GENERAL OVERVIEW

The incidence of seafood poisoning appears to be on the rise due to increasing seafood consumption, as well as international trade and tourism. In the United States, 1 in 6 food poisoning outbreaks are due to fish, shellfish, and other marine organisms. A wide variety of etiologic agents may be responsible, including toxins, bacteria, viruses, and parasites. It is incumbent on the travel medicine practitioner to advise travelers on ways to avoid seafood poisoning.

TOXINS

Marine Toxins

Marine toxin diseases are caused by a myriad of natural toxins produced by minute organisms called dinoflagellates and diatoms. These phytoplankton move up the food chain into shellfish and carnivorous fish where they concentrate in viscera, affecting those who consume them. Because these toxins are tasteless, odorless, and heat and acid stable, normal screening and food preparation procedures will not prevent intoxication.

The marine toxin diseases are categorized into 2 groups depending on their vectors: shellfish and fish. Shellfish harbor the toxins that produce paralytic shellfish poisoning (PSP), neurotoxic shellfish poisoning (NSP), diarrheic shellfish poisoning (DSP), and amnesic shellfish poisoning (ASP). (See Table 1.) On the other hand, fish carry the toxins responsible for ciguatera (see below) and tetrodotoxin (fugu or pufferfish) poisoning. The shellfish-associated diseases generally occur in association with algal blooms or "red tides," which may be characterized by patches of discolored water and dead or dying fish. The primary target of marine toxins is the neurologic system, including the gastrointestinal tract.

Ciguatera Poisoning

Epidemiology

Ciguatera fish poisoning is the most frequently reported food-borne disease associated with eating fish in the United States and Canada. Ciguatera is endemic throughout the Caribbean and South Pacific islands and is common in tropical or subtropical regions between Lat 35°N and 35°S. The disease has been linked to more than 400 species of fish, particularly large, carnivorous reef fish such as barracuda, grouper, moray eel, parrot fish, red snapper, surgeon fish, trigger fish, amberjack, wrass, and mullet.

Ciguatera poisoning results from the ingestion of fish contaminated with several different marine toxins, all produced by small sea algae which adhere to dead coral and multiply rapidly with disturbances of coral reefs by such activity as underwater dredging or storms. Outbreaks occur when humans ingest toxin-laden carnivorous fish. The toxin becomes more concentrated in the viscera, liver, and gonads of affected fish. Unfortunately for humans, the toxin is tasteless, odorless, and temperature stable. Cooking, freezing, salting, drying, smoking, or marinating fish will not eliminate it.

Clinical manifestations

Clinical manifestations of ciguatera fish poisoning depend on the amount and parts of the fish eaten, species, and size. Progressively more severe symptoms occur with each new exposure. The disease is characterized by an acute neurological disease manifested by transient gastrointestinal symptoms (diarrhea, abdominal cramps, and vomiting) occurring within 12 hours of ingestion, followed within hours by neurological symptoms (perioral and limb paresthesia, tooth pain, pruritus, myalgia, blurred vision, dysuria, depression, and fatigue). Classically, heat/cold reversal occurs, a symptom that is characterized by a burning sensation of skin when it comes in contact with a cold object, liquid, or air; the reverse occurs when hot material is touched. In severe cases, ataxia, limb paralysis, respiratory failure, seizures, or coma may occur. Cardiac symptoms due to damage to nerves that innervate the heart include labile blood pressure, arrhythmia, hypotension, or shock. Neurologic symptoms usually resolve within several weeks but may persist for many months, especially weakness and paresthesia. They may recur with ingestion of marine or fresh water fish, ethanol, caffeine, and nuts up to 6 months after initial presentation. Acute fatality ranges from 0.1% to 12% of reported cases.

Diagnosis

The diagnosis is usually made on the basis of clinical symptoms and history of recent fish ingestion. In the differential diagnosis are toxic syndromes due to other marine toxins, especially neurotoxic shellfish poisoning (NSP) and paralytic shellfish poisoning (PSP); the former may demonstrate heat/cold reversal. At present the diagnosis can be made with certainty only from the contaminated fish in a mouse bioassay or using electrophysiological measures.

Management

Until recently, medical treatment, to a large extent, has been symptomatic. Early induction of vomiting and gastric lavage followed by activated charcoal is recommended. Atropine sulphate is indicated for bradycardia, and dopamine or calcium gluconate for shock. Opiates and barbiturates should be avoided since they may cause hypotension. Other symptomatic therapies include amitriptyline, tocainide, or carbamazepine to treat paresthesia and other neurological symptoms.

The most important breakthrough in the treatment of ciguatera poisoning came with the use of mannitol, which reduces the severity and duration of neurological symptoms. Mannitol must be administered in a high dose of 1 gram/kg over 30 minutes, ideally within 24 hours of ciguatoxin ingestion. Hydration with intravenous fluids before administration of mannitol may be necessary to prevent hypotension.

Prevention

Unfortunately, underreporting of outbreaks of ciguatera poisoning and insufficient public education make it difficult for the traveler to know when local fish are contaminated. However, in endemic areas several precautions may reduce but not eliminate the risk:

• Never eat barracuda or moray eel and be cautious with grouper and red snapper.
• Avoid viscera of reef fish and large predatory reef fish, especially after severe climatological changes such as hurricanes or storms.
• The larger the fish, the higher the dose of toxin; therefore, smaller fish should be selected, smaller than the plate on which it is served, assuming that the fish isn't being served on an oversized dinner plate.

BACTERIAL TOXINS

Seafood diseases caused by bacterial toxins generally are associated with improper food preparation and storage. Scombroid poisoning (see below) is the most common. Clostridium botulinum type E produces a toxin on smoked fish, fish eggs, and uneviscerated and salted whitefish. Staphylococcus aureus elaborates a toxin on improperly stored seafood, especially if the fish is garnished with cream sauces or mayonnaise.

Scombroid Poisoning

Epidemiology

After ciguatera poisoning, scombroid is the most commonly reported fish-borne illness reported worldwide and is particularly common in countries with diets high in fish. Scombroid poisoning results from the eating of spoiled fish of the Scombroidea or Scomberesocidae families. Typically, this has included consumption of tuna, mackerel, skipjack, and bonito. However, non-scombroid fish, such as mahi-mahi (dolphin fish), bluefish, amberjack, swordfish, herring, sardines, anchovies, salmon, and trout, have produced scombrotoxism. The phenomenon occurs with the consumption of both fresh and canned fish.

Scombroid is caused by bacterial overgrowth associated with inadequate storage of fish that naturally contain high levels of histidine. These surface bacteria decarboxylate histidine to produce high levels of histamine, the source of "histamine toxicity." Optimal conditions for poisoning occur when the fish is improperly stored in a range from 20° to 30°C, temperatures that favor bacterial growth. Once the bacterial overgrowth and decarboxylation have taken place, neither refrigeration nor cooking can prevent scombroid.

Clinical presentation

The onset of symptoms occurs within an hour of ingesting spoiled fish, with a range of minutes to 4 hours after ingestion. Signs and symptoms usually last for several hours and usually resolve within 24 hours even without treatment. Scombroid often is mistakenly diagnosed as "fish allergy" because the illness resembles an IgE-mediated reaction and responds rapidly to antihistamines. These symptoms typically include flushing, a bright erythematous rush, headache, and palpitations. Dizziness, breathlessness, and gastrointestinal symptoms (diarrhea, nausea, vomiting, and abdominal pain) may also develop. Urticaria, angioedema, and conjunctival suffusion are well described. Most symptoms resolve within 3 to 8 hours.

Diagnosis

The main differential diagnosis is hypersensitivity reaction to fish that is often incorrectly ascribed to food allergy or, rarely, Anisakiasis. The diagnosis usually is made clinically but can be confirmed by measuring the histamine content of the leftover fish.

Treatment

Treatment of scombroid poisoning is often unnecessary because it is a short-lived, self-limited illness; however, H1 or H2 antihistamines (such as Benadryl, Tagamet, or Zantac) provide symptomatic relief as do bronchodilators when necessary. Adrenaline may be required in rare, severe cases.

Prevention

Travelers should be counseled to avoid eating fish which have a "peppery" taste or which are associated with mouth tingling.

CHEMICAL TOXINS

Industrial activities release heavy metals from the earth and send them into bodies of water (fresh or salt water) where they bioaccumulate through the food chain and return to humans in the form of contaminated seafood. Well-known toxins include methyl mercury, the cause of Minamata Disease in Japan; other heavy metals; PCBs; organochlorides; pesticides; and radioactive waste.

BACTERIA

Historically, the vibrios have been important causes of bacterial seafood poisoning. Vibrio cholerae, the most infamous, is often acquired from unhygienic food handling in the home and on the street. In Latin America, seviche (raw fish) is a common source. Since the organism requires alkaline medium in which to grow, the addition of citrus juice (an acid) will reduce, but not eliminate, the risk. Other vibrios include V. parahaemolyticus, an organism that causes diarrhea, and V. vulnificus, which can cause fatal septicemia in a person with liver disease or an immunocompromised host. Wound infections may occur in those who swim in contaminated waters. Listeria monocytogenes, on the surface of fish, may cause severe illness in a neonate born to an infected mother. Salmonella and Aeromonas species are also a risk through seafood.

VIRUSES

Shellfish harvested in waters contaminated with raw or inadequately treated sewage are extremely efficient vectors of seafood pathogens because they are filter feeders that concentrate the organisms. Hepatitis A is the most common cause of seafood-associated hepatitis and is most often acquired from the consumption of raw or inadequately prepared shellfish. Small, round, structured viruses (such as Norwalk-like viruses) that cause gastroenteritis are not reliably eliminated by cooking shellfish.

PARASITES

Parasite infections from ingestion of inadequately cooked fish are relatively uncommon but preventable. Anisakiasis, a rare roundworm, is acquired through the consumption of raw fish, especially cod, herring, mackerel, and salmon. It is associated with abdominal pain and eosinophilia in symptomatic individuals. Diphyllobothriasis due to fish tapeworm has been reported with the ingestion of raw Pacific salmon and gefilte fish.