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CARIBBEAN RESEARCH INSTITUTE cbt 0, S Zeyy FISH POISONING IN THE EASTERN CARIBBEAN Robert W. Brody Ciguatera Study Caribbean Research Institute College of the Virgin Islands St. Thoms, U S. Virgin Islands 00801 Fer Presentation Gulf and Caribbean Fisheries Institute 24th Annual Session Miami, Florida 15-18 Novenber, 1971 CONTENTS Page I, INTRODUCTION I. TYPES OF FISH POISONING III. SYMPTOMOLOGY AND PUBLIC HEALTH 10 ASPECTS 16 IV. GEOGRAPHIC DISTRIBUTION SPECIES REPORTED AS CIGUATOXIC 21 V. VI. CHEMISTRY AND PHARMACOLOGY 23 VIL. BIOGENESIS AND TRANSMISSION OF 26 CIGUATOXIN VIII. EFFECTS OF CIGUATERA POISONING ON THE DEVELOPMENT OF FISHERIES 31 36 Ix, SUMMARY AND CONCLUSIONS xX. ACKNOWLEDGEMENTS 38 XI. LITERATURE CITED 39 INTRODUCTION "When I first got here I thought that I would be able to practically exist on fish....."; "I was poisoned fifteen times —— I left my father's house. He always liked to buy big fish because there was more meat....."; "I can't get a contract for grouper or snapper with any of the hotels. They buy the same fish from Santo Domingo for ten cents a pound more....."; “Where are all the seafoodrestaurants ? I thought this was an island!" These comments and others like them represent a biotoxicological problem which has always plagued the eastern Caribbean. Ciguatera fish poisoning, scombroid poisoning, and to a lesser extent "clupeoid", tetraodontoid and elasmo- branch poisoning have beenreported since pre-Columbian time and the problem shows no sign of lessening. This paper will present the basic facts of fish poisoning in the eastern Caribbean area as we presently know them. It will not attempt to review the voluminous literature from the Pacific; the reader is referred to excellent summar ies of Halstead (1967) and Banner (1971). At the present time we have very little "hard data''on the chemistry, biogenesis and biology and pharmacology of the fish poisoning problem in the area. We have yet to confirm that the most important type of poi- soning, ciguatera, is in fact identical to the toxin from the Pacific. The sections on ciguatera aretherefore based on our local observations and inferences from studies in the Pacific are noted. Il. TYPES OF FISH POISONING Fish poisoning in the eastern Caribbean can be broken down intothree major groupings. The endotoxins from the puff- er-like fishes with the additional rarely reported cases of clupeoid, elasmobranch and hallucinogenic fish poisoning form the first group. These incidents represent a very small per- centage of the total number of cases reported; several years of casual data-gathering and six months of active research have only produced two accounts in the last four years, both of clupeiotoxism. The biology, chemistry, and pharmacology of puffer fish poisoning have been accurately summarized else where (Bagnis, 1970). Although the world-wide fatality rate is high (61%), very few cases of tetraodon poisoning are reported in the Caribbean, probably because the puffers are not highly esteemed as a food fish. This may also be the reason for the low in- cidence of reports of elasmobranch poisoning in the area. Shark has been harvested recently in an effort to produce a packaged seafood product ("Sea Flake") with generally good customer acceptance; there have been no instances of elasmo- branch poisoning brought to our attention as aresult. Hallu- cinatory fish poisoning (icthyoallyeinotoxism) is also an ap- parently rare event in the eastern Caribbean; it has been described to us by an herbalist on St. Thomas but an actual case history has not been received. Cleupeoid poisoning is a form of icthyosarcotoxism caused by ingestion of the flesh of fishes of the order Clu- peiformes. The symptoms are frequently violent with an ex- tremely high case fatality rate. The onset of symptoms is noted with a sharp, metallic taste in the mouth followed rapidly by severe gastrointestinal upset with distinct indications of vascular collapse (drop in blood pressure, cyanosis). This may be accompanied or rapidly followed by neurological dis- turbances nervousness, dilated pupils, violent headache, tingling, and in severe cases respiratory distress, convulsions, coma, anddeath. Thetoxin is apparently particularly virulent: death may occur within fifteen minutes. The literature reports that persons have died while in the act of eating the fish - "part of the fish was stillin the victim's mouth at the time of death” (Halstead, 1967). Fishin the families Clupeidae (herrings), Engraulidae (anchovies), Albulidae (bonefishes), and Elopidae (tarpons) have been reported as toxic in the Caribbean; our experience has been limited to two cases involving the clupeoid fishes Herengula humeralis (yellow-billed sprat) and Opisthonema oglinum (thread herring). One case isreported from a fisher - man on Tortola, B. V.I. who (with his family of five) ate "yellow bill sprat" (probably Opisthonema oglinum from his descrip- tion of a "spine on the back fin") caught in Great Harbor, Peter Island, B.V.I. He reported "bad fish poisoning" symptoms generally similar to ciguatera poisoning; the rapid onset re- ported above was present. He forced all of the members ofhis family to vomit and alltook a "heavy dose of sulphur" (a patent medicine). He did not contact public health authorities. The family recovered from acute symptoms within 36 hours. (This incident took place in late 1967 and was reported in April 1971; the interview was thus clouded by time and atleast two subse- quent incidents of ciguatera poisoning.) The second case is reported by Halstead (1970) from Antigua, W.I. from 1968 (?) when "some small surface-feeding 'herring-like' fish were eaten". Two people died in this outbreak. Halstead suggests that local terminology of ''yellow-billed sprat'' is applicable to Iferengula humeralis. The violence of the episode suggests that this case was an example of classic clupeiotoxism while the Tortola case is not definitely separable from ciguatoxism. -5- The chemical nature and biogenesis of clupeiotoxism is not presently known. Numerous authors have suggested that fish caught during the summer months are more likely to be toxic. All reported incidents are from fish caught close to tropicalislands. There are several references inthe literature to planktonic blooms as the causative organism, specifically a '"monad" (dinoflagellate ?) (Halstead, 1967), Skujaella, (Trichodesmium) (Randail, 1958) or to "swarming of palolo worms" (Halstead, 1967). It is probable that the toxin is pro- duced by some planktonic form as the clupeoid fishes are for the most part plankton feeders, this may add strength to the position that clupeiotoxism is a separate entity from ciguatera poisoning. Clupeiotoxin is not thought tobe degraded by normal cooking and the degree of freshness does not seem to have effect on the toxicity. Clupeiotoxism may pose a wider threat to public health than the occasional locally consumed fish. If the toxin is in- deed caused by "blooming" plankton organism the likelihood of a large school of toxic fish cannot be overlooked. The sardine and anchovy groups are frequently thought of as ideal fish for Fish Protein Concentrate production; we have no data on the ability of current FPC technology to eliminate the toxin from the raw fish. The second major group of poisonings experienced in the eastern Caribbean ig: the result of bacterial decomposition of fresh fish. In the Virgin Islands and throughout the northern Leeward Islands fish are typically sold ''fresh'' from the boat. Very few fishermen use ice or gut the fish before sale, in fact there is a strong feeling among older citizens that such pre- servation is usedto camouflage the true "freshness". Eastern Caribbean fishermen do not use live-wells and fish frequently spend a good part of the day inthe sun. These conditions ob- viously tend to promote bacterial decomposition of the fish and the consequent toxicity problem; it is interesting that the younger people in St. Thomas, U. S. V. I. who tend to buy fish in the supermarket report a significantly lower incidence of fish poi- soning attributable to scombroids. We presume that an undetermined proportion of the poisonings reported are the result of some sort of bacterial de- composition. In many "mild'’ cases the only complaint is of gastrointestinal distress; the neurological symptoms specific to ciguatera and ciguatera-like toxins are not noted. Many of these cases may be attributable to scombroid poisoning but the symptoms may not be sufficiently pronounced for a proper -7T- diagnosis to be made. The distinct histamine -like toxicity caused by bacterial degradation of the flesh of fish of the family Scombridae is a relatively common type of fish poisoning throughout the Carib- bean. The symptomology includes a distinct "sharp" or "peppery" taste upon eating the fish followed by intense head- ache, dizziness, a variety of circulatory disfunctions, gastro- intestinal distress, dryness of the mouth, and inability to swallow. These symptoms are followed by generalized erythema, the face becomes swollen and flushed, eyes are sunken, and an urticarial eruption may develop covering the entire body. In severe cases there may be additional compli- cations of shock and respiratory distress. Death has been re- ported in a few cases but acute symptoms generally dissipate in eight to twelve hours. This toxic reaction is brought about by the bacterial degradation of histidine in scombroid muscle tissue which produces a substance designated as scombrotoxin. Scombrotoxin probably has a combination of chemical con- stituents including saurine, histidine, and possibly other toxic compounds. The disease responds wellto treatment with anti- histaminic drugs; this specific treatment has mitigated the severity of scombroid poisoning as a public health problem in recent years. Inthe eastern Caribbean scombroid poisoning has been reported from Acanthocybium solandri (wahoo) Scomberomorus cavalla (kingfish or king mackerel). Scomberomorus regalis (spanish mackerel), and S. maculatus (cero). Weare not aware of cases reported recently from the eastern Caribbean in the tunas (Auxis, Euthynnus, Sarda, Scomber, Thunnus) but these genera may also be incriminated. There probably is no true seasonality to scombroid poisoning although the incidence in any one area can be correlated with local "runs" of the particular species involved. Thus there seem to be more poisonings during the tourist season when sport fishing pressure is high. The third general type of fish poisoning is described as ciguaterafish poisoning. Evidence from the Pacific suggests that there are at least three (probably more) distinct toxins capable of producing the ciguatera syndrome. Many authors (and many physicians in the eastern Caribbean area) have not separated the diagnosis or treatment of ciguatera from that of scombroid poisoning and some confusion has resulted. Both ciguatera and scombroid poisoning have been occasionally re- ported from the same fish in the Pacific (Halstead, 1967); we have no such report from the Caribbean in recent years. Ill SYMPTOMOLOGY AND PUBLIC HEALTH ASPECTS OF CIGUATERA In the absence of precise chemical and biogenic data we have defined ciguatera in terms of its symptomology. The following symptoms are extracted from Halstead (1967), Bag- nis (1970), and Banner (1971) and are quotedas they appear in Teytaud and Brody (1971): "Ciguatera fish poisoning in its simplest un- complicated form develops within 3 to 5 hours after the fish is eaten. There is a sudden onset of abdominal pain followed by nausea, vomiting, and a watery diar- rhea. The gastrointestinal symptoms will occur in about 40 to 75 percent of the cases. The victim feels weak, generally ill, and may experience muscle aches throughout the back and thighs in about 10 percent or more of the cases. Soon after, the victim complains of numbness and tingling in and about the mouth which then extends to the extremities (present in about 50 percent or more of the cases). Fever, headache, and rash are generally absent, and the patient has no de- sire for food. The acute symptoms usually subside in about 8 to 10 hours, and within 24 hours after onset most of the patient's symptoms will have completely subsided except for a feeling of weakness. However, the numbness andtingling may continue to alesser ex- tent for a period of 4 to 7 days. The foregoing re- sume is typical of the majority of uncomplicated ciguatoxications that are generally encountered by the practicing physician. in an endemic ciguatoxic locality. Ciguatera, like many other diseases, may vary greatly in its clinical manifestations depending upon the toxicity of the fish that is eaten, the individ- ual's sensitivity to the poison, amount of fish ingested, and other factors. In a broader sense ciguatera fish poisoning may be characterized as follows: the onset «10+ of symptoms may vary from almost immediately to within a period of 30 hours after ingestion of the fish, but is usually within a period of 6 hours. The initial symptoms in some cases are gastrointestinal in nature, consisting of nausea, vomiting, watery diarrhea, metallic taste, abdominal cramps, and tenesmus, whereas in other patients the initial symptoms consist of tingling and numbness about the lips, tongue, and throat. This may be accompanied by a sensation of dryness of the mouth. The muscles of the mouth, cheeks, and jaws may become drawn and spastic with an accompanying sensation of numbness throughout. Generalized symptoms of headache, anxiety, malaise, prostration, dizziness, pallor, cvanosis, insomnia, chilly sensations, fever, proiuse sweating, rapid weak pulse, weight loss, myalgia, and back and joint aches may be present in varying degrees, or one or more of the symptoms may be entirely absent. The victims usually complain of a feeling of profound ex- haustion and weakness. The feeling of weakness may become progressively worse untilthe patient is unable to walk. Muscle pain are generally described as a dull, heavy ache, or cramping sensation, but on occasion may be sharp, shooting, and affect particu- larly the arms andlegs. Victims complain of their teeth feeling loose and painful in their sockets. Visual disturbances consisting of blurring, temporary blind- ness, photophobia, and scotoma are common. Pupils are usually dilated and the reflexes diminished. Skin disorders are frequently reported that are usually initiated by an intense generalized pruritus, accom- panied by erythema, and maculopapular eruptions , blisters, extensive areas of desquamation - particu- larly of the hands and feet - and occasionally ulcera- tion. There may alsc be a loss of hair and nails. In severe intoxications the neurotoxic com- ponents are especially pronounced. Paresthesias in- volve the extremities, and paradoxical sensory dis- turbances may be present in whichthe victim interprets coldas a "tingling, burning, dry-ice or electric-shock sensation", or hot objects may give a feeling of cold. In regard to the paradoxical sensory disturbance (P. S. D.), a classic example is that of a naval officer who was poisoned by an amberjack. Four weeks later he “Lie was observed subconsciously blowing on his ice cream, which was “burning his tongue", in order to cool it. Ataxis and generalized motor incoordination may be- come progressively worse. The reflexes may be di- minished, muscular paralyses may develop, accom-- panied by clonic and tonic convulsions, muscular twitchings, tremors, dysphonia, dysphagia, coma, and death by respiratory paralysis. The limited morbidity statistics show a case fatality rate of about 12 percent. Death may occur within 10 minutes, but generally re- quire several days." Table 1 vimaeioes the symptoms occuring during the first 24 hours after ingestion as they were reported by 25 persons who were interviewed following ciguatoxications of minor to moderate severity in St. Thomas U.S. V.I. during 1971. Several of these reports represent the symptoms produced in different individuals by a single fish; they therefore do not represent 25 separate outbreaks. TABLE 1. Summary of Symptoms Symptom Percent Reporting abdominal pain 96 (96) nausea 88 (92) vomiting 68 (68) diarrhea 96 (96) numbness, tingling about mouth 56 (64) headache 48 (48) numbness in extremeties 48 (56) metallic taste 24 (36) weakness 96 (96) muscle aches 40 (48) paradoxical sensory disturbance 32 (32) itching 64 (68) Summary of symptoms manifested by 25 ciguatoxicated indi- viduals during first 24 hours after ingestion of fish. (Percent- ages in parentheses represent change in original descriptions following questions by the interviewer.) -12- Several additional symptoms were reported by three or fewer (less than 12%) of the persons interviewed. These symptoms include lack of coordination, muscle spasm, high fever, visual disturbances, diminished reflexes, and skin rash. It is notable that none of these persons required hos- pitalization and only three reported visiting a physician (several others contacted a physician by telephone during the time period 24 - 72 hours after ingestion). Virtually all of the persons interviewed reported no- ticeable symptoms of ciguatoxication for several days after the onset of the incident. Most commonly reported was ex- treme weakness and lethargy lasting up to two weeks. Many victims reported gastrointestinal symptoms well into the third day along with itching and/or skinrash. Those persons report - ing the paradoxical sensory disturbance stated that it persisted for at least three days, in some cases ten days or two weeks. The bulk ofthe other symptoms noted were reported as having dissipated within the first 24 hours. We are currently undertaking a more extensive epi- demiology reporting program in cooperation with local media, physicians, and public health authorities. Data from this sur- vey combining questionnaire and interview procedures should -13- be available early in 1972. At this time we have no accurate estimate of the magnitude of the ciguatera poisoning problem in the Virgin Islands or for that matter anywhere in the eastern Caribbean. Outbreaks in Puerto Rico are sufficiently notable toreceive coverage inthe major English-language media which suggests that they are infrequent. The officials responsible for public health record-keeping in St. Thomas, on the other hand, estimate three or four cases per week are seen in the emergency room; ifour 25 cases reportedin table 1 represent typical reporting ratios there may be as many as 30 cases per week in St. Thomas. These figures probably represent the maxima however and cannot be confirmed. Reports of cigua- toxication in the British Virgin Islands have stated that virtually "everybody" has been poisoned at least once (some as many as fifteen times) but medical advice is almost never sought. Interestingly the British Virgin Islands are the only demo- graphic unit mentioned by Halstead (1970) where fish poisoning is "not regarded as deterrent to the development of the fisheries programme”. The pattern of sporadic reporting of ciguatera poi- soning despite the relatively high incidence of the disease is commonthroughout the northern Leeward Islands. Information a from Halstead (1970) and our own contacts withfishermen, in- ter-islandtraders, charterboat operators and fishery personnel in the region suggests that the problem is indeed severe. Vir- tually every person contacted from St. Kitts, St. Maarten, St. Eustatius, Anguilla, and Montserrat had either been a victim himself or knew of a close friend or relative who had been poisoned within the last five years. Very few of these cases were brought to the attention of a physician; most public health officials believe that "only the very severe cases are brought to the attention of the medical authorities" (Antigua); Halstead,(1970). One long-time resident of St. Kitts estimates only about one case in ten receives medical attention; as might be expected the bulk of the cases reported involve tourists and non-native residents. = 5 IV. GEOGRAPHIC DISTRIBUTION The geographic distribution of ciguatoxic fish in the Virgin Islands is shown in Figure 1. The island of St. Croix, on a separate geologic platform, is not reported as producing ciguatoxic fish in any appreciable quantity and has been omitted from this figure. A large number of the areas indicated have been reported as producing toxic fish for centuries. It cannot be presumed that these are the only localities; toxic fish are frequently caught in other areas. In the Virgin Islands there is an extremely strong feeling among the fishermen that the south side of the Virgin Bank from Sail Rock east to Peter Island consistently pro- duces toxic fish. Other fishermen would extend this area east and north to include most of the coastline of Virgin Gorda, some would include the Horseshoe Reef and Anegada. Still others (particularly those who regularly fish this southern Bank) state that only specific locations in this area produce toxic fish and that reef areas or "banks" only a few miles away are free of ciguatera. Virtually all fishermen feel that the entire north side (the Atlantic side) of the Bank is free of toxicity with the exception of a very few species. This pattern of geographic «1 G- YSTJ OTXOR easy _OOL * Hhutonpoid se pejziodez seere a ~~, gO gO care aeactceeel™ aAIND swouzey OOT ----: - eare spueTsSI utbata ayy fo dep T agundIa N ° ia 3 8 ueA 3s0r O Y <x - oO i f 7 nee oe Oe A ao Samad wt ee Fe 4 xf Joo , Ni . @BoysesIoH ; / / f / i SUNBeZ OOT - s, ss distribution of ciguatoxic fishes seems consistent with those areas teported by earlier authors (Walker, 1922; Arcisz, 1950; Brown, 1945; de Sylva, 1956, Mann, 1938). Other writers quoted in Halstead (1967) notably Hill (1868) Rogers (1899) and Gilman (1942), are contradicted by local fishermen, atleast for the bulk of the species implicated elsewhere in the Virgin Is- lands. In almost allreports on the geographic locality where toxic fish are caught the interviewee was referring to depths of 30 fathoms or less; the bulk of — refer to reef areas in eight - fifteen fathoms, but this may be an artifact of fishing methods rather than abiological distribution. The relationship of depth to capture of ciguatoxic fishes is discussed in a later section. The areasreported (by our contacts and by Halstead, 1970) as producing toxic fish in the northern Leeward Islands are shown in Figure 2. These data are plotted along withareas mentioned as toxic by various authors in Halstead (1967) and do not represent an intensive survey. More.specific data will be presented in a later paper. The more southerly group of islands in the eastern Caribbean (Martinique south to Trinidad: the Windward Islands) have not commonly been reported as pro- ducing ciguatoxic fish in this century. Earlier authors make =9§~ reference to a variety of species and locations but this is not confirmed by present residents. Although no quantitative data are available it seems clear that the majority of ciguatera poisoning outbreaks in the eastern Caribbean occur in a rather small area from Mont- serrat north to the VirginIslands including all of the northern Leeward Islands and portions of Saba and Anguilla Banks. Be- yond this area ciguatera poisoning is limited to sporadic out- breaks which generally involve large specimens of only a few species. 29s FIGURE 2 Map of the Leeward Islands - . - . - . 100 fathoms curve areas reported as producing toxic fish f-0 —n Ve ¢ — rd — _— Pied sv 7 Anguilla Bank 7 er eae Anguilla ‘Nos Py 7 Ap Pg , es Bees “ee e- ot dae Barts ee f+ ed ~~ Barbuda », GE sa a ~ ian’ St. Bustatius — Ss Ay ~ wo Saba Bank e St. Kitts won ee. ! Nevis Antigua . as. ee end eee ans, Find Montserrat @-. oe V. SPECIES REPORTED AS CIGUATOXIC More than 400 species of fish have been implicated in ciguatera poisoning on a global basis (Bagnis, 1970). Ofthese 400, 91 species could conceivably be found in the eastern Ca- ribbean. It is possible that an -even larger number could be associated with ciguatoxications if they were desirable as food fish. There are also a number ofreports of molluscs, crabs, and lobsters producing the disease. Appendix I lists the 24 fish most frequently reported as toxic in the Virgin Islands. All of these species are valued as food fish with the exception of barracuda and amberjack; these two species have such a bad reputation as ciguateric that only the smallest specimens can be sold. It is somewhat surprising that the moray eel is as highly esteemed as it is, considering reports of toxicity from the Pacific. In St. Thomas eels are typically purchased by individuals from Spanish Caribbean cultures (Puerto Rico, Dominican Republic, Cuba), areas where ciguatera is less frequently reported. The fish at the top of the list tend to be reported as toxic more frequently than those lower down. In general the larger specimens of these species are frequently incriminated in ciguatera poisoning incidents. The fish generally can be considered 'shore-fishes" or "reef - aed fishes" and for the most part conform to the pattern noted by other authors (Randall, 1958; Halstead, 1967; Banner, 1971): toxic fishes are not common at depths greater than 80 - 100 fathoms. Two notable exceptions in the Virgin Islands are the blackfin snapper, Lutjanus buccanella and misty grouper, Epinephalus mystacinus. We have data on two outbreaks af- fecting five people from blackfin snapper caught in deep water and three additional outbreaks implicating misty grouper (which has not been taken at depths of less than 55 fathoms) involving at least ten persons during mid-1971. These data appear in Appendix II. Additional data on ciguatera from deep-living species is noted in a later section of this report. Although Banner (1971) states "true ciguateric fishes appear to be only those fishes tied directly to the flora and fauna of coral reef..." there is excellent clinical data to support these outbreak re- ports; several members of our staff were among the victims. Samples have been retained for extraction and bioassay to quantify the toxicity of these fish (see also section on fisheries development). VI. -CHEMISTRY AND PHARMACOLOGY Our knowledge of ciguatera poisoning in the eastern Caribbean is presently based upon clinical reports and is only beginning to be qantified by chemical and biological assays. On the basis of symptomology and from the species implicated it is highly probable that ciguatera poisoning in the eastern Caribbean is produced by very similar (if not identical) com- pounds to those known from the Pacific. Scheuer and other workers at the University of Hawaii have isolated what they consider to be the primary toxin and, in cooperation with Hashimoto and his colleagues at the University of Tokyo; several secondary toxins. The primary toxin (deemed cigua- toxin) is insoluable in water, soluable in polar organic sol- vents, heat stable to 100°C, stable below 0°C as a crude toxin but unstable in the semipurified or purified form unless ex- tracted, purified, and stored in an inert atmosphere at low temperatures. The non-crystalline product has the empirical formula (C35Hg5NO3)n and the molecule has indications of a quaternary nitrogen atom, one or more hydroxy] groups and a carbonyl function. It is not a phospholipid. Acry stalline product currently undergoing analysis to determine its structur - al formula (Banner 1971). a99- Present evidence (againfrom the University of Hawaii group) suggests that ciguatoxin acts upon excitable membranes to increase the permeability of Na + ions, upsetting the ionic balance of the membrane. Ciguatoxin is not an anticholinesterase in vivo, despite earlier papers and various therapies for cigua - toxications based on stimulation of cholinesterase cannot be endorsed at the present time. The toxin is active at the level of 0.025 mg/kg when injected into mice with a toxin yield of 5 - 10 mg/kg from highly toxic flesh. The toxin is carried at a uniform level eraser the musculature of toxic fish but may be 50 to 100 times as concentrated in the viscera, par- ticularly the liver. Our laboratory in St. Thomas is currently using an acetone - diethyl ether extraction with purification by column chromatography developed by Scheuer (per. comm. ) and bio- assay using intraperitoneal injection into 20+ gram Charles River CD-1 mice. We have previously used other extraction techniques including crude aqueous extraction with emulsifiers and a variety of experimental bioassay techniques. Our con- clusions are basically the same asthe workers in Hawaii al- though based on much less experience: careful solvent ex - traction and purification are necessary, rigidly controlled bioassay procedures are required, and experienced laboratory -94- personnel are an absolute re quire ment. To date there has been no rapid, simple colorimetric or other chemical test for ciguatoxin developed. Screening programs are exceedingly ex- pensive and difficult to manage and are only in operation in Japan on a limited basis for selected samples from highly suspect areas. As much as we might desire it, we are not very close to a rapid means of identifying ciguatoxic fish in the laboratory and even further from a simpletest which might be part of a housewife's shopping kit. The traditional West Indian methods of determining if a fish is ciguatoxic have been discussed at length by previous authors. Appendix III lists these methods as reported to us by natives of the Virgin and Leeward Islands. Many housewives swear by some particular method utilizing visual inspection of external characters of the fish. Most admit that in practice both the visual methods and those requiring addition of some indicator are unreliable. We have submitted each of these methods to an assay with at least two known toxic fish and two non-toxic fish and have not found them reliable. VII. BIOGENESIS AND TRANSMISSION OF CIGUATOXIN At the present time we have no accurate data on the mechanisms of biogenesis of ciguatoxin (or its related compounds) nor information on its transmission through the food chain. Banner, Helfrich, Randall, and others at the Univers ity of Hawaii have concentrated a good deal of effort on these prob - lems in the Pacific and their findings to date are summarized below (from Banner, 1971): 1. No causative agent or organism has yet been identified as producing toxins similar to ciguatoxin. 2. No definite evidence has been found to suggest that: a) copper or other metallic ions act as chelators, trace minerals or catalysts in the formation of the toxin; b) no demonstrable increase in ciguateric fishes was noted in areas where "new surfaces" were exposed by natural disasters, dredging, blasting, predation by Acanthaster; c) contamination of the marine environment by pollutants (specifically wax esters at Wake Island) have no effect on ciguatera. 3. Normally non-toxic omnivores can be made toxic when fed small amounts of toxic fish over a period of time. -265 4. Toxic Lutjanus bohar retain toxicity for up to 30 months when fed a non-toxic diet. 5. Adetrital feeding acanthurid (Ctenochaetus striatus) has demonstrable ciguatoxin in the flesh, viscera, and gut contents. 6. Most carnivores seem to carry the same toxin (ciguatoxin) although additional toxins (eg: Aluterin, ciguaterin) may also be present. It should be noted that Dr. Banner will present a paper entitled "Biological Origin and Transmission of Ciguatoxin" tomorrow (18 November 1971), which could shed some new light on this subject. Given the similar symptoms and species distribution reported in Pacific and eastern Caribbean ciguatera poisonings it is reasonable to assume that similar biogenesis and trans- mission of the toxin can be expected. There are several per- sistent beliefs among eastern Caribbean fishermen which will be repeated here although we have been unable to confirm them. 1. Ciguatera is produced by fish which eat the fruit or leaves of manchineel (Hippomane mancinella). This theory has been proposed since 1511 (by Peter Martyr of Anghera; -27- Halstead, 1967) and is probably based on advise to early ex- plorers from Caribbean Indians. Hippomane is certainly toxic but its pharmacological action is quite different. It is doubtful that this theory is correct. 2. The most persistent theory inthe Virgin and Leeward Islands involves copper. Natural copper deposits ("copper banks’') are presumed to exist and fish which feed on these banks become toxic. Some of the more sophisticated fishermen suggest that it is not actually the copper metal but a small "sea moss” (which grown in areas where copper con- centrations are high) which actually manufactures the toxin or a precursor. The "sea moss’ responsible has been pointed out to us by several fishermen (actually) three species: Enteromorphia lingulata from shallow water at Buck Island, St. Thomas; Cladophora sp. from fish pot warps of Flanagan Is- land, U.S. V.I.; Chaetomorphia sp. from rocky subtidal at Buck Island, St. Thomas). None of these algae showed toxic activity when extracted with Tween and injected I. P. into mice; we plan to repeat this experiment with solvent - solvent ex- traction and column chromatography when these algae can be collected from historically toxic areas. Most fishermen suggest that the production of:toxic "sea moss" is seasonal -28- with peak growth in late spring or early summer. The asso- ciation of ciguatoxin with copper is not limitedto copper banks by fishermen; it is proposed that shipwrecks (particularly older wrecks with copper-sheathed bottoms) and copper antifouling paints supply all of the copper needed. We can in no way con- firm the theory of copper-induced ciguatoxin at this time. 3. A theory proposed by a few fishermen and com- pletely unproven at this time attempts to explain the high con- centrations of toxic fish on the south of the Virgin Bank (with the lower toxicity reported from the same species on the north side of the Bank) and in the area from Antigua north to the Anegada Passage. It is proposed that the toxin is produced by some organism (presumably a primary producer) which is found only in areas where deep, cold, nutrient-laden water is upwelling. The theory is reasonable when applied to the southern Virgin Bank and the southeastern portions of Saba Bank, both noted as producing toxic fish, as there is good evidence that upwelling does indeed occur in the Anegada Passage. The upwelling pro- cess cannot be confirmed in the St. Kitts - St. Eustatius - Redondo area at the present time due to lack of data. The specific organisms(s) responsible and the mechanism of toxin production are not known by the proponents of this theory. -29- We are therefore no closer to an accurate description of the biogenesis or transmission mechanisms of ciguatoxin than purely theoretical considerations. We have proposed a series of studies similar to those undertaken by the University of Hawaii group including chemical, ecological, and epidemiological programs for the next three years to attempt a better under- standing of this problem. «30~ Vl. EFFECTS OF CIGUATERA POISONING ON THE DEVELOPMENT OF FISHERIES We have every reason to believe that ciguatera poisoning is a major impediment to the sale of local finfish in the Virgin Islands and thus is a strong deterrent to expansion of the com- mercial fisheries. Interviews by Halstead (1970) suggest that this is true throughout the Leeward Islands too, although re sidents of Antigua, St. Kitts, and St. Maartc : express the opinion that there is little alternative to continued buying of local fish and risk of intoxication. In Dammann's 1967-68 survey of commercial fisheries of the Virgin Islands slightly more than half of total finfish con- sumption was from local (U.S. and British V.I.) sources (1, 672, 400 of 3,084, 373). We have no data on how much of the fish imports could be replaced by local production if ciguatera were not a problem, Interviews with fishermen suggest that very few hotels and restaurants catering to the tourist trade would purchase locally caught grouper, snapper, jacks, and kingfish because of fear of fish poisoning. Dammann's Table 9 "Fisherman-reported problems inthe Virgin Islands commer cial fishery" doesnot include any dataon this subject, however Table 12 indicates that only two percent (two of 79) of the fishermen “Z1< contacted felt that there were "no fish" (commonly reported as ciguatoxic) so one might assume that ciguatera was indeed con- sidered a problem. Two investigations of fisheries development potential in the Virgin Islands area have recently been completed. The first (Dammann et al., 1970) developedlines of approach carried out in the second project (Brownell and Rainey, 1971) for ex- panding the VirginIslands fisheries through exploitation of deep water stocks. This effort was motivated by several natural limiting factors on the shallow water fish populations, among them the risk of ciguatera poisoning. It now appears that even species previously considered non-toxic because their normal depth-range is greater than 100 fathoms are implicated in ciguatoxications. Brownell and Rainey (1971) report three out- breaks from mir’y grouper Epinephelus mystacinus taken at 130-135 fathoms and the only documented case of ciguatera from a silk snapper Lutjanus vivanus from 110 fathoms. Two questionable outbreaks are reported by Dammann et al. (1970) from Epinephelus nigri tus (actually E. mystacinus). In addition to the outbreaks reported for E. mystacinus and Lutjanus buccanella in Appendix II, we are aware of several outbreaks from L. buccanella attributed to fish caught during the exploratory -32- fishing projects of the UN/FAO Caribbean Fisheries Development Programme (CFDP)in 1970 and 71. Weare currently extracting and bioassaying about two tons of fish caught on UN/FAO cruises from areas where toxicity is reported. These data will be re- ported in early 1972. Although these data will provide us with a more precise estimate of the proportion of ciguatoxic fishes in the deep shelf - shel!f-slope-populations, we have already ascertained that this resource is not free of ciguatoxin. The toxic blackfin snappers caught by the CTDP came from Saba and Anguilla Banks; fishermen in Montserrat report that most known poisonous fish had been captured in deep water - up to 250 fathoms. It is highly probable that the abrupt drop- off to depths of 200 fathoms or more surrounding many of the Leeward Islands harbor excellent stocks of food fish but it is quite likely that some ofthese species carry ciguatera poisoning. Halstead's 1970 survey found that fishermen, fisheries officers, and public health officials were almost unanimous that ciguatera was a deterrent todevelopment of the commercial fisheries. Most Islands reported ciguatera in fish from depths of 0-60 fathoms and the most frequently toxic are all among the first ten species listed in Appendix I. At least two large com- mercial fishing operations in St. Maarten have given up shallow -~33- water fishing because of repeated ciguatoxications by their catch; several fishermen have reported having to discard large catches of jacks and grouper because their previous catches had caused poisoning. In the small communities of the Virgin and Leeward Islands an individual fishermen is occasionally completely boy- cotted because of his reputation for regularly landing toxic fish. Fishermen are expected to be able to determine whether or not a particular fish is toxic; an occasional instance is accepted, however. The fisheries of the Virgin and Leeward Islands do not lend themselves to exploitation by large vessels with modern ground fishing gear. The pelagic stocks are apparently not sufficient to support a muchlarger fishing effort than is currently in progress. There are probably not sufficient stocks in the shelf-edge populations to withstand intensive fishing pressure equivalent to the Gulf of Mexico - Florida Straits snapper in- dustry. The majority of fishermen in the eastern Caribbean are owner -operators of small boats (20 feet or less) who rarely go more than ten miles from their home port. These fishermen could be trained and proper gear could be utilized for exploiting the area's natural stocks both in shallow and deep water but fish poisoning cases would be likely to increase. A thorough under- = standing of the ciguatera problem must be developed before ex- pansion of the fishery can be effectively accomplished. IX. SUMMARY AND CONCLUSIONS 1. Fish poisoning in the eastern Caribbean is reported from all of the islands ofthe northern Virgin and Leeward Islands group. PuertoRico, Hispaniolaand St. Croix havea muchlower incidence rate as do the Windward Islands (Trinidad to Martinique). 2. Although clupeoid, elasmobranch, tetraodontoid, and hallucinatory fish poisoning are reported from the eastern Caribbean, scombroid poisoning and ciguatera poisoning are con- sidered to be most important. Because scombroid poisoning can be prevented by modern preservationtechniques andtreatment of the disease is specific and effective, it is considered a less se- vere problem than ciguatera poisoning. 3. Epidemiological reporting of ciguatoxications has only been begun in the last month throughout the Virgin Islands and a careful survey ofthe Leeward Islands must await additional funding. Ciguatera is presently reportedas a severe public health problem with only afraction of the cases reaching medical atten- tion. The problem seems most severe in the area from Mont- serrat north to the British Virgin Islands including the south- east portion of Saba Bank and the southern shelf of the Virgin Is- lands plateau. ~36- 4. The chemistry, pharmacology, and ecology of ciguatoxin and closely allied compounds are at present poorly understood. The symptomology and species distribution of the toxins in the eastern Caribbean strongly suggest that a situation exists which is very similar to that described from the Pacific islands by the Marine Biotoxin group at the University of Hawaii over the past sixteen years. 5. Toxicity in eastern Caribbean fishes seems to be more prevalent among the large carnivores of reef or reef-re- lated habitats. There are a number of data which suggest that ciguatoxin(s) are produced by some organism in the reef food web and that the toxin is passed through the food web without a signi- ficant modification and concentrated by the larger carnivores. 6. Development of the commercial fisheries in the eastern Caribbean is severely impeded by the prevalence of ciguatoxin in commercially desirable species. There is good evidence that the shelf-edge stocks of snapper and grouper are not free from ciguatera poisoning as previously proposed and that exploitation of this presently underutilized resource may be impeded by this toxicity. xX. ACKNOWLEDGEMENTS This report was prepared with the cooperation of the staff of the Ciguatera Project, Caribbean Research Institute, College of the Virgin Islands. The Ciguatera Project is supported by a Sea Grant (1-35368) from the National Oceanic and Atmospheric Agency of the U. S. Department of Commerce with matching con- tributions from the United Nations Food and Agriculture Agency's Caribbean Fisheries Development Programme, the College of the Virgin Islands, and the Government ofthe U. S. Virgin Islands. RBs XI, LITERATURE CITED Arcisz, W. 1950. U.S. Fish & Wildlife Serv. Sp. Sci. Rep. no. 27, 1-27 Bagnis, R. etal. 1970. Bull. World Health Org. 42:69-88. Banner, A.H. 1971. Tech. Report #1 (Final Report) ONR Contract #N00014-67-C-0127. Brown H.H. 1945. Develop. Welfare West Indies, Bull. 20: 34-37 Brownell, W. N. & W.E. Rainey 1971. Carib. Res. Inst. Rept. VIERS no. 3. Dammann, A, E,, W. Swingle & J. Yntema 1969. Carib. Res. Inst. Spec. Rept. VIERS no. 1 , etal. 1970. Carib. Res. Inst. Spec. Rept. VIERS no. 2. de Sylva, D. 1956. Mar.Lab. Univ. Miami. Spec. Serv. Bull., v. 13:1-9. Gilman, C.L. 1942. U.S, Nav. Med. Bull. 40(1):19-27. Halstead, B.W. 1967. Poisonous and Venomous Marine Animals U.S. G. P.O. 1970. UN/FAO CFDP working paper FI:SF/CAR Reg. 189. Hill, R. 1868. Proc. Sci. Assoc. Trinidad 1 (5)210-223. Mann, W.L. 1938. U.S. Nav. Med. Bull. 36(4):631-634. Randall, J. E, 1958. Bull. Mar. Sci. Gulf Caribbean 8(3):236-267. Rogers, J.M. 1899. Pop. Sci. Monthly 55:680-685. Teytaud, A.R. & R.W. Brody 1971. Carib. Res. Inst. Spec. Pub. Cig. no. 1. -39- APPENDIX I Species Most Commonly Reported as Toxic in the Virgin Islands Area Species Sphyraena barracuda Seriola dumerili Caranx latus Caranx ruber Caranx hippos Lutjanus jocu Mycteroperca venemosa Scomberomorus cavalla Caranx fusus Gymnothorax funebris Epinephelus adscensionis Mycteroperca bonaci Scomberomorus regalis Caranx lugubris Lutjanus griseus Lutjanus buccanella Epinephelus mystacinus Epinephelus guttatus Seriola rivoliana Caranx bartholomaei Apsilus dentatus Epinephelus morio Lachinolaimus maximus Belistes vetula Common Name Great barracuda; barra Amberjack; amber Horse-eye jack Bar jack; carang Crevalle jack Dog Snapper; dog tooth Yellowfin grouper; gramminix Kingfish; king mackerel Blue runner; hard nose Green moray (probably Conger or Congo eel) Rock hind Black grouper Cero (often mistaken for "spanish mackerel") Black jack Grey snapper Blackfin snapper Misty grouper (often erroneously called Warsaw grouper) Red hind Almaco jack Yellow jack Black snapper Red grouper Hogfish Queen triggerfish; old wife APPENDIX II Outbreak reports from fishes caught at depths greater than 500 feet during 1970-71 (data from interviews; Ciguatera Case Repository numbers refer to CRI files) CCR-71-011. Blackfin snapper - Lutjanus buccanella - about four lbs. Fishcaught southof Frenchcap Cay, U.S, V. I. at about 40 fathoms bylocal fishermen. Fishwas eaten by three people all of whom reported abdominal pain, bowels, nausea, vomiting in that order. Onset between three and six hours after ingestion. Secondary symptoms included extreme weakness, listlessness, itching which developed 12-24 hours after ingestion and lasted for several five - seven days. None of the victims reported | previous intoxication. CCR-71-018. Blackfin snapper - Lutjanus buccanella - about three lbs. Fish was purchased on the waterfront at St. Thomas by young couple visiting relatives on the island. Fish was broiled with sauce, no symptoms developed until about eight hours after ingestion. Vomiting, diar- rhea, weakness in the knees, dull headache persisted all the following day. Late afternoon produced P.S. D. for manbut not wife. Returned to mainlandthree days after ingestion, no followup available. CCR-71-008. Misty grouper - Epinephelus mystacinus - 36 lbs. Fish purchased at the dock - caught (apparently) south of St. John. Victims brought five lbs. (tw large steaks); refrigeratedthem and cooked fishnext evening. Four persons had dinner of this fish; three young men and a young lady - one man andthe lady reported nausea, vomiting, and weakness within six hours; headache, nausea, weakness persisted for "three or four days". The third victim had no violent symptoms of gastro- intestinal origin but was lethargic and felt ''weak in the joints'' next day. The fourth person did not report any illness. CCR-71-021. Misty grouper - Epinephelus mystacinus - 56 lbs. Fish caught bylocal sport-commercial fishermen at the ''Warsaw Pocket'’ (misnamed since the area pro- duce misty groupers) - about 3-1/2 miles south of Nor- man Island, B.V.1. at depth of about 120fathoms. Fish was filleted and headed; at least six persons ate fillets with no ill effects. Two more people made soup of the head; they reported some intestinal discomfort and weak- ness, tingling sensations and lethargy the following day. Five other persons fried a small section of the liver: each reported eating "not more than a few bites" that night. All awoke within three hours with violent abdominal cramps, vomiting, and violeni headache. Severity of gastrointestinal symptoms continued for six hours or so, then extreme \.ecakness, sinus-like head- ache, and watery bowels persisted for two - four days. P.S.D. and tingling and numbness in the lips were re- ported about sixteenhours after ingestion by three of the five. Allreported persistent symptoms of weakness and soreness in all body joints for seven - ten days. PS. D, persisted for at least a week in two victims. CCR-71-023. Misty grouper - Epinephelus mystacinus - a- bout 30 lbs. Steaks were sold to about four persons none of who apparently developed ciguatera symptoms. A soup was made of the head and eaten by three persons. All described gastrointestinal distress, diarrhea, and nausea withinthree - six hours; apparently the symptoms disappeared within about 24 hours for two of the victims; the third reported listlessness, weakness, and achy joints which lessened by the third day after ingestion. APPENDIX IIl Methods for identifying ciguatoxic fish as described in the folk- lore of the Virgin and Leeward Islands (from interviews; Dam - mann et al., 1969; Halstead, 1967) Il. Ill. ? External characters of the fish or fish flesh which indicate toxicity: -More yellow or brassy color, especially about the head -Stripes (in species where they are not normally obvious) -Darker coloration -Red coloration to the eyes -Yellow mucus on inner lining of gullet -Green tint to raw flesh -Tiny black "veins" running through the musculature -Brassy or coppery odor to the flesh -Teeth are black -Suspect specifies with roe is toxic -Enlarged or bloated stomach -Flesh tastes bitter or hot in mouth Indicator organisms which suggest toxicity: -Worms in the flesh (particularly jacks and mackerel) (Worms in the stomach indicate a non-toxic fish) -Igopod ectoparasites ("cockroach") are not found on toxic fish (jacks) -Flies will not land on flesh -Ants will not eat Methods employing an indicator: -Silver turns black when boiled with toxic fish -Sweet potato turns black when boiled with toxic fish