NATURALLY OCCURRING FISH AND SHELLFISH POISONING

High risk groups • • • Consumers of raw molluscan shellfish Consumers of recreational fishery pro ducts Consumers of subsistence fishery products

Various types of naturally occurring fish and shellfish poisoning: • • • • • • • Diarrhetic shellfish poisoning ( DSP ) Ciguatera poisoning Scombro id poisoning Paralytic shellfish poisoning ( PSP ) Neurotoxic shellfish poisonin g ( NSP ) Puffer fish poisoning Amnesic shellfish poisoning ( ASP )

Diarrhetic Shellfish Poisoning (DSP) • caused by ingestion of mussels, scallops or clams that have been feeding on th e dinoflagellate Dinophysis fortii or D. acuminata and other species of Dinophys is and possibly Prorocentrum sp. ( Elder and Hageltorn, 1990; Yasumoto and Murat a, 1990 ) common in Japan and has become a problem in Europe •

Symptoms • • • • • Diarrhea Nausea Vomiting Abdominal pain Onset of symptoms occurs from 30 minutes to a few hours after eating toxic shellfish, and the duration is usua lly short with a maximum of a few days in severe cases The disease is not life t hreatening •

• • • At least five toxins have been isolated from dinoflagellates and shellfish. Okad aic acid is most commonly encountered in Europe where D. acuminata is the usual agent. Mixtures of okadaic acid, dinophysistoxins and pectenotoxins are detected in cases in Japan, usually involving D. fortii ( Yasumoto and Murata, 1990 ). T here is a mouse assay for the toxins. •

Ciguatera poisoning • Clinical syndrome caused by eating the flesh of toxic fish caught in tropical reef and island waters Toxin originates in a microscopic dinoflagellate alga, Ga mbierdiscus toxicus that grows on reefs (Bangnis et al., 1980) Other benthic alg ae have also been implicated Fish eating the algae become toxic, and the effect is magnified through the food chain so that the large, predatory fish become the most toxic • Ciguatera poisoning • •

• • occurrence of toxic fish - localized >400 species of fish have been implicated i n ciguatera poisoning • fish most commonly implicated: • Amberjack • Snapper • G rouper • Barracuda • Goatfish • Reef fish belonging to the family Carangidae Ciguatera poisoning

• • The disease affects both the gastro-intestinal and neurological systems Gastro-i ntestinal symptoms: • Diarrhea • Nausea • Vomiting • Abdominal pain Appear 3-5 h ours after ingestion of the fish and are of short duration Neurological symptoms begin 12-18 hours after consumption of the fish and may be moderate to severe C ommonly last for 1 - 82 days but may persist for several months. Ciguatera poisoning • • •

• In rare cases, symptoms may last for years, and get worse in association with fi sh consumption or possibly alcohol. Symptoms typically include: • hot-cold inversion (hot coffee taste cold, ice cre am tastes hot) • muscular aches • tingling and numbness of lips. tongue and peri oral region • metallic taste • dryness of mouth • anxiety • extreme physical wea kness • dizziness, chills, sweating, dilated pupils, blurred vision and temporar y blindness • paralysis and death may occur in a few extreme cases Ciguatera poisoning

• • Several toxic compounds have been isolated from ciguatoxic fish and from Gambier discus. The principal toxin called “ciguatoxin” is a small, lipid-soluble polyet her with a molecular weight of 1,112 (Schueuer et. al., 1967). This toxin has be en purified and its structure determined (Murata et. al., 1990). Ciguatoxin ( CT X ) has a molecular formula of C60H88O19 and is a brevitoxin-type ether, about 1 00 times more potent than tetrodotoxin. Ciguatoxin opens voltage-dependent sodiu m channels in cell membranes (Bidard, 1984), and studies in vitro of tissue prep arations suggest that the toxin causes a nerve conduction block after initial ne ural stimulation. • Ciguatera poisoning • •

• • • Another lipid-soluble neurotoxin from ciguateric fish is called “scaritoxin”. Th e pharmacological action is close to that of ciguatoxin, and they may be related compounds. Another toxin found, called “maitotoxin”, is a water-soluble toxin t hat may interfere with or modify calcium movement or calcium conductance in tiss ues. Ciguatera poisoning

• In the USA, the reported incidence of ciguatera is about 15 - 20 outbreaks per y ear, involving 50 100 cases. For the majority of US consumers, the disease can b e contracted only from fish imported from endemic areas. For the residents in en demic areas, safety depends on abstinence from eating reef fish. The Amberjack ( Seriola dumerii Kahala ) is not sold commercially in Hawaii because of the known high incidence of ciguatoxic fish of this species. • Ciguatera poisoning • •

• • Control options are limited by the impossibility of detecting toxic fish by orga noleptic inspection. At present, the only ciguatera screening programme in exist ence is that employed by the Tokyo Central Wholesale Fish Market in Japan. Muscl e extracts are prepared and tested on cats and mice for evidence of ciguatoxicit y. This is a lengthy and expensive screening technique. Ciguatera poisoning •

• A radioimmunoassay (RIA ) was developed by Hokama and co-workers in Hawaii ( Hok ama et. al., 1977 ) and then modified to a simpler enzyme immunoassay (Hokama 19 85). The method has been further simplified to a “stick” test that has been used to screen fish landed in Hawaii and holds promise as a practical basis for cont rol (Hokama et. al., 1989b). The stick test measures ciguatoxin and polyether co mpounds, including okadaic acid. This whole area needs further research, particu larly because of the concern over falsepositive results from the stick test. • Ciguatera poisoning • •

• Research is needed into methods for predicting the development of ciguateric con ditions in reef fishing areas, perhaps by assessing Gambierdiscus or other toxig enic microorganism populations and somehow closing such areas to fishing when th e risk is high. The risk of contracting ciguatera poisoning are low for most con sumers in the mainland United States. Risks are much higher in Hawaii, other Pac ific islands, Puerto Rico and the Virgin Islands. There are moderate risks in ar eas such as Miami. • Ciguatera poisoning

Paralytic shellfish poisoning (PSP) Paralytic shellfish poisoning (PSP) • Results from ingesting bivalve molluscs (mussels, clams, oysters, scallops) whic h have consumed toxigenic dinoflagellates (Halstead and Schantz, 1984; Schantz, 1973). Toxins are assimilated and temporarily stored by the shellfish. Outbreaks occur mostly when these shellfish are gathered and eaten by recreational collec tors from closed areas. In the USA, during 1978-1986, 12 outbreaks involving 134 people with one death were recorded. • • •

• Paralytic shellfish poisoning (PSP) PSP is potentially life threatening because the toxins involved are among the mo st poisonous known. Symptoms are neurological and normally appear within an hour of eating toxic shellfish. They include: • Tingling • Numbness • burning sensat ion of the lips and fingertips • Ataxia • Giddiness • Staggering • Drowsiness • Dry throat and skin • Incoherence • Rash and fever •

• In severe cases, respiratory paralysis occurs, which can cause death during the first 24 hours. No antidote is known. Immunity is not conferred and multiple inc idence can occur. The cause of PSP is a complex of toxins known as saxitoxins, i ncluding saxitoxin, neotoxin and gonyautoxins. In the USA, the toxic dinoflagell ates of importance are Gonyaulax catenella and G. tamarensis. Paralytic shellfish poisoning (PSP) • • • •

• Paralytic shellfish poisoning (PSP) The saxotoxins are neurotoxins which act by blocking the flow of sodium (Na+) io ns through the sodium channels of the nerves. The lethal dose for humans is 1 4 mg expressed as saxitoxin equivalents (Schantz, 1986) FDA action limit is 80µg of toxin per 100g of shellfish tissue. The classic method for analysis of saxit oxins is by mouse bioassay. • • •

• Paralytic shellfish poisoning (PSP) The chemical analytical methods which have used include column separation, thinlayer chromatography, and fluorescence assays, either directly or after separati on by high performance liquid chromatography (HPLC). Recently, immunoassay metho ds have been developed and reported (Sullivan and Iwaoka, 1983). These involve r abbit serum antibody preparations and monoclonal antibodies, and both radioimmun oassays and enzyme-linked immunoabsorbant assays ( ELISA ) have been used (Chu a nd Fan, 1985). So far, these methods are not acceptable for regulatory use. • •

• Paralytic shellfish poisoning (PSP) The occurrence of blooms of toxic dinoflagellates are not predictable. When thes e blooms occur, shellfish become toxic and remain toxic for several weeks after the bloom subsides. Protection of the consumer is achieved by closure of shellfi sh harvesting in affected areas. Warnings are issued through the media, posted o n public beaches and a surveillance system is carried out. Commercial producers are required to submit samples for testing. • • • •

Neurotoxic shellfish poisoning (NSP) • Also known as brevetoxic shelling poisoning (BSP) Caused by ingesting shellfis h which have fed on the red tide organism, Gymnodinium breve. The red tides can be observed as a red colouration of the seawater, and the organisms can be seen under the microscope. Irritant aerosols, produced by wind and wave action, cause respiratory distress. If there is more than 5,000 G. breve cells per litre of s eawater, a ban on shellfish harvesting is imposed. Surveillance and closure syst ems have been found to be effective. Neurotoxic shellfish poisoning • • •

Symptoms include: • • • • • • Tingling Numbness of the lips, tongue, throat and perioral area Musc ular aches Gastrointestinal upset Dizziness The symptoms appear to be due to two brevetoxins produced by G. breve that bind to nerve cells (Baden et. al.,1984). The intoxication is usually not fatal. There is no antidote. Neurotoxic shellfish poisoning •

Puffer fish poisoning • Results from the ingestion of the flesh of certain species of fish belonging t o the family Tetraodontidae. The toxin involved is called tetrodotoxin. The toxi city of poisonous puffers fluctuates greatly. It has recently been shown that ce rtain common marine vibrios can produce a form of the toxin, and because they oc cur as part of the microflora of puffer fish, may be implicated in toxicity deve lopment (Narita et. al., 1987). • Puffer fish poisoning • •

• • • There are 20 - 100 deaths from puffer fish (fugu) poisoning each year. The sympt oms are similar to those described for paralytic shellfish poisoning. Tetradotox in also blocks sodium channels. No antidote has been identified. The lethal dose for humans is 1 - 4 mg of tetradotoxin. Puffer fish poisoning • •

Amnesic Shellfish Poisoning (ASP) Amnesic Shellfish Poisoning (ASP) • • € The severe symptoms of this poisoning are caused by domoic acid. The toxin is present in some varieties of the diatom, Nitzchia pungens and accumulated in mussels and clams. Symptoms include: • Vomiting • Abdominal cramps • Diarrhea • Disorientation and memory loss ( Perl et. al., 1988; Teitelbaum et al., 1990 ). • Short term memory loss is the most common symptom.

Amnesic Shellfish Poisoning (ASP) • • • Autopsies on three fatalities showed necrosis of the hippocampus. The poisoning has a particularly severe effect among older people. Canadian authorities now en force closure of beds when levels of 20 µg /g are detected in the tissues of mus sels and clams (Gilgan et. al., 1989).

Conclusion • € The most effective measure to prevent illness and fatalities from fish and s hellfish poisoning: • Education of the fish-eating public about which fish and s hellfish may be naturally toxic. There is a need for materials to be made availa ble to the fishing industry, public health workers, divers and sport fishermen. •

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