consideration in symptomatic returned travelers and a high index of suspicion is necessary to avoid misdiagnosis. A careful food history is always important. Specific diagnostic tests are not readily available.
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