CARIBBEAN RESEARCH INSTITUTE



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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



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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



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areas reported as



producing toxic fish



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PAGE 20

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