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Increased education of the consuming public, sports fishers, and health professionals on the hazards and symptoms of ciguatera is also recommended. Scombroid poisoning reportedly caused about the same number of outbreaks as ciguatera but was much more widespread in occurrence. Tuna, mahimahi dolphin , and bluefish were implicated as the major cause of scombroid poisoning in the United States. The disease is generally mild and self-resolving, and symptoms can be ameliorated by antihistamine drugs. Because the histamine that causes scombroid poisoning is produced after the fish have been caught as a consequence of improper temperature control, the disease can be prevented by rapidly cooling fish after capture.

A system based on the Hazard Analysis Critical Control Point would ensure this for commercially handled fish, but the education of subsistence and recreational fishers is also necessary. Paralytic shellfish poisoning was reported as a minor cause of seafood-borne illness in with only two deaths. This is a remarkable record in view of the annual occurrence of toxic situations among shellfish on both the East and the West coasts of the United States and indicates that current control measures applied by coastal states are highly effective.

However, the increasing occurrence of toxic dinoflagellate blooms and changing eating practices among some sectors of the consuming public require increased surveillance and the development of more rapid and simple tests for toxic shellfish. Although other natural seafood intoxications have not been reported recently in U. Increased vigilance concerning imported products, based on a requirement for certified nontoxicity, is recommended. Moreover, both state and federal laboratories should be prepared to test for these "other" toxins, and procedures should be in place to deal with outbreaks.

The toxic diseases from fish and shellfish of importance to American consumers include ciguatera, scombroid fish poisoning, paralytic shellfish poisoning, neurotoxic brevetoxic shellfish poisoning, puffer fish poisoning, diarrhetic shellfish poisoning, and amnesic shellfish poisoning Hughes and Merson, ; Mills and Passmore, ; Ragelis, ; Todd, In all cases, illness is due to ingestion of tissues containing heat-resistant toxins that are not destroyed by normal cooking and whose presence is undetectable by organoleptic means.

Except for scombroid poisoning, toxins usually accumulate in fish or shellfish through the food chain, so that the fish or shellfish are toxic at the time of harvest. Scombroid poisoning is caused by bacterial-induced chemical changes resulting from mishandling of fish after capture, which is more readily susceptible to human control Taylor, Fish poisoning, principally ciguatera and scombroid fish poisoning, was responsible for Reports were approximately evenly split between the two principal toxicoses: ciguatera outbreaks involving cases, and outbreaks of scombroid with cases Table However, as noted elsewhere in this report, CDC data are highly skewed, in this case due to the limited area within which ciguatera occurs, which enhances the visibility of this disease, and to the different symptoms associated with scombroid poisoning.

Thirteen outbreaks of paralytic shellfish poisoning PSP , the most dangerous of the intoxications, were reported and involved cases, most of which 94 were from two large California outbreaks in No cases of puffer fish or diarrhetic shellfish poisoning were reported to CDC in this period. The actual incidences of cases of ciguatera and PSP with milder symptoms are probably higher than indicated due to underreporting, as evident from a comparison of CDC data with those obtained in incidence studies in defined geographical areas Mills and Passmore, ; Morris et al.

Ciguatera is a clinical syndrome caused by eating the flesh of toxic fish caught in tropical reef and island waters. The toxin is believed to originate in a microscopic dinoflagellate alga Gambierdiscus toxicus that grows on reefs Bagnis et al. However, other benthic algae have also been implicated. Fish eating the algae become toxic, and the effect is magnified through the food chain so that large predatory fish become the most toxic. The occurrence of toxic fish tends to be localized, but localization is not consistent and toxic fish may occur sporadically anywhere in a reef or island location Engleberg et al.

More than species have been implicated in ciguatera poisoning Randall, , but the fish most commonly implicated include amberjack, snapper, grouper, barracuda, goatfish, and reef fish belonging to the Carrangidae Table A particularly high incidence was reported from Guam Haddock, , and a few cases have been reported in other states caused by fish shipped from Florida. Cases are frequently associated with travel to endemic ciguatera areas such as Hawaii and the Virgin Islands, and there is concern that many cases are not recognized by mainland U. The disease affects both gastrointestinal and neurological systems Bagnis et al.

Gastrointestinal symptoms, including diarrhea, nausea, vomiting, and abdominal pain, appear hours after ingestion of the fish and are of short duration. Neurological symptoms begin hours after consumption and may be moderate to severe; they commonly last for days but may persist for several months. In rare cases, symptoms may last for years, with exacerbation associated with fish consumption or possibly alcohol Halstead, Symptoms typically include hot-cold inversion hot coffee tastes cold, ice cream tastes hot ; muscular aches;.

Paralysis and death may occur in a few extreme cases. Symptoms may be extremely debilitating, resulting in extended periods of disability. Intravenous mannitol may relieve acute symptoms Palafox et al. There is considerable individuality in patient response Engleberg et al. Not all species in each category are necessarily toxic. 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, Scheuer et al.

Ciguatoxin CTX has a molecular formula of C 60 H 88 O 19 and is a brevitoxin type polyether, approximately times more potent than terodotoxin. Ciguatoxin opens voltage-dependent sodium channels in cell membranes Bidard, , and studies with in vitro tissue preparations suggest that the toxin causes a nerve conduction block after initial neural stimulation. In animal models, low doses of ciguatoxin cause mild hypotension and brachycardia.

Another lipid-soluble neurotoxin from ciguateric fish is called "scaritoxin. Generally, the pharmacological action is close to that of ciguatoxin, and they may be related compounds Legrand and Bagnis, Maitotoxin is a water-soluble toxin that may interfere with or modify calcium movement or calcium conductance in tissues. Other lipid-soluble toxins have been reported, but their structures and pharmacologic roles are not understood Ragelis, The reported incidence of ciguatera as indicated by CDC data is on the order of outbreaks per year, involving 50 to cases.

However, these numbers appear to reflect significant underreporting. In a randomized, stratified community survey conducted in the U. An incidence rate of The average annual incidence in Hawaii for was only 8. These data emphasize the striking regional nature of this disease and its very real importance as a cause of morbidity in endemic areas.

There is some evidence from the Pacific region that changes in the reef environment due to construction or other underwater activities can cause an increase in the occurrence of ciguatoxic fish Anderson et al. For the vast majority of U. For residents of south Florida, the Caribbean, and Hawaiian or other Pacific islands, absolute safety depends on individual abstinence from eating reef fish.

The risk may be greatly reduced by. These data are not included in calculation of total outbreaks and cases. However, hot spots may persist for extended periods of time or may change Cooper, ; Halstead, Voluntary action by commercial fish distributors in some areas has been quite effective. Thus amberjack Seriola dumerili , Kahala is not sold commercially in Hawaii because of the known high incidence of ciguatoxic fish of this species. Other suspect species coming to market in Hawaii may be tested by the "stick test. In areas where reef fish are part of the regular diet of inhabitants or visitors, and particularly where significant quantities of fish are caught and consumed by recreational or small-boat fishermen, it seems unlikely that ciguatera can be completely prevented.

The impossibility of detecting toxic fish by organoleptic inspection and the sporadic occurrence of such fish limit control options. The availability of a simple reliable test would greatly improve the situation. At present, the only ciguatera screening program in existence is that employed by the Tokyo Central Wholesale Fish Market in Japan. Hygiene inspectors examine incoming shiploads of fish that have originated in tropical island regions. Suspect specimens are removed for testing. Muscle extracts are prepared and tested on cats and mice for evidence of ciguatoxicity Halstead, This is a lengthy and expensive screening technique that is impractical when dealing with large numbers of samples.

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. Kits are being developed for use by sports fishers that could partly resolve the cost problem. In any case it would be desirable to limit testing to high-risk fish. 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.

Reef closure would probably be feasible in discrete Pacific islands where there is limited movement of fish from one reef area to another. However, this might not be the case in the Caribbean where fish movement between reefs is easier and more common. Obviously, there should be some follow-up on the reports of a relationship between reef disturbance and increased occurrence of ciguateric fish because this may result from human activity that can be controlled Gollop and Pon, Estimates of the economic consequences of ciguatera are not easily made.

However, they are significant for island communities largely dependent on tourism. In summary, the risks of contracting ciguatera fish poisoning are low for most consumers of seafood in the mainland United States. Risks are much higher in Hawaii, other Pacific islands, Puerto Rico, and the Virgin Islands, with more moderate risks in areas such as Miami that border endemic zones. For mainland consumers, protection could be afforded by strict control of imports and intrastate shipments.

4. Naturally Occurring Fish and Shellfish Poisons | Seafood Safety | The National Academies Press

However, such an approach may be unnecessarily severe and does not address the. A more reasonable and potentially cost-effective approach would be to emphasize development of an inexpensive but reliable assay for ciguatoxic fish, similar to the stick test proposed by Hokama The stick test measures ciguatoxin and polyether compounds including okadaic acid Hokama et al.

In a recent outbreak in Hawaii due to Philippine fish, the test was positive for a fish that was then shown to contain palytoxin Kodama et al. It has been suggested that palytoxin, previously reported from parrot fish and crab in Japan, is one of the toxins "under the rubric of ciguatera" Kodama et al. Obviously, this whole area needs further research, particularly because of the concern over false-positive results from the stick test.

If such an assay were widely available, it might be applied both by regulation and voluntarily to reduce the incidence of disease in endemic areas, particularly if consumers were knowledgeable and insisted on purchasing only fish that had been screened for toxicity. Similarly, interstate shipment and imports of potentially high-risk fish grouper, jack could be restricted to fish certified to be nontoxic. This is particularly important in view of the increased production and export of fish to the United States from Pacific islands and reef fishery areas of Southeast Asia, such as the Philippines Miller, Scombroid intoxication results from ingestion of fish containing high levels of free histamine.

Initially, the disease was associated with consumption of scombroid fish such as tuna, mackerel, bonito, and saury. More recently, other types of fish have been identified as causing the intoxication, including mahimahi, bluefish, jack, mackerel, amberjack, herring, sardine, and anchovy. In the United States, scombroid fish poisoning has been caused dominantly by mahimahi, tuna, and bluefish CDC, see Table Scombroid food poisoning has a wider geographic occurrence in the United States than ciguatera, with incidents reported from 45 states during This reflects the fact that the disease, although associated with warm ambient temperatures, is not due solely to tropical or subtropical species of fish.

Thus, the risk of scombroid poisoning is widespread among fish-eating consumers. Fortunately, the disease is mild, of short duration, and self-resolving without any sequelae in the vast majority of cases. Moreover, because the toxic condition is a consequence of improper handling or storage of the fish and there are effective testing methods to identify toxic fish, control and prevention are possible.

The mildness and transient nature of scombroid poisoning make it likely that this disease is underreported. Fish imported to the United States from warmwater countries, particularly mahimahi, have been implicated as a cause of scombroid poisoning; this reflects both the high ambient water and air temperatures in the originating area, and the poor handling conditions on boats and in markets permitting growth of the bacteria that convert histidine to histamine.

The disease is correctly described as histamine poisoning Taylor, ; it includes gastrointestinal, neurological, hemodynamic, and cutaneous symptoms such as. The most frequent symptoms are tingling and burning sensations around the mouth "peppery tasting" , gastrointestinal complaints, and a rash with itching. The illness is generally mild and self-resolving, with rapid onset of symptoms and duration of only a few hours.

Normally, treatment is unnecessary but antihistamine drugs will provide relief. The histamine is produced in the fish flesh by decarboxylation of free histidine, which is naturally present at high levels in species of fish implicated in scombroid fish poisoning Lukton and Olcott, The production of histamine is due to the action of histidine decarboxylase, an enzyme produced by bacteria growing on the fish. Histidine decarboxylase production is not widespread among bacteria and is found principally among species of the Enterobacteriaceae, Clostridium, Lactobacillus Taylor, , and possibly Vibrio Van Spreekens, The enteric bacteria Morganella morganii, Klebsiella pneumoniae , and Hafnia alvei have been isolated and identified from fish implicated in histamine poisoning Havelka, ; Kawabata et al.

Other enteric bacteria, Clostridium perfringens , and halophilic vibrios have also been reported, but M. These organisms are not commonly isolated from living fish and may be added during catching and handling Taylor, Bacteria must grow to a large enough population for significant production of histamine to occur. Thus, histamine production in fish is a consequence of improper handling and storage of fish after capture.

Indeed, histamine content may be used as an index of spoilage in certain fish.


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There is uncertainty regarding the threshold toxic dose because potentiators of toxicity are present in fish that lower the effective dosage compared with pure histamine. The occurrence of scombroid fish poisoning in recent years, based on CDC reports, is between 12 and 20 outbreaks involving fewer than cases per year higher numbers were recorded in , , and This is, without question, a considerable underestimate because the illness is generally mild, passes rapidly with no after effects, and is thus not usually reported to health authorities.

Above this level the fish is considered hazardous. Fish histamine poisoning is preventable by proper handling of fish at the time of capture and during subsequent storage, processing, and distribution. Fish should be chilled as rapidly as possible after capture by using ice, refrigerated seawater or brine, or mechanical refrigeration. Histamine levels should be monitored routinely by the industry in susceptible species where proper prior handling cannot be ensured. The level at which testing is performed will depend on the species and product form e. In the United States, the highest-risk fish commercially is probably imported fresh or frozen fish from tropical areas.

High histamine levels may be present in such fish when other overt signs of spoilage bad odor, discoloration are absent.

Marine toxins: origin, structure, and molecular pharmacology [1990]

Imported fish should be subject to controls. Domestically caught species in normal commercial channels are probably less of a problem because of the widespread use of ice and refrigeration. Bluefish and sport caught tuna or mackerel present a more intractable control problem because they are caught by individuals and either do not enter commercial channels or do so in an unconventional way.

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Some local or state control may be possible where licensed charter fishing boats are involved, perhaps by requiring that adequate facilities are provided for rapid chilling of fish and for their storage in a chilled state until landed. In the absence of a simple litmus test, control for most sports fishers and their families depends on education. States should be encouraged to provide advisory bulletins to sports fishers.

However, it should be emphasized that this is a mild disease that is neither long lasting nor life threatening, and that symptoms can be relieved quickly by antihistamines. Paralytic shellfish poisoning results from ingesting bivalve molluscs mussels, clams, oysters, scallops that have consumed toxigenic dinoflagellates Halstead and Schantz, ; Schantz, The toxins are assimilated and temporarily stored by the shellfish.

Very few outbreaks have occurred in other areas of the United States from shellfish harvested in coastal states, reflecting the effectiveness of current testing and control measures for commercially produced shellfish. Most disease incidents involve mussels, clams, and scallops gathered and eaten by recreational collectors often from closed areas. The CDC listed 12 outbreaks involving people with one death during Table A report by Nishitani and Chew , based on data from the West Coast, lists cases as follows: 68 from Alaska, 98 from California, 1 from Oregon, and 12 from Washington.

Thus, there is some evidence of underreporting of cases to CDC. Although PSP is an extremely dangerous disease that can cause death, there is reason to believe that mild cases due to consumption of marginally toxic clams by recreational diggers are never reported to health authorities or are misdiagnosed. Paralytic shellfish poisoning 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; in nonlethal cases they usually subside within a few days.

Symptoms include tingling, numbness, and burning of the lips and fingertips; ataxia; giddiness; staggering; drowsiness; dry throat and skin;. Cases Reported by Nishitani and Chew a. In severe cases, respiratory paralysis occurs, which can cause death usually during the first 24 hours, so that the prognosis for recovery is good for patients surviving this period.

No antidote is known, but respiratory support is given when paralysis occurs. There are no sequelae, and patients recover completely. Immunity is not conferred by a poisonous episode and multiple incidents can occur. The cause of PSP is a complex of toxins known as saxitoxins because all can be considered forms or derivatives of saxitoxin, whose structure was reported by Schantz et al. Saxitoxin, neosaxitoxin, and gonyautoxins II and III are roughly equal in toxicity, whereas the others are somewhat weaker Hall and Reichardt, In the United States, the toxigenic dinoflagellates of importance are Gonyaulax catenella and G.

Strains of these microorganisms develop characteristic toxin profiles that usually contain six to eight saxitoxins. Shellfish feeding on blooms of these Gonyaulax ingest all toxins but seem to selectively retain or biologically modify some derivatives because the toxin profiles in clams or scallops may differ from those of the Gonyaulax on which they have been feeding Schantz et al.

The classical method for analysis of saxitoxins is by mouse bioassay Schantz et al. Suitable groups of mice are challenged by injection of toxin extracts, and their responses are compared with those of mice injected with known toxin at different concentrations. This method is used by state laboratories in surveillance activities.

The chemical analytical methods that have been used, mostly in research, include column separation, thin-layer chromatography, and fluorescent assays either directly or after separation by high-performance liquid chromatography HPLC. The HPLC method is quite rapid and has been considered as a possible replacement of the mouse bioassay Sullivan and Iwaoka, Recently, immunoassay methods have been developed and reported. These involve rabbit serum antibody preparations and monoclonal antibodies, and both radioimmunoassays and enzyme-linked immunoabsorbent assays ELISA have been used Chu and Fan, However, so far these methods are not acceptable for regulatory use.

Blooms of the toxigenic dinoflagellates Gonyaulax catenella West Coast and G. The occurrence of blooms is not predictable with the present state of knowledge. When these blooms occur, shellfish become toxic and remain toxic for several weeks after the bloom subsides. Some species of bivalve molluscs in a few areas remain constantly toxic e. Protection of the consumer is primarily the responsibility of the state in which potentially toxic shellfish originate and is achieved by closure of shellfish harvesting in affected areas.

Closure may be absolute for certain species over a long period e. Because clam digging and oyster gathering from public beaches are popular recreational activities in coastal states, the authorities issue warnings through the media when dangerous conditions exist and post warning notices multilingual in the West on public beaches. Each of the affected states has a surveillance system involving regular sampling and testing of shellfish from different areas during the season for blooms April to October.

Toxicity tests are normally run in state public health laboratories by using the standardized mouse bioassay AOAC, , whereas the collection of samples and posting of beaches are frequently the responsibility of local e. Commercial producers are required to submit samples for testing, and many voluntarily send shellfish to the state laboratories. This system, although expensive for the states, has served the U. In , these involved only twelve outbreaks with cases. Only two outbreaks, both due to mussels from the same source California , were of commercial origin.

All other outbreaks were among recreational clam diggers shellfish gatherers. Despite the seriousness of the intoxication, there have been only two. West Coast state records show a somewhat higher number of outbreaks, which have typically involved recreational shellfish gatherers but with no serious consequences Nishitani and Chew, The present system of testing and control by the states appears to provide adequate protection to the consumer of domestically produced shellfish.

Neurotoxic shellfish poisoning sometimes referred to as brevetoxic shellfish poisoning, BSP is caused by ingesting shellfish that have fed on the red tide organism Gymnodinium breve formerly Ptychodiscus brevis. Red tides occur sporadically in the Gulf of Mexico and off the coast of Florida Baden et al.

They may be carried north in the Gulf Stream, occasionally affecting the coastline of adjacent states. The dinoflagellate blooms are easily observed as a red coloration of seawater, and the organisms can be detected microscopically. Red tides usually cause massive fish kills, and the carcasses wash ashore. Irritant aerosols are produced by wind and wave action, which may cause respiratory distress. Filter feeding molluscs ingest the dinoflagellates and retain the toxin in their tissues for some time.

Reports of respiratory irritation affecting people in coastal areas were received on October 29 and 30, ; oyster harvesting was closed on November 2. The basis for closure was the occurrence of more than 5, G. Notwithstanding this incident, which occurred as a result of the first bloom of G. Symptoms resulting from the ingestion of shellfish containing brevetoxins include tingling and numbness of the lips, tongue, throat, and perioral area; muscular aches; gastrointestinal upset; and dizziness.

The intoxication is usually not fatal. Onset is rapid and symptoms subside within a few hours or days at most. There is no antidote. The symptoms appear to be due to two brevetoxins produced by G. They may be analyzed chemically, but this is not done routinely. Identification of a dangerous condition is readily made by observation of red tide conditions, including characteristic fish kills, and of the organisms themselves in the water.

Local authorities then routinely close shellfish harvesting to industries and the public. Diarrhetic shellfish poisoning is caused by ingestion of mussels, scallops, or clams that have been feeding on Dinophysis fortii or D. There have been no confirmed outbreaks in the United States, but the disease is common in Japan and has become a problem in Europe. One confirmed DSP episode occurred in Canada in Symptoms include diarrhea, nausea, vomiting, and abdominal pain.

Onset 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 Yasumoto et al. At least five toxins have been isolated from dinoflagellates and shellfish.

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Okadaic acid is most commonly encountered in Europe where D. There is a mouse bioassay for the toxins. For the U. Shellfish should be imported only from countries with whom the United States has a memorandum of understanding MOU. Testing for shellfish toxins should be part of the general practice under the MOU. Nevertheless, because Dinophysis does occur in U. Puffer fish poisoning results from ingestion of the flesh of certain species of fish belonging to the Tetraodontidae Halstead, The toxin involved is called tetrodotoxin and was originally believed to be a true ichthyosarcotoxin produced by the fish itself.

The toxicity of poisonous puffers fluctuates greatly Halstead, Recent observations that cultured puffer fish are atoxic has supported a food chain origin for the toxin, but this has not yet been confirmed Mosher and Fuhrman, It has recently been shown, however, that certain common marine vibrios can produce a form of the toxin Narita et al. Puffer fish poisoning has not been reported in mainland United States in recent years, but incidents were reported in the past. Seven cases were reported in Florida between and , including three fatalities Benson, ; Hemmert, They appear to have been caused by the consumption of locally caught species of Sphoeroides.

The common puffer fish, Arothron hispidus , has been implicated in at least seven fatalities in Hawaii HDH, There are deaths from fugu poisoning in Japan each year, where various species of puffer fish are eaten as a delicacy; this occurs despite very stringent controls imposed by Japanese authorities on the marketing and restaurant preparation of the dish Ogura, The symptoms of puffer fish poisoning are similar to those described for paralytic shellfish poisoning, including initial tingling and numbness of lips, tongue, and fingers leading to paralysis of the extremities; ataxia; difficulty in speaking; and finally, death by asphyxiation due to respiratory paralysis.

Nausea and vomiting are common early symptoms. The similarity in symptoms is not surprising because tetrodotoxin, although chemically different from the saxitoxins, also blocks sodium channels. The toxicity of tetrodotoxin is similar to that of saxitoxin, and mg constitutes a lethal dose for humans. There is disagreement concerning the toxicity of U.

Atlantic puffer fish. However, Hemmert shows a table indicating that the viscera, skin, and some flesh of S. Larson et al. The species Arothron hispidus has been implicated in at least seven fatalities in Hawaii. The wholesaling, preparation, and selling of puffers as food in Japan, even under the most rigid public health conditions by trained and certified puffer cooks, has not eliminated the danger of eating these fish.

The fugu puffer still remains a major cause of fatal food intoxications in Japan. In brief, eating poisonous puffers is at best a game of Russian roulette. All of the U. There are too many variables in the puffer business, and sale of these should be prohibited in the United States. This subject has been documented and discussed at great length by Halstead , In view of these reports, it would seem prudent to exclude puffer fish, whether domestic or imported, from U. Even though very strict requirements have been imposed in an attempt to ensure that the fish are nontoxic, the continuing Japanese experience should raise questions concerning the safety of this process for the U.

Amnesic shellfish poisoning has been proposed by Todd as a name for the syndrome caused by domoic acid. This severe disease has been identified only in a series of outbreaks in Canada in November and December involving people. The toxin is present in some varieties of the diatom Nitzschia pungens and accumulated in mussels and clams in Atlantic Canada during a period of blooms of the diatom.

Symptoms included vomiting, abdominal cramps, diarrhea, disorientation, and memory loss Perl et al. Short-term memory loss was the most persistent symptom and lasted over a year in several cases. Autopsies on three fatalities showed necrosis of the hippocampus. The disease is particularly severe among older people, some of whom died in the Canadian outbreak.

Clearly, this is a toxin to be considered in U. Nitzschia pungens and N. States in the northeastern United States are now testing mussels for domoic acid. There are sporadic reports of other intoxications from seafoods from time to time Halstead, ; Wekell and Liston, , but these have not been investigated sufficiently to identify the toxic agent. As noted earlier, the somewhat variable symptoms defined as ciguatera and the reported association of polyether substances and palytoxin Hokama et al.

One well-defined syndrome reported to occur in Hawaii is "hallucinogenic fish poisoning. Hallucinations, insomnia, intense dreaming, weakness, and burning of the throat are common soon after eating the fish Halstead and Schantz, Terrifying nightmares have been reported and constrictive chest pains occur. The condition is short-lived and self-resolving Halstead, ; HDH, There does not seem to be any analytical test for this toxin.

Diseases caused by natural fish poisoning are listed in Table Three of these are of direct significance to the U. Of these three, PSP, which has potentially the most severe health consequences, is well controlled by state surveillance and harvest closure practices. Ciguatera, for which the largest number of cases is reported, has a major public health impact in Hawaii, Guam, and Caribbean island communities and a small effect in Florida. Prevention of ciguatera can be ensured only by interdiction of the supply of potentially toxic tropical reef fish to the U. This is theoretically possible through banning imports to the U.

Such action would probably be unacceptable in the island states and possessions, where local fishing provides essential employment and is closely tied to the tourist industry. Furthermore, blanket rejection of such species as groupers, which are mostly nontoxic, would greatly reduce consumer choice and adversely affect the income of fishermen and others in areas remote from the toxin problem.

Fortunately, current research at the University of Hawaii provides good promise of early development of a simple reliable test for ciguatoxic fish. Such a test is urgently needed to enable selective rejection of toxic fish by testing either on board the fishing vessel or at dockside. On a longer-term basis, research should be directed toward the prediction of developing toxic conditions so that closure of fishing areas can be applied before human intoxications occur.

Scombroid fish poisoning is unquestionably a consequence of improper handling or processing of certain types of fish. Control of this hazard at the commercial level can be ensured, to a reasonable degree, by proper application of temperature control in handling and processing fish with known high content of free histidine. Where uncertainty exists concerning the quality of primary handling, as for some imported fish, reliable analytical tests may be used to determine whether fish or fish products exceed the limit for histamine content used by FDA.

There seems to be no easy solution to the problem of recreationally caught fish mostly tuna and bluefish because it is unlikely that a mandatory inspection and testing program could be imposed. Education on proper fish handling to avoid the hazard and warnings issued by states to their recreational anglers and to businesses supporting such activity charter boats, gear suppliers, etc. The other intoxications discussed in this chapter are rare and apparently under control in the United States e. Nevertheless, agencies responsible for ensuring the safety of the U. Appropriate tests should be sought and laboratories prepared for their use.

Importers should be required to ensure that seafood products from countries where such intoxications have occurred are not toxic. This is best done by controlling imports through an MOU that would include provisions for toxicity testing. Organoleptic inspection systems have little value in protecting the consumer from seafood intoxications. Toxic fish and shellfish usually look and smell perfectly normal. Protection of the consumer requires a multifaceted approach involving industry practices and regulations, control of harvest and distribution, and as a last resort, testing, seizure, and detention.

This requires action by states and local authorities from different departments e. In the final analysis the most effective measure is likely to be education of the fish-eating public about which fish and shellfish may be naturally toxic. Except for scombroid poisoning, toxicity is a function of the normal feeding habits of wild animals and cannot be controlled.

Thus, potentially toxic fish may enter the food supply. Fortunately, the serious life-threatening intoxications are controllable so that most incidents of fish poisoning are of short duration and are self-resolving. Nevertheless, research aimed at the detection and elimination of toxic fish from the food supply and at methods of treatment for intoxications such as ciguatera that can have long-lasting and even disabling effects should be encouraged.

There is a need for educational materials to be made available to the fishing industry, public health workers, divers, and sports fishers. A number of popular handbooks have been published dealing with the potential health hazards caused by marine organisms Halstead, , ; Halstead et al. However, much of this information does not reach regulatory, clinical public health, and poison control centers Freudenthal, In dealing with this subject matter, it is essential that the educational materials be fully illustrated, preferably in color. More charts and informational pamphlets are required.

Toxic dinoflagellates: Gonyaulax catenella Pacific ; G. Numbness, paralysis after eating; death hours; prognosis good after 24 hours. Abdominal pain, nausea, vomiting, severe diarrhea within 4 hours after eating; rarely fatal. Feeling of nausea from red tide spray, symptoms like ciguatera from eating bivalves. Itching, redness, allergic symptoms, headache, dizziness, diarrhea, peppery taste. Vomiting, cramps, diarrhea, memory loss and disorientation; memory loss has lasted a year. Remarks: In most cases toxic shellfish are not detectable by organoleptic means.

It is therefore important that practical chemical or biological tests, specific for the detection of the toxins, be developed. Although not all the listed diseases are problems in the United States, seafood inspectors and processors should always be aware that toxigenic dinoflagellates, or other microorganisms producing toxins that get into fish and shellfish, may become established in areas where fish and shellfish are harvested for U.

An example: diarrhetic shellfish poisoning is not a problem in the United States, but the dinoflagellate that produces the toxin may become established in shellfish areas that supply U. Fish of species reported by health authorities to have caused ciguatera, which are to be imported to the United States from regions of high ciguatera incidence, should carry certification of nontoxicity. States and territories in which ciguatera is a problem should license marine sports fishers and, at the point of issuance of the license, issue clear and specific warnings regarding the dangers of ciguateric fish.

Pamphlets on poisonous fish should be generally available to the public in areas where ciguatera is endemic. When feasible, reef fishing should be closed in areas where ciguatoxic fish are present. This closure should apply to sports fishers as well as to commercial vessels.

Research should be accelerated on the development of simple, rapid tests for toxicity such as the Hokama stick test. Research should also be directed toward analysis of the events leading to the appearance of toxic fish in particular reef environments, with the objective of developing predictive indices that can be used to close areas to fishing before human intoxications occur. This should be controlled by routine lot testing. Similar temperature records should be maintained for such species during processing and shipment on land. Advisory leaflets describing the causes of scombroid poisoning and providing advice on how to handle fish to minimize risk of the disease should be made widely available to sports fishers who target potentially scombrotoxic species.

Research to develop a rapid field test for PSP toxicity in shellfish should be strongly encouraged and supported. Such a test could be applied directly by commercial growers and recreational shellfish gatherers. Nevertheless, state agencies should continue to monitor the PSP condition of local shellfish. The consumption of puffer fish should be strongly discouraged, and their importation to the United States should be banned.

Regulatory agencies should maintain awareness of potential toxin problems, such as diarrhetic shellfish poisoning and amnesic shellfish poisoning, and their technical personnel should be trained and equipped to run definitive analyses on these and other toxins. Shellfish should be imported only under an MOU that includes a provision for toxicity testing. In view of the complexity of seafood intoxications, the federal government should establish or support two to three centers of research into such toxins to enlarge understanding of the phenomena, provide possible remedies, and develop particular tests.

Because of the highly localized impact, primary responsibility for control of seafood toxins should reside at the state level, with funding, quality control, and specialist assistance from a federal seafood safety agency. The toxigenic strains have also been designated Protogonyaulax , and more recently, the genus name Alexandrium has been proposed. Anderson, B. Sims, N. Wiebenga, and M. The epidemiology of ciguatera fish poisoning in Hawaii Arnold, S.

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OJIKA, Makoto

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Paralytic Shellfish Poisoning (PSP) Toxins

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