4
Naturally Occurring Fish and Shellfish Poisons

ABSTRACT

Incidents of illness due to naturally occurring seafood toxins reported to the Centers for Disease Control in the period 1978-1987 were limited to ciguatera, scombroid fish poisoning, and paralytic shellfish poisoning. Other intoxications, including puffer fish poisoning and neurotoxic (brevetoxic) shellfish poisoning, were reported earlier, and diarrhetic shellfish poisoning and amnesic shellfish poisoning are prospective risks that should be anticipated. Naturally, toxic fish and shellfish cannot be distinguished from nontoxic animals by sensory inspection, and the toxins are not destroyed by normal cooking or processing. Except for scombroid fish poisoning, natural intoxications are both highly regional and species associated, and toxins are present in the fish or shellfish at the time of capture. Scombroid poisoning is due to histamine produced by bacteria multiplying on certain fish that are mishandled after capture, and illnesses are widely reported from different states.

Ciguatera is a sometimes severe disease caused by consuming certain species of fish in tropical waters usually associated with islands or reefs. The disease is most common (endemic) in the Caribbean and Pacific islands, with some outbreaks in southern Florida and sporadic cases in other states due to imported fish or tourist travel to endemic areas. Ciguatera was responsible for about half of all reported outbreaks of seafood intoxications in 1978-1987. Treatments are largely supportive, but mortality is low. There are presently no effective control systems in place for prevention of ciguatera because a generally accepted test for toxic fish is not available. Warnings and advisories concerning the hazards of ciguatera and the risks of consuming particular species of fish from ciguatera areas are issued by states. Active control based on regulation of fishing dangerous species, supported by testing suspect fish at dockside or on board the catching vessel to detect and reject ciguatoxic fish, is proposed. 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



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Seafood Safety 4 Naturally Occurring Fish and Shellfish Poisons ABSTRACT Incidents of illness due to naturally occurring seafood toxins reported to the Centers for Disease Control in the period 1978-1987 were limited to ciguatera, scombroid fish poisoning, and paralytic shellfish poisoning. Other intoxications, including puffer fish poisoning and neurotoxic (brevetoxic) shellfish poisoning, were reported earlier, and diarrhetic shellfish poisoning and amnesic shellfish poisoning are prospective risks that should be anticipated. Naturally, toxic fish and shellfish cannot be distinguished from nontoxic animals by sensory inspection, and the toxins are not destroyed by normal cooking or processing. Except for scombroid fish poisoning, natural intoxications are both highly regional and species associated, and toxins are present in the fish or shellfish at the time of capture. Scombroid poisoning is due to histamine produced by bacteria multiplying on certain fish that are mishandled after capture, and illnesses are widely reported from different states. Ciguatera is a sometimes severe disease caused by consuming certain species of fish in tropical waters usually associated with islands or reefs. The disease is most common (endemic) in the Caribbean and Pacific islands, with some outbreaks in southern Florida and sporadic cases in other states due to imported fish or tourist travel to endemic areas. Ciguatera was responsible for about half of all reported outbreaks of seafood intoxications in 1978-1987. Treatments are largely supportive, but mortality is low. There are presently no effective control systems in place for prevention of ciguatera because a generally accepted test for toxic fish is not available. Warnings and advisories concerning the hazards of ciguatera and the risks of consuming particular species of fish from ciguatera areas are issued by states. Active control based on regulation of fishing dangerous species, supported by testing suspect fish at dockside or on board the catching vessel to detect and reject ciguatoxic fish, is proposed. 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

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Seafood Safety to 10°C or lower and holding them at or below this temperature at all times before cooking and eating. 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 1978-1987 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.S. consumers (except for an outbreak of neurotoxic shellfish poisoning in North Carolina in 1987), the potential for their occurrence either from domestically produced seafoods or from imports is real. 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. INTRODUCTION 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, 1976; Mills and Passmore, 1988; Ragelis, 1984; Todd, 1989). 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, 1986). Fish poisoning, principally ciguatera and scombroid fish poisoning, was responsible for 17.8% of all confirmed food-borne disease outbreaks listed by the Centers for Disease Control (CDC) in 1978-1987. Reports were approximately evenly split between the two principal toxicoses: 179 ciguatera outbreaks involving 791 cases, and 157 outbreaks of scombroid with 757 cases (Table 4-1). 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 134 cases, most of which (94) were from two large California outbreaks in 1980. 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, 1988; Morris et al., 1982b; Nishitani and Chew, 1988).

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Seafood Safety TABLE 4-1 Illness Due to Natural Seafood Toxins in the United States Reported to CDC   Ciguatera Scombroid PSP   Outbreaks Cases Outbreaks Cases Outbreaks Cases 1978 19 56 7 30 4 10 1979 21 97 14 134 1 3 1980 15 52 28 151 5 116 1981 30 219 9 93 - - 1982 8 37 18 58 0 5 1983 13 43 13 271 - - 1984 18 78 12 53 - - 1985 26 104 14 56 2 3 1986 18 70 20 60 - 0 1987 11 35 22 95 - 0 Total 179 791 157 757 13 137 SPECIFIC INTOXICATIONS Ciguatera 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., 1980). 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., 1983). More than 400 species have been implicated in ciguatera poisoning (Randall, 1980), but the fish most commonly implicated include amberjack, snapper, grouper, barracuda, goatfish, and reef fish belonging to the Carrangidae (Table 4-2). In the United States, ciguatera occurs principally in Hawaii, Puerto Rico, the Virgin Islands, Guam, and Florida (CDC, 1989). A particularly high incidence was reported from Guam (Haddock, 1989), 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.S. physicians. The disease affects both gastrointestinal and neurological systems (Bagnis et al., 1979; Morris et al., 1982a). Gastrointestinal symptoms, including diarrhea, nausea, vomiting, and abdominal pain, appear 3-5 hours after ingestion of the fish and are of short duration. Neurological symptoms begin 12-18 hours after consumption and may be moderate to severe; they commonly last for 1-82 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, 1967). Symptoms typically include hot-cold inversion (hot coffee tastes cold, ice cream tastes hot); muscular aches;

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Seafood Safety tingling and numbness of lips, tongue, and perioral region; metallic taste; dryness of mouth; anxiety; prostration; dizziness; chills; sweating; dilated eyes, blurred vision, and temporary blindness. 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., 1988), provided it is given within several hours of consumption, with amitriptyline (Bowman, 1984) or tocainide (Lange et al., 1988) suggested for more chronic manifestations. There is considerable individuality in patient response (Engleberg et al., 1983). TABLE 4-2 Fish Reported as a Vehicle of Ciguatera to CDC 1978-1987 Ordered by Frequency of Reported Involvementa Common Fish Name Genus or Family Name Amberjack Seriola species Snappersb Lutjanidae Groupers Serranidae Goatfish Mullidae Po'ou Cheilinus species Jacks Carangidae Barracuda Sphyrenidae Ulua Caranx species Wrasse Labridae Surgeon fish Acantharidae Moray eel Muraeinidae Papio Trachinotus species Roi Cephalopolis species Rabbit fish Siganus species Parrot fish Scaridae Miscellaneous reef fish   a See Halstead (1967) for a more complete listing of fish species involved in Ciguatera outbreaks. b These categories include a number of different species commonly referred to by the vernacular name. Not all species in each category are necessarily toxic. SOURCE: CDC (1981a-c, 1983a,b, 1984, 1985, 1989) and Haddock (1989). 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 (Scheuer 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 polyether, approximately 100 times more potent than terodotoxin. Ciguatoxin opens voltage-dependent sodium channels in cell membranes (Bidard, 1984), 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. Higher doses give a biphasic response with an initial brachycardia/hypotension followed by tachycardia/hypertension; very high doses produce a phrenic nerve block with respiratory arrest (Gillespie et al., 1986). Another lipid-soluble neurotoxin from ciguateric fish is called "scaritoxin." This toxin has been shown to depress oxidative metabolic processes in rat brain and has a depolarizing action on excitable membranes.

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Seafood Safety Generally, the pharmacological action is close to that of ciguatoxin, and they may be related compounds (Legrand and Bagnis, 1984). 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, 1984). The reported incidence of ciguatera as indicated by CDC data is on the order of 15-20 outbreaks per year, involving 50 to 100 cases. Cases reported to the CDC occur almost exclusively in Hawaii, Puerto Rico, the Virgin Islands, and Florida (Table 4-3). However, these numbers appear to reflect significant underreporting. In a randomized, stratified community survey conducted in the U.S. Virgin Islands, the calculated incidence rate was 73 cases/10,000 population/year (Morris et al., 1982b). In Puerto Rico, 45 cases were reported to the Puerto Rico Poison Control Center in 1982. In an associated telephone survey, 7% of persons contacted reported that at least one family member had at one time had ciguatera (Holt et al., 1984). In Miami, 129 cases of ciguatera were reported to the Dade County Health Department between 1972 and 1976, for an annual incidence of 5 cases/100,000 population; the actual incidence was estimated to be 10-100 times this figure (i.e., 50-500 cases/100,000 population) (Lawrence et al., 1980). An incidence rate of 234.9 cases/100,000 population was reported for the Marshall Islands during 1982-1987 (Ruff, 1989). The average annual incidence in Hawaii for 1984-1988 was only 8.7 cases/100,000 population, but this varied greatly from island to island: in 1988 the rate per 100,000 population was 3.2 on Oahu, 12.5 on Kauai, 11.1 on Maui, 33.9 on Hawaii (the largest island), and 7.5 for the state (Gollop and Pon, 1991). 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., 1983; Ruff, 1989). For the vast majority of U.S. consumers, the disease can be contracted only through consumption of fish imported from endemic areas. 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 TABLE 4-3 Outbreaks and Cases of Ciguatera in the United States Reported to CDC 1978-1987 State Outbreaks Cases Percentage of Outbreaks Percentage of Cases California 1 2 0.6 0.3 Florida 9 35 5.0 4.4 Guama 60 117 56.0 48.0 Hawaii 144 560 80.0 71.0 Louisiana 1 6 0.6 0.8 Puerto Rico 13 73 7.0 9.0 Vermont 1 3 0.6 0.4 Virgin Islands 9 110 5.0 14.0 Washington 1 2 0.6 0.3 Total 179 791     a From Haddock (1989). These data are not included in calculation of total outbreaks and cases.

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Seafood Safety avoidance of particular species of fish from known "hot-spot" areas (Randall, 1980). However, hot spots may persist for extended periods of time or may change (Cooper, 1964; Halstead, 1967). 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." Also, the Hawaii Department of Health (HDH, 1988) publishes a warning pamphlet on Fish Poisoning in Hawaii and periodically issues advisories on dangerous species and the areas from which they have been taken. 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, 1970). This is a lengthy and expensive screening technique that is impractical when dealing with large numbers of samples. 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). However, even this test costs $1 to 2 per fish, and it would not be possible to test each reef fish landed. 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, 1991). Estimates of the economic consequences of ciguatera are not easily made. However, they are significant for island communities largely dependent on tourism. Ragelis (1984) quoted an estimate of an annual loss to fishermen in the Caribbean region and Hawaii of $10 million as a result of restricted fishing, but this may be low. 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. However, such an approach may be unnecessarily severe and does not address the

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Seafood Safety much more significant problems that exist in endemic areas. 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 (1990). The stick test measures ciguatoxin and polyether compounds including okadaic acid (Hokama et al., 1989a). 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., 1989). 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., 1989). 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, 1991). Scombroid (Histamine) Fish Poisoning 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, 1989) (see Table 4-4). Scombroid food poisoning has a wider geographic occurrence in the United States than ciguatera, with incidents reported from 45 states during 1978-1988. The TABLE 4-4 Fish Reported to CDC as Vehicles of Scombroid Poisoning in the United States, 1978-1986a Common Name Genus Reported Outbreaks Mahimahi Coryphaena 55 Tuna Thunnus 41 Bluefish Pomatomus 13 Salmon (raw) Oncorhynchus 2 Marlin Makaira 1 Mackerel Scomber 1 Blue Ulua Caranx 1 Opelu Dicapterus 1 Redfish Sebastes 1 a Data not available for 1987.

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Seafood Safety highest number of outbreaks (45) and cases (171) occurred in Hawaii, but mainland states reported a total of 111 outbreaks and 582 cases (see Table 4-5). 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, 1986); it includes gastrointestinal, neurological, hemodynamic, and cutaneous symptoms such as TABLE 4-5 Scombroid Fish Poisoning in the United States Reported to CDC, 1978-1987 State Outbreaks Cases Alaska 3 17 Arizona 3 7 California 18 (12%) 69 (9%) Connecticut 8 47 District of Columbia 1 3 Florida 1 20 Hawaii 45 (29%) 170 (23%) Idaho 1 4 Illinois 3 35 Indiana 1 4 Kentucky 1 7 Maine 3 54 Maryland 1 10 Michigan 3 25 Minnesota 1 24 Nebraska 1 10 New Jersey 4 42 New Mexico 1 2 New York 30 (19%) 122 (16%) North Carolina 1 10 Pennsylvania 2 4 Texas 2 11 Vermont 3 6 Virginia 2 13 Virgin Islands 1 5 Washington 16 35 Wisconsin 1 1 Total 157 757

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Seafood Safety nausea, vomiting, diarrhea, cramping, headache, palpitations, flushing, tingling, burning, itching, hypotension, rash, urticaria, edema, and localized inflammation. 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, 1958). 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, 1986), and possibly Vibrio (Van Spreekens, 1987). The enteric bacteria Morganella morganii, Klebsiella pneumoniae, and Hafnia alvei have been isolated and identified from fish implicated in histamine poisoning (Havelka, 1967; Kawabata et al., 1956; Taylor et al., 1979). Other enteric bacteria, Clostridium perfringens, and halophilic vibrios have also been reported, but M. morganii and K. pneumoniae are most frequently implicated. These organisms are not commonly isolated from living fish and may be added during catching and handling (Taylor, 1986). Bacteria must grow to a large enough population for significant production of histamine to occur. These are mesophilic bacteria that require temperatures higher than 15°C. In tropical areas of the world, fish temperatures at capture frequently exceed 20°C, and on small vessels it is not unusual for fish to be held on deck at even higher temperatures for several hours. Histamine production is optimal at 30°C (Arnold et al., 1980). Once a large population of bacteria has been established, residual enzyme activity continues slowly at refrigeration temperatures (0-5°C) though bacterial growth ceases. 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. The Food and Drug Administration (FDA) considers a level of 20 milligrams (mg) of histamine per 100 grams (g) of flesh, or 200 parts per million (ppm), an indication of spoilage in tuna and 50 mg/100 g (500 ppm) an indication of hazard (Federal Register, 1982). This is close to the toxic dose estimate of 60 mg/100 g made by Simidu and Hibiku (1955). 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 100 cases per year (higher numbers were recorded in 1973, 1979, and 1980). 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. Good chemical tests are available for histamine in fish flesh (Taylor, 1986), which has allowed FDA to set an action level for histamine in tuna at 50 mg/100 g of flesh. 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. Flesh temperature should be brought below 15°C and preferably below 10°C within 4 hours; this should be

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Seafood Safety normal practice in commercial systems. 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.g., tuna for canning, hot smoked mackerel). 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. 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. 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 (PSP) Paralytic shellfish poisoning results from ingesting bivalve molluscs (mussels, clams, oysters, scallops) that have consumed toxigenic dinoflagellates (Halstead and Schantz, 1984; Schantz, 1973). The toxins are assimilated and temporarily stored by the shellfish. In the United States, PSP is a problem primarily in the New England states on the East Coast and in Alaska, California, and Washington on the West Coast. 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 134 people with one death during 1978-1986 (Table 4-6). The outbreaks occurred in Alaska, California, Massachusetts, Tennessee (due to mussels from California), and Washington (Table 4-7). The Northeast Technical Support Unit (NETSU) compilation shows a total of 282 cases for the period, including cases from Maine, Alaska, and Massachusetts. A report by Nishitani and Chew (1988), 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;

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Seafood Safety TABLE 4-6 PSP Incidents in the United States Reported by CDC, 1978-1985   Outbreaks Cases Deaths Alaska 2 7 — California 2 94 2 Massachusetts 1 15 — Tennessee 1 5 — Washington 7 16 — TABLE 4-7 PSP Incidents in the United States Listed Elsewhere   NETSU Cases Cases Reported by Nishitani and Chew (1988)a Alaska 54 75 California 132b 98 Maine 73 — Massachusetts 41 — Oregon - 1 Tennessee 5 — Washington 15 12 a 1978-1987: West Coast states only. b 1969-1980. incoherence; aphasia; rash; and fever. 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. (1975). The 12 most commonly encountered include saxitoxin, neosaxitoxin, gonyautoxins (I, II, III, IV), B1, B2, C1, C2, C3, and C4, which vary in their toxic effects on mice (Boyer et al., 1978; Shimizu and Hsu, 1981). Saxitoxin, neosaxitoxin, and gonyautoxins II and III are roughly equal in toxicity, whereas the others are somewhat weaker (Hall and Reichardt, 1984). In the United States, the toxigenic dinoflagellates of importance are Gonyaulax catenella and G. tamarenses,1 the first being most dominant on the West Coast and the second on the East Coast (Taylor, 1988). 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., 1975; Sullivan et al., 1983).

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Seafood Safety of Dinophysis and possibly Prorocentrum (Edler and Hageltorn, 1990; Yasumoto and Murata, 1990). 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 1990. 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., 1984). 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, and mixtures of okadaic acid, dinophysistoxins, and pectenotoxins are detected in Japanese cases usually involving D. fortii (Yasumoto and Murata, 1990). There is a mouse bioassay for the toxins. For the U.S. consumer, DSP would appear, at present, to be a hazard only for imported products and should be controllable by import regulation. 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.S. coastal waters, regulatory agencies in the United States should be alert for the possibility of an outbreak (Freudenthal and Jijina, 1988). Puffer Fish Poisoning (PFP) Puffer fish poisoning results from ingestion of the flesh of certain species of fish belonging to the Tetraodontidae (Halstead, 1967). 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, 1988). 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, 1984). It has recently been shown, however, that certain common marine vibrios can produce a form of the toxin (Narita et al., 1987), and because vibrios occur as part of the microflora of puffer fish, they may be implicated in toxicity development (Sugita et al., 1989). 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 1951 and 1974, including three fatalities (Benson, 1956; Hemmert, 1974). 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, 1988). There are 20-100 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, 1971). 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. No

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Seafood Safety antidote has been identified for tetrodotoxin and treatment is supportive. The toxicity of tetrodotoxin is similar to that of saxitoxin, and 1-4 mg constitutes a lethal dose for humans. There is disagreement concerning the toxicity of U.S. Atlantic puffer fish. A recent advisory from the National Oceanic and Atmospheric Administration (NOAA, 1988) describes the northern puffer (Sphoeroides maculatus) as nontoxic and notes that the fish were marketed along the Atlantic Coast as "sea squab" during World War II. However, Hemmert (1974) shows a table indicating that the viscera, skin, and some flesh of S. maculatus caught in the Atlantic were toxic (Lalone et al., 1963). Larson et al. (1959, 1960) also reported that S. maculatus is toxic. From the West Coast, Goe and Halstead (1953) reported that the Pacific species S. annulatus is often toxic. 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.S. puffers may be potentially toxic. 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 (1967, 1988). In view of these reports, it would seem prudent to exclude puffer fish, whether domestic or imported, from U.S. commercial channels at least until a proper assessment is made of the extent of risk they may present. The FDA has recently approved the importation of the Japanese puffer for fugu restaurants in the United States. 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.S. public (Halstead, 1988). Amnesic Shellfish Poisoning (ASP) Amnesic shellfish poisoning has been proposed by Todd (1989) 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 1988 involving 103 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., 1988; Teitelbaum et al., 1990). 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. Canadian authorities now analyze mussels and clams for domoic acid and enforce closure of beds when levels in excess of 20 µg/g are detected in their tissues (Gilgan et al., 1989). Clearly, this is a toxin to be considered in U.S. testing regimes, and there should be close cooperation between U.S. and Canadian regulatory agencies on the movement of imported Canadian shellfish into the United States. Nitzschia pungens and N. pseudodelicatissima reportedly occur in northern U.S. and Canadian waters, and there

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Seafood Safety is potential for development of toxicity in shellfish growing in these areas. States in the northeastern United States are now testing mussels for domoic acid. Other Toxins There are sporadic reports of other intoxications from seafoods from time to time (Halstead, 1988; Wekell and Liston, 1982), 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., 1989a; Kodama et al., 1989) in fish implicated in such cases raise questions about the toxicity of reef-associated fish. One well-defined syndrome reported to occur in Hawaii is "hallucinogenic fish poisoning." This illness follows consumption of mullet and a number of reef fish and occurs seasonally, usually during summer months. Hallucinations, insomnia, intense dreaming, weakness, and burning of the throat are common soon after eating the fish (Halstead and Schantz, 1984). Terrifying nightmares have been reported and constrictive chest pains occur. The condition is short-lived and self-resolving (Halstead, 1988; HDH, 1988). There does not seem to be any analytical test for this toxin. CONCLUSIONS AND RECOMMENDATIONS Diseases caused by natural fish poisoning are listed in Table 4-8. Three of these are of direct significance to the U.S. consumer: ciguatera, scombroid poisoning, and paralytic shellfish poisoning. 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.S. consumer. This is theoretically possible through banning imports to the U.S. mainland of fish known to become ciguatoxic and through strict control of fishing in dangerous areas by fishery management agencies, accompanied by rejection of suspect species at the point of landing. 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.

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Seafood Safety 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.) appear to be the only available solution. However, because imported mahimahi was reportedly responsible for 47% of identified scombroid poisoning, embargoing this fish could have a significant effect. The other intoxications discussed in this chapter are rare and apparently under control in the United States (e.g., NSP and PFP), or not reported as a cause of sickness here (e.g., DSP and ASP). Nevertheless, agencies responsible for ensuring the safety of the U.S. food supply should maintain constant vigilance to avoid the importation of such problems. 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.g., fisheries and health), and a national program involving a single federal agency would probably not be effective without extensive state involvement. 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, 1959, 1990; Halstead et al., 1990). However, much of this information does not reach regulatory, clinical public health, and poison control centers (Freudenthal, 1990). 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.

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Seafood Safety TABLE 4-8 Information on Diseases Caused by Natural Toxins and Poisons Found in Fish and Shellfish   Paralytic Shellfish Poisoning (PSP) Puffer Fish Poisoning (PFP) Ciguatera Diarrhetic Shellfish Poisoning (DSP) Neurotoxic Shellfish Poisoning (NSP) Scombroid Fish Poisoning Amnesic Shellfish Poisoning (ASP) Seafood Involved Mussels, clams, some fish; poison in digestive gland, siphon Puffer or globefish (tetrodon), poison in liver, gonads, and roe Most common in barracuda, kahala, snapper, and grouper Mussels, clams, scallops; toxin in digestive gland Bivalves and most plankton feeders Mahimahi, tuna, bluefish, mackerel, skipjack Mussels and clams Source of poison or toxin Toxic dinoflagellates: Gonyaulax catenella (Pacific); G. tamarensis (Atlantic) May be produced by fish, some evidence from food chain Not definitely known, possible Gambierdiscus toxicus Dinoflagellates: Dinophysis fortii, D. acuminata Dinoflagellate: Gymnodinium breve Bacterial action on fish with high levels of histidine Diatom: Nitzschia pungens Areas commonly found NW and NE North America, south Chile, North Sea area, Japan Areas of Pacific around China and Japan, rare in U.S. Tropical areas around world, in U.S. mainly around Florida Heaviest around Japan and Europe, no cases in U.S. Mostly west coast of Florida, Caribbean Worldwide Eastern Canada; northeast U.S. Method of assay Mouse unit is minimum intraperitoneal dose to kill in 15 minutes, HPLC, ELISA (specific toxicity 7 µg/kg mouse) Use mouse assay for PSP, HPLC (specific toxicity 7 µg/kg mouse) Mouse test (poor), RIA, ELISA, immunological stick test under development Mouse unit minimum intraperitoneal dose to kill in 24 hours (specific toxicity in mouse, 500 µg/kg) Mouse test Chemical methods for histamine HPLC Type of poison or toxin Neurotoxin, purine base, very water soluble Neurotoxin, slightly water soluble Lipid-soluble, polyether multicomponent Okadaic acid, dinophysis toxin Brevetoxin, lipidsoluble polyether Histamine and histamine-like substances Neurotoxic and cytotoxic, domoic acid Extent of U.S. and worldwide problem Local areas worldwide, few cases now Important seafood in Japan; 100 cases, 50 deaths per year; rare in U.S. Largest seafood problem, 50,000 cases per year, <0.1 mortality High morbidity rate, potentially worldwide problem, none in U.S. Massive fish kills, environmental problems Japan 100-1,000 cases, some in U.S. Canada (1987) 103 cases and 3 deaths; no known cases in U.S. Stability Stable to cooking, most stable at pH 7 and below Stable to cooking, stable between pH 4 and 9 Stable to cooking Stable to cooking Heat stable Heat stable Heat stable Symptoms of poisoning in humans Numbness, paralysis after eating; death 2-12 hours; prognosis good after 24 hours Very similar to PSP Abdominal pain, diarrhea, vomiting, neurological symptoms; rarely fatal 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 Dangerous and lethal human dose per 100 g of edible meat 1 mg (sickness) 2 mg or more (death) Same as for PSP Actual dose not known; any amount is dangerous Actual dose not known Actual dose not known Dose varies with individual 2 mg or more per 100 g of meat Treatment No antidote; artificial respiration, rest No antidote; artificial respiration, rest No effective antidote; mannitol may be effective in acute cases No specific treatment No specific treatment Unnecessary for short duration, antihistamines Rest, symptomatic Control measures FDA limit 80 µg/100 g of meat, minimum cases due to good management Education on identification of toxic species No harvesting where toxic fish are found None in U.S. close shellfish beds No established controls, close shellfish harvest Education on care of freshly caught fish; keep below 10°C Close shellfish beds when domoic acid is detected 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.S. consumption. 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.S. markets.

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Seafood Safety The committee recommends the following: 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. All imported fish of species known to be a cause of scombroid poisoning should be certified as having histamine levels of less than 20 mg/100 g of fish. This should be controlled by routine lot testing. Vessels fishing potentially scombrotoxic species should be required to maintain time/temperature records to ensure proper cooling and refrigerated storage of fish. 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.

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Seafood Safety NOTE 1.   The toxigenic strains have also been designated Protogonyaulax, and more recently, the genus name Alexandrium has been proposed. REFERENCES Anderson, B.S., J.K. Sims, N. Wiebenga, and M. Sugi. 1983. The epidemiology of ciguatera fish poisoning in Hawaii 1975-1982. Haw. Med. J. 42:326-334. Arnold, S.H, R.J. Price, and W.D. Brown. 1980. Histamine formation by bacteria isolated from skipjack tuna, Katsuwonas pelamis. Bull. Jpn. Soc. Sci. Fish 46:991-995. AOAC (Association of Official Analytical Chemists). 1984. P. 344 in S. Williams, ed. Official Methods of Analysis of the Association of Official Analytical Chemists, 14th ed. AOAC, Arlington, Va. Baden, D.G., T.J. Mende, M.A. Poli, and R.E. Block. 1984. Toxins from Florida's red tide dinoflagellate Ptychodiscus brevis. Pp. 359-367 in E.P. Ragelis, ed. Seafood Toxins. American Chemical Society, Washington, D.C. Bagnis, R., T. Kuberski, and S. Laugier. 1979. Clinical observations on 3009 cases of ciguatera (fish poisoning) in the South Pacific. Am. J. Trop. Med. Hyg. 28:1067-1073. Bagnis, R., S. Chanteau, E. Chungue, J.M. Hurtel, T. Yasumoto, and A. Inoue. 1980. Origins of ciguatera fish poisoning: A new dinoflagellate Gambierdiscus toxicus Adachi and Fukuyo, definitely involved as a causal agent. Toxicon 18:199-208. Benson, J. 1956. Tetradon (blowfish) poisoning. A report of two fatalities. J. Forensic Sci. 1:119-126. Bidard, J.N., H.P.M. Vijuerbert, C. Frelin, E. Chungue, A.M. Legrand, R. Bagnis, and M. Lazdunski. 1984. Ciguatoxin is a novel type of Na+ channel toxin. J. Biol. Chem. 359:8353-8357. Bowman, P.B. 1984. Amitriptyline and ciguatera. Med. J. Australia 140:802. Boyer, G.E., J. Schantz, and H.K. Schnoes. 1978. Characterization of 11-hydroxysaxitoxin sulfate. J. Chem. Soc. London Chem. Comm. 20:889-893. CDC (Centers for Disease Control). 1981a. Salmonella Surveillance, Annual Summary, 1978. HHS Publ. No. (CDC)81-8219. Public Health Service, U.S. Department of Health and Human Services, Atlanta, Ga. 25 pp. CDC (Centers for Disease Control). 1981b. Annual Summary of Foodborne Disease, 1978. HHS Publ. No. (CDC)81-8185. U.S. Department of Health and Human Services, Atlanta, Ga. 53 pp. CDC (Centers for Disease Control). 1981c. Annual Summary of Foodborne Disease, 1979. HHS Publ. No. (CDC)8185. U.S. Department of Health and Human Services, Atlanta, Ga. 40 pp. CDC (Centers for Disease Control). 1983a. Food-Borne Disease Outbreaks, Annual Summary, 1980. HHS Publ. No. (CDC)83-8185. Public Health Service, U.S. Department of Health and Human Services, Atlanta, Ga. 32 pp. CDC (Centers for Disease Control). 1983b. Food-Borne Disease Outbreaks, Annual Summary, 1981. HHS Publ. No. (CDC)83-8185. Public Health Service, U.S. Department of Health and Human Services, Atlanta, Ga. 41 pp. CDC (Centers for Disease Control). 1984. Food-Borne Disease Outbreaks, Annual Summary 1983: Reported morbidity and mortality in the United States. Morbid. Mortal. Weekly Rep. (annual suppl.). 32 pp. CDC (Centers for Disease Control). 1985. Food-Borne Disease Outbreaks, Annual Summary 1982. HHS Publ. No. (CDC)85-8185. Public Health Service, U.S. Department of Health and Human Services, Atlanta, Ga. 38 pp. CDC (Centers for Disease Control). 1989. Annual Summary of Foodborne Disease, unpublished dates from 1983 to 1986. U.S. Department of Health and Human Services, Atlanta, Ga. 1989. Chu, F.S., and T.S.L. Fan. 1985. Indirect enzyme-linked immunosorbent assay for saxitoxin in shellfish. J. Assoc. Off. Anal. Chem. 68:13-16. Cooper, M.J. 1964. Ciguatera and other marine poisonings in the Gilbert Islands. Pacific Sci. 18:411-440. DNR (Department of Natural Resources, Florida). 1985. Pp. 1-10 in Contingency Plan for Control of Shellfish Potentially Contaminated by Marine Biotoxins. Bureau of Marine Research, St. Petersburg, Fla.

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Seafood Safety Edler, L., and M. Hageltorn. 1990. Identification of the causative organism of a DSP outbreak on the Swedish west coast. Pp. 345-349 in E. Graneli, B. Sundström, L. Edler, and D.M. Anderson, eds. Toxic Marine Phytoplankton. Elsevier, Amsterdam, The Netherlands. Engleberg, N.C., J.G. Morris, Jr., J. Lewis, J.P. McMillan, R.A. Pollard, and P.A. Blake. 1983. Ciguatera fish poisoning: A major common source outbreak in the U.S. Virgin Islands. Ann. Intern. Med. 98:336-337. FDA (Food and Drug Administration). 1989 revision. Sanitation of shellfish growing areas. National Shellfish Sanitation Program Manual of Operations Part I. Center for Food Safety and Applied Nutrition, Division of Cooperative Programs, Shellfish Sanitation Branch, Washington, D.C. Federal Register. 1982. Department of Health and Human Services. Food and Drug Administration. Defect action levels for histamine in tuna: Availability of a guide. Fed. Reg. 470:40487-40488. Freudenthal, A.R. 1990. Public health aspect of ciguatera poisoning contracted on tropical vacations by North American tourists. Pp. 463-468 in E. Graneli, B. Sundström, L. Edler, and D.M. Anderson, eds. Proceedings of the 4th International Conference on Toxic Marine Phytoplankton. Elsevier, Amsterdam, The Netherlands. Freudenthal, A.R., and J.L. Jijina. 1988. Potential hazards of Dinophysis to consumers and shellfisheries. J. Shellfish Res. 7:695-701. Gilgan, M.W., B.G. Burns, and G.J. Landry. 1989. Distribution and magnitude of domoic acid contamination of shellfish in Atlantic Canada during 1988. Pp. 469-474 in Proceedings of the 4th International Conference on Toxic Marine Phytoplankton. Elsevier, Amsterdam, The Netherlands. Gillespie, N.C., R.J. Lewis, J.H. Pearn, A.T.C. Bourke, M.J. Holmes, J.B. Bourke, and W.J. Shields. 1986. Ciguatera in Australia: Occurrence, clinical features, pathophysiology and management. Med. J. Aust. 145:584-590. Goe, D.R., and B.R. Halstead. 1953. A preliminary report of the toxicity of the Gulf puffer, Sphoeroides annulatus. Calif. Fish and Game 39:229-232. Gollop, J.H., and E.W. Pon. 1991. Ciguatera fish poisoning: Review of pathogenesis, clinical manifestations and epidemiology in Hawaii 1984-1988. Hawaii Med. J. (in press). Haddock, R.L. 1989. Letter report on food-borne disease incidence, dated September 8, 1989, from Dr. Robert L. Haddock, Territorial Epidemiologist, Department of Public Health and Social Services, Government of Guam to Dr. Farid E. Ahmed, Project Director, Committee on Evaluation of the Safety of Fishery Products, Institute of Medicine, National Academy of Sciences, Washington, D.C. Hall, S., and P.B. Reichardt. 1984. Cryptic paralytic shellfish toxins. Pp. 113-124 in Ragelis, E.P. ed. Seafood Toxins. American Chemical Society, Washington, D.C. Halstead, B.W. 1959. Dangerous Marine Animals. Cornell Maritime Press, Cambridge, 146 pp. Halstead, B.W. 1967. Poisonous and Venomous Marine Animals of the World, Vol. I, pp. 83-87; Vol. II, pp. 679-844. U.S. Government Printing Office, Washington, D.C. Halstead, B.W. 1970. Poisonous and Venomous Marine Animals of the World. U.S. Government Printing Office, Washington, D.C. 1006 pp. Halstead, B.W. 1988. Poisonous and Venomous Marine Animals of the World, 2nd rev. ed. Darwin Press, Princeton, N.J. 1168 pp. Halstead, B.W. 1990. Dangerous Aquatic Animals of the World: A Color Guide. Darwin Press, Princeton, N.J. 288 pp. Halstead, B.W., and W.M. Lively. 1954. Poisonous fishes and ichthyosarcotoxism. Their relationship to the Armed Forces. U.S. Armed Forces Med. J. 5:157-175. Halstead, B.W., and E.J. Schantz. 1984. Paralytic shellfish poisoning. WHO Offset Publication No. 79:1-60. Geneva, Switzerland. Halstead, B.W., P.S. Auerbach, and D. Campbell. 1990. A Colour Atlas of Dangerous Marine Animals. Wolfe Medical Publications, Ipswich, England. 192 pp. Havelka, B. 1967. Role of Hafnia bacteria in the rise of histamine in tuna fish meat. Cesk. Hyg. 12:343. HDH (Hawaii Department of Health). 1988. Fish Poisoning in Hawaii. Advisory Leaflet. Honolulu, Hawaii. Hemmert, C.D. 1974. Tetraodon (puffer fish) poisoning. Memorandum of Florida Department of Health, Tallahassee, Fla. Hokama, Y. 1985. A rapid simplified enzyme immunoassay stick test for the detection of ciguatoxin and related polyethers from fish tissue. Toxicon 23:939-946. Hokama, Y. 1990. Simplified solid-phase immunobead assay for detection of ciguatoxin and related

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Seafood Safety polyethers. J. Clin. Lab. Anal. 4:213-217. Hokama, Y., A.H. Banner, and D. Boyland. 1977. A radioimmunoassay for the detection of ciguatoxin. Toxicon 15:317-325. Hokama, Y., S.A.A. Honda, A.Y. Asahina, J.M.L. Fong, C.M. Matsumoto, and T.S. Gallacher. 1989a. Cross-reactivity of ciguatoxin, okadaic acid, and polyethers with monoclonal antibodies. Food Agric. Immunol. 1:29-35. Hokama, Y., S.A.A. Honda, M.N. Kobayashi, L.K. Nakagawa, A.Y. Asahina, and J.T. Miyahara. 1989b. Monoclonal antibody (MAb) in detection of ciguatoxin (CTX) and related polyethers by the stick-enzyme immunoassay (S-EIA) in fish tissues associated with ciguatera poisoning. Pp. 303-310 in S. Natori, K. Hashimoto, and Y. Ueno, eds. Mycotoxins and Phycotoxins '88. Elsevier Science Publishers, Amsterdam, The Netherlands. Holt, R.J., G. Miro, and A. Del Valle. 1984. An analysis of poison control center reports of ciguatera toxicity in Puerto Rico for one year. Clin. Toxicol. 22:177-185. Hughes, J.M., and M.H. Merson. 1976. Fish and shellfish poisoning. N. Engl. J. Med. 295:1117-1120. Kawabata, T., K. Ishizaka, T. Miura, and T. Sasaki. 1956. Studies on the food poisoning associated with putrefaction of marine products. VII. An outbreak of allergy-like food poisoning caused by sashimi of Parathunnus mebachi and the isolation of the causative bacteria. Bull. Jpn. Soc. Sci. Fish 22:41-47. Kodama, A.M., Y. Hokama, T. Yasumoto, M. Fukui, S.J. Manea, and N. Sutherland. 1989. Clinical and laboratory findings implicating palytoxin as cause of ciguatera poisoning due to Decapterus macrosoma (mackerel). Toxicon 27:1051-1053. Lalone, R.C., E.D. DeVillez, and E. Larson. 1963. An assay of the toxicity of the Atlantic puffer fish Sphoeroides maculatus. Toxicon 1:159-164. Lange, W.R., S.D. Kreider, M. Hattwick, and J. Hobbs. 1988. Potential benefit of tocainide in the treatment of ciguatera: Report of three cases. Am. J. Med. 84:1087-1088. Larson, E., L.R. Rivas, R.C. Lalone, and S. Coward. 1959. Toxicology of the Western Atlantic Puffer Fish of the Genus Sphoeroides . The Pharmacologists 1:70 (Abstract). Larson, E., R.C. Lalone, and L. Rivas. 1960. Comparative toxicity of the Atlantic pufferfishes of the genera Sphoeroides, Lactophrys, Lagocelhalus and Chilomycterus. Fed. Proc. 19:388 (Abstract). Lawrence, D.N., M.B. Enriquez, R.M. Lumish, and A. Maceo. 1980. Ciguatera fish poisoning in Miami. J. Am. Med. Assoc. 244:254-258. Legrand, A.M., and R. Bagnis. 1984. Mode of action of ciguatera toxins. Pp. 217 in E.P. Ragelis, ed. Seafood Toxins. American Chemical Society, Washington, D.C. Lukton, A., and H.S. Olcott. 1958. Content of free imidazole compounds in the muscle tissue of aquatic animals. Food Res. 23:611-618. Miller, M.D. 1991. Ciguatera Seafood Toxins. CRC Press, Boca Raton, Fla. 176 pp. Mills, A.R., and R. Passmore. 1988. Pelagic paralysis. Lancet 1:161-164. Morris, J.G., Jr., P. Lewin, N.T. Hargrett, C.W. Smith, P.A. Blake, and R. Schneider. 1982a. Clinical features of ciguatera fish poisoning: A study of the disease in the U.S. Virgin Islands. Arch. Intern. Med. 142:1090-1092. Morris, J.G., Jr., P. Lewin, C.W. Smith, P.A. Blake, and R. Schneider. 1982b. Ciguatera fish poisoning: Epidemiology of the disease on St. Thomas, U.S. Virgin Islands. Am. J. Trop. Med. Hyg. 31:574-578. Mosher, H., and F.A. Fuhrman. 1984. Occurrence and origin of tetrodotoxin. Pp. 333-334 in E.P. Ragelis, ed. Seafood Toxins. American Chemical Society, Washington, D.C. Murata, M., A.M. Legrand, Y. Ishibashi, M. Fukui, and T. Yasumoto. 1990. Structures and configurations of ciguatoxin from the moray eel Gymnothorax javanicus and its likely precursor from the dinoflagellate Gambierdiscus toxicus. J. Am. Chem. Soc. 112:4380-4386. Narita, H., S. Matsubara, N. Miwa, S. Akahane, M. Murakami, T. Goto, M. Nara, T. Noguchi, T. Shida, and K. Hashimoto. 1987. Vibrio alginolyticus a TTX-producing bacterium isolated from the starfish Astropecten polyacanthus. Nippon Suisan Gakk. 53:617-621. Nishitani, L., and K. Chew. 1988. PSP toxins in the Pacific Coast states: Monitoring programs and effects on bivalve industries. J. Shellfish Res. 1:653-669. NOAA (National Oceanic and Atmospheric Administration). 1988. Japan's "Fugu" (Puffer Fish) Market Advisory. Doc/NOAA/NMFS, Washington, D.C. 1 p. Ogura, Y. 1971. Fugu (puffer fish) poisoning and the pharmacology of crystalline tetrodotoxin in poisoning. Pp. 139-159 in L.L. Simpson, ed. Neuropoisons, Vol. I. Plenum Press, New York. Palafox, N.A., L.G. Jain, A.Z. Pinano, T.M. Gulick, R.K. Williams, and I.J. Schatz. 1988. Successful

OCR for page 87
Seafood Safety treatment of ciguatera fish poisoning with intravenous mannitol. J. Am. Med. Assoc. 259:2740-2742. Perl, T.M., L. Bédard, T. Kosatsky, J.C. Hockin, E.C.D. Todd, and R.S. Remis. 1988. An outbreak of toxic encephalopathy caused by eating mussels contaminated with domoic acid. N. Engl. J. Med. 322:1775-1780. Ragelis, E.P. 1984. Ciguatera seafood poisoning: An overview. Pp. 25-36 in E.P. Ragelis, ed. Seafood Toxins. American Chemical Society, Washington, D.C. Randall, J.E. 1980. A survey of ciguatera at Eniwetok and Bikini Marshall Islands, with notes on the systematics and food habits of ciguatoxic fish. Fish Bull. 78:201-249. Ruff, T.A. 1989. Ciguatera in the Pacific: A link with military activities. Lancet 1:201-205. Schantz, E. 1973. Seafood toxicants. Pp. 424-447 in Toxicants Occurring Naturally in Foods, 2nd ed. National Academy Press, Washington, D.C. Schantz, E. 1986. Chemistry and biology of saxitoxins and related toxins. Ann. N.Y. Acad. Sci. 479:15-23. Schantz, E.J., E.F. McFarren, M.L. Schafer, and K.H. Lewis. 1958. Purified shellfish poison for bioassay standardization. J. Off. Agric. Chem. 41:160-170. Schantz, E.J., V.E. Ghazarossian, H.K. Schnoes, F.M. Strong, J.P. Springer, J.D. Pezzanite, and J. Clardy. 1975. The structure of saxitoxin. J. Am. Chem. Soc. 97:1238-1239. Scheuer, P.J., W. Takahashi, J. Tsutsumi, and T. Yoshida. 1967. Ciguatoxin: Isolation and chemical nature. Science 155:1267-1268. Shimizu, Y., and C. Hsu. 1981. Confirmation of the structure of gonyautoxins I-IV by correlation with saxitoxin. J. Chem. Soc. Chem. Comm. pp. 314-315. Simidu, W., and S. Hibiku. 1955. Studies on putrefaction of aquatic products. XXIII. On the critical concentration of poisoning for histamine. Bull. Jpn. Soc. Sci. Fish 21:365-367. Sugita, H., J. Iwata, C. Miyajima, T. Kubo, T. Noguchi, K. Hashimoto, and Y. Deguchi. 1989. Changes in microflora of a puffer fish Fugu niphobles with different water temperatures. Marine Biology 101:299-304. Sullivan, J.J., and W.T. Iwaoka. 1983. High pressure liquid chromatographic determination of toxins associated with paralytic shellfish poisoning. J. Assoc. Off. Anal. Chem. 66:297-303. Sullivan, J.J., W.T. Iwaoka, and J. Liston. 1983. Enzymatic transformation of PSP toxins in the littleneck clam (Protothacis staminea). Biochem. Biophys. Res. Commun. 114:465-472. Taylor, S.L. 1986. Histamine food poisoning: Toxicology and clinical aspects. C.R.C. Crit. Rev. Toxicol. 17:91-128. Taylor, S.L. 1988. Marine toxins of microbial origin. Food Tech. 42:94-98. Taylor, S.L., L.S. Guthertz, M. Leatherwood, and E.R. Lieber. 1979. Histamine production by Klebsiella pneumoniae and an incident of scombroid fish poisoning. Appl. Environ. Microbiol. 37:274-278. Teitelbaum. J.S., R.J. Zatorre, S. Carpenter, D. Gendron. A.C. Evans, A. Gjedde, and N.R. Cashman. 1990. Neurologic sequelae of domoic acid intoxication due to the ingestion of contaminated mussels. N. Engl. J. Med. 322:1781-1787. Tester, P.A., and P.K. Fowler. 1990. Brevetoxin contamination of Mercenaria mercenaria and Crassostrea virginica: A management issue. Pp. 499-503 in E. Graneli, B. Sundström, L. Edler, and D.M. Anderson, eds. Proceedings of the 4th International Conference on Toxic Marine Phytoplankton. Elsevier, Amsterdam, The Netherlands. Todd, E.C.D. 1989. Amnesic shellfish poisoning–A new seafood toxin syndrome. Pp. 504-508 in E. Graneli, B. Sundström, L. Edler, and D.M. Anderson, eds. Proceedings of the 4th International Conference on Toxic Marine Phytoplankton. Elsevier, Amsterdam, The Netherlands. Van Spreekens, K. 1987. Histamine production by the psychrophilic flora. Pp. 309-318 in D.E. Kramer and J. Liston, eds. Seafood Quality Determination. Elsevier Science Publishers, Amsterdam, The Netherlands. Wekell, J., and J. Liston. 1982. Pp. 111-155 in P. Newberne, ed. Seafood Biotoxicants in Trace Substances and Health: A Handbook Part II. Marcel Dekker, New York. Yasumoto, T., and M. Murata. 1990. Polyether toxins involved in seafood poisoning. Pp. 120-132 in S. Hall and G. Stricharty, eds. Marine Toxins. Origin, Structure and Molecular Pharmacology. American Chemical Society, Washington, D.C. Yasumoto, T., M. Murata, Y. Oshima, G.K. Matsumoto, and J. Clardy. 1984. Diarrhetic shellfish poisoning. Pp. 207-216 in E.P. Ragelis, ed. Seafood Toxins. American Chemical Society, Washington, D.C.