FISH & SHELLFISH POISONING

Click here to load reader

  • date post

    10-Apr-2015
  • Category

    Documents

  • view

    826
  • download

    25

Embed Size (px)

description

FISH & SHELLFISH POISONING

Transcript of FISH & SHELLFISH POISONING

NATURALLY OCCURRING FISH AND SHELLFISH POISONING

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

Various types of naturally occurring fish and shellfish poisoning: Diarrhetic shellfish poisoning ( DSP ) Ciguatera poisoning Scombroid poisoning Paralytic shellfish poisoning ( PSP ) Neurotoxic shellfish poisoning ( 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 the dinoflagellate Dinophysis fortii or D. acuminata and other species of Dinophysis and possibly Prorocentrum sp. ( Elder and Hageltorn, 1990; Yasumoto and Murata, 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 usually short with a maximum of a few days in severe cases The disease is not life threatening

At least five toxins have been isolated from dinoflagellates and shellfish. Okadaic 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 ). There 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, Gambierdiscus toxicus that grows on reefs (Bangnis et al., 1980) Other benthic algae 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 in ciguatera poisoning fish most commonly implicated: Amberjack Snapper Grouper Barracuda Goatfish Reef fish belonging to the family Carangidae

Ciguatera poisoning

The disease affects both the gastro-intestinal and neurological systems Gastro-intestinal symptoms: Diarrhea Nausea Vomiting Abdominal pain Appear 3-5 hours 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 Commonly 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 fish consumption or possibly alcohol.

Symptoms typically include: hot-cold inversion (hot coffee taste cold, ice cream tastes hot) muscular aches tingling and numbness of lips. tongue and perioral region metallic taste dryness of mouth anxiety extreme physical weakness dizziness, chills, sweating, dilated pupils, blurred vision and temporary blindness paralysis and death may occur in a few extreme cases

Ciguatera poisoning

Several toxic compounds have been isolated from ciguatoxic fish and from Gambierdiscus. The principal toxin called ciguatoxin is a small, lipid-soluble polyether with a molecular weight of 1,112 (Schueuer et. al., 1967). This toxin has been purified and its structure determined (Murata et. al., 1990). Ciguatoxin ( CTX ) has a molecular formula of C60H88O19 and is a brevitoxin-type ether, about 100 times more potent than tetrodotoxin. Ciguatoxin opens voltage-dependent sodium channels in cell membranes (Bidard, 1984), and studies in vitro of tissue preparations suggest that the toxin causes a nerve conduction block after initial neural stimulation.

Ciguatera poisoning

Another lipid-soluble neurotoxin from ciguateric fish is called scaritoxin. The pharmacological action is close to that of ciguatoxin, and they may be related compounds. Another toxin found, called maitotoxin, is a water-soluble toxin that may interfere with or modify calcium movement or calcium conductance in tissues.

Ciguatera poisoning

In the USA, the reported incidence of ciguatera is about 15 - 20 outbreaks per year, involving 50 100 cases. For the majority of US consumers, the disease can be contracted only from fish imported from endemic areas. For the residents in endemic 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 organoleptic inspection. At present, the only ciguatera screening programme in existence is that employed by the Tokyo Central Wholesale Fish Market in Japan. Muscle extracts are prepared and tested on cats and mice for evidence of ciguatoxicity. This is a lengthy and expensive screening technique.

Ciguatera poisoning

A radioimmunoassay (RIA ) was developed by Hokama and co-workers in Hawaii ( Hokama et. al., 1977 ) and then modified to a simpler enzyme immunoassay (Hokama 1985). 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 control (Hokama et. al., 1989b). The stick test measures ciguatoxin and polyether compounds, including okadaic acid. This whole area needs further research, particularly because of the concern over falsepositive results from the stick test.

Ciguatera poisoning

Research is needed into methods for predicting the development of ciguateric conditions in reef fishing areas, perhaps by assessing Gambierdiscus or other toxigenic microorganism populations and somehow closing such areas to fishing when the risk is high. The risk of contracting ciguatera poisoning are low for most consumers in the mainland United States. Risks are much higher in Hawaii, other Pacific islands, Puerto Rico and the Virgin Islands. There are moderate risks in areas such as Miami.

Ciguatera poisoning

Paralytic shellfish poisoning (PSP)

Paralytic shellfish poisoning (PSP)

Results from ingesting bivalve molluscs (mussels, clams, oysters, scallops) which 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 collectors 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 most poisonous known. Symptoms are neurological and normally appear within an hour of eating toxic shellfish. They include: Tingling Numbness burning sensation 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 incidence can occur. The cause of PSP is a complex of toxins known as saxitoxins, including saxitoxin, neotoxin and gonyautoxins. In the USA, the toxic dinoflagellates 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+) ions 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 80g of toxin per 100g of shellfish tissue. The classic method for analysis of saxitoxins is by mouse bioassay.

Paralytic shellfish poisoning (PSP)

The chemical analytical methods which have used include column separation, thin-layer chromatography, and fluorescence assays, either directly or after separation by high performance liquid chromatography (HPLC). Recently, immunoassay methods have been developed and reported (Sullivan and Iwaoka, 1983). These involve rabbit serum antibody preparations and monoclonal antibodies, and both radioimmunoassays and enzyme-linked immunoabsorbant assays ( ELISA ) have been used (Chu and 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 these blooms occur, shellfish become toxic and remain toxic for several weeks after the bloom subsides. Protection of the consumer is achieved by closure of shellfish harvesting in affected areas. Warnings are issued through the media, posted on 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 shellfish 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 seawater, a ban on shellfish harvesting is imposed. Surveillance and closure systems have been found to be effective.

Neurotoxic shellfish poisoning

Symptoms include: Tingling Numbness of the lips, tongue, throat and perioral area Muscular 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 usua