4

Poisonous FishesMAN'S KNOWLEDGE of poisonous fishes

dates back to ancient times. At least oneof the Mosaic laws is believed to have been aimeddirectly at eliminating poisonous fishes from theIsraelite diet, "These ye shall eat of all that arein the waters: all that have fins and scales shallye eat: And whatever hath not fins and scalesye may not eat: it is unclean unto you" (Deuter-onomy 14: 9-10). The French archeologistClaude Gaillard reported that hieroglyphicsand figures of the deadly Tetraodon lineatuws ap-pear frequently on ancient Egyptian tombs (1),and according to the Egyptologist Keimer, thisscaleless species was recognized as poisonousduring the time of the Pharaohs. Galen is saidto have reported in his De Alimentis that theflesh of the moray is dangerous to eat (2).Alexander the Great forbade his soldiers to eat

BRUCE W. HALSTEAD, M.D.

fish during conquests because he believed thatsome species produced skin disorders.

Peter Martyr, the first historian of the WestIndies, made the earliest reference to ciguaterain 1555 (3). In de Landa's famous Relacion deLas Cosas de Yucatan, written in 1566, the lethalqualities of puffers are mentioned (4).

Beginning with the 19th century, hundreds ofpublications appeared on the subject of fish

Dr. Halstead is generally regarded as the world'sleading authority on poisonous fishes. He is chair-man of the section of natural products, School ofTropical and Preventive Medicine, CoUege of Medi-cal Evangelists, Loma Linda, Calif. Until July 1,1958, he is on military leave with the Division ofPreventive Medicine, Naval Medical School, Na-tional Naval Medical Center, Bethesda, Md.

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poisoning, including some comprehensive re-views and bibliographies (3, 5-11).

Because of their somewhat sporadic and un-predictable appearance, generally affecting onlysmall numbers of persons at any one time,poisonous fishes have not attracted a great dealof attention in medical circles. However, thepublic health significance of poisonous fisheswas pointed up in the series of outbreaks whichoccurred in Midway, Johnston, and the LineIslands, beginning about 1943 and reaching apeak about 1946 (12, 13).

Recent mass intoxications in the westernPacific have once again directed attention to thepublic health importance of poisonous marineorganisms. These outbreaks began about 1952,became increasingly severe during 1955, andhave continued until the present time, intoxicat-ing a number estimated at more than 40,000 per-sons. The bulk of the outbreaks have takenplace in Japan, the Philippine Islands, andmore recently in Viet Nam. The causativeagents were octopus, Octopus8vugaris, 0. dof-leini, squid, Omna8trephes sloani pacificus, Jap-

anese horse mackerel, Trachurus japonics, com-mon Japanese mackerel, Scomber japonicue,flying fish, Prognichthys agoo, and oceanic bo-nito, Katewuonus pelamd. All of the out-breaks have been seasonal, taking place duringJune to the middle of September. Bacteriolog-ical tests have been negative, and the degree offreshness of the organisms seems to have nobearing on the matter. The symptoms are simi-lar to those produced by bacterial food poison-ing, but no human pathogens have been isolatedby Japanese epidemiologists. The mortalityrate in the largest series of Japanese fish out-breaks in 1955 was 0.77 percent (14).According to a report received from the Bu-

reau of Fisheries of the Philippine Govern-ment, another series of outbreaks of fish poison-

Some fishes associated with ciguatera are illustratedacross the top of these pages. They are: 1. Trigger-fish, Odonus niger. 2. Wrasse, Epibulus insidiator.3. Jack, Carano melampygus. 4. Surgeonfish, Acan-thurus triostegus. 5. Snapper, Monotazia grandoculis.6. Seabass, Variola louti. 7. Grouper, aephalopholisargus. 8. Red Snapper, LutjaMus vaigiensis.

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ing took place in April 1957. The completeniumber of persons inivolved has not been deter-mined as yet, but several deatlhs have been re-ported. The cauisative agent in most of thePhilippine poisonings has been the oceanicbonito, K. pelamis. Philippine public healthauthorities are establishing regulations prolib-iting the sale of the oceanic bonito in some lo-calities. Some intoxications fronm fishes havebeen reported in Viet Nam, but as yet no detailsare available as to the nature of the outbreaks.

Since intoxications resultinog from poisonousfishes are frequently confused witlh a variety ofother ailments, a review of the epidemuiologicaland clinical aspects of the problem of iclhtlhyo-sarcotoxism is timely. The chemistry of thesepoisons has been reviewed elsewhere (31).

Epidemiology

Judging from the public lhealtlh anid toxico-logical reports that lhave appeared to date, anymarine fish can under certain circumstances be-come poisonous as a result of its food lhabits.Toxicity is not species specific, except possiblyin puffers or tetraodontoid fishes. More tlhan300 species of marine fishes have been incrimi-nated as causative agents in producing hunianintoxications of the ciguatera type alone. Mostpoisonous fishes are shore forms rather tlhanoceanic inhabitants. Fishes captured in deepwaters far from shore are generally safe to eat.Some of the more common families of marinefishes which have caused lhuman intoxicationsare listed under the various clinical types of fislhpoisoning.

Poisonous fishes are largely circumtropical indistribution, but on occasion occur in temnper-ate waters. With the exception of 2 or 3 borealspecies they are currently believe(d to have amaximum distributional range of 450 northand 450 soutlh of the Equator. Particularlylarge populations of poisonous fishes are knowinto occur in the central Indo-Pacific area anid inthe West Indies. They are more common nearislands than along continental slhores. Withlillthese general areas, poisonous fishes seem to bequite circumscribed in distribution. They mayvary considerably in their distribution about asingle island. A species may be toxic in one

part of the island, but edible in another.Lagoon fishes are more likely to be poisonousthian those living on seaward reefs.The toxicity of puffers or tetraodontoid fishes

generally follows closely their reproductivecycle. Th-e toxin content of the fish is greatestijist prior to spawning. For most puffers,spawning takes place during late spring orearly summer. Toxin content is lowest duringfaldl and wiinter. There is some evidence thatthle barracuda (Sphyraena spp.) may follow asini ilar, but less pronouunced, seasonal pattern.IHowever, in most other species there is no evi-dence of a seasonal fluctuation.The poison in tetraodontoid fishes is usually

more concentrated in the liver, gonads, andskin, but other parts of the viscera may alsobe toxic. Puffer musculature is generally non-poisonous. Tlhe (listribution of poison is ex-ceedingly variable in other kinds of fishes. Ifa fish is toxic, the musculature will be found tobe poisonous in about 50 percent of the speci-niens, and the viscera, in about 90 percent ormore. However, the distribution of the poisoniin the body of the fish varies from one inidivid-ual to the next.No consistent patterni has been observed as to

the relationship between the size of the fishand its toxicity. It has been observed that un-usually large specimens of jacks (Caranx spp.),grouper (Epinephelus spp.), and barracuda(Sphyraena spp.) are more likely to be toxicthan smaller specimens. This has not beenfound to be necessarily true in otlher species.

Aboriginal peoples have numerous methodsby which they attempt to distinguish a poi-sonous fish from an edible one. The signifi-cance of color change in silver coins, color ofthe fish, condition of the gills, position of thescales, ad infinitum, is generally without scien-tific foundationi. To the best of our knowledge,one cannlot detect a poisonous fish by its appear-anice. The most reliable field method is to feeda small sample of the fish to a kitten or a dog.If the animal remains asymptomatic for 12lhours, the fish is generally safe to eat. Investi-gationls are currently in progress at the Schoolof Tropical and Preventive Medicine, LomaLinda, Calif., witli the lhope of developing areliable rapid chemical fiel-d test.

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Origin of the Poison

The origin of ichthyosarcotoxins in naturehas been the subject of much speculation andfolklore. Numerous theories have been pro-pounded, but few have any scientific basis(15, 16). It is certain, with the single excep-tion of scombroid poison, the poisons are notbacterial in origin. Putrefactive processes donot play a part in the production of fish poisons.There is no evidence of any relationship be-tween the presence of ichthyosarcotoxins andradioactive substances in the water. It is be-lieved that most of these poisons are derivedfrom the food which the fish eats. Food prob-ably plays an important role in the direct pro-duction of even puffer poison.The most widely accepted theory propounds

the idea that' the toxic substances, or theirprecursors, are obtained directly from marinelittoral algae. It is doubtful that planktonplay any role in the mechanism. Herbivoresfeed on the plants. Carnivores feed on theherbivores and man may become poisonedfrom eating either of them. Stomach contentanalyses have revealed that algae are morefrequently present in poisonous fishes than anyother types of food (17), and toxicological testsof these algae have shown some of them to con-tain toxic substances (18). Moreover, con-trolled laboratory feeding tests demonstratethat it is possible to induce toxicity in carnivo-rous species without evidence of detrimentaleffects on the fish, by feeding them toxic fishflesh. Further chemical and stomach analyseswill be required before the toxin-food chaintheory can be definitely established. Experi-mental work in attempting to determine theorigin of fish poisons in nature is currently inprogress by the author.The incidence of fish poisoning cannot be

accurately determined since the disease is fre-quently misdiagnosed and generally unre-ported. In the past, several hundred cases ofpuffer poisoning were reported each year inJapan, during some years accounting for asmuch as 44 percent of all fatal cases of foodpoisoning in that country. Japanese publichealth authorities state that puffers continue tobe their greatest single cause of food fatalities(19, 20). Probably the second most common

type of fish poisoning is ciguatera. Third onthe list would be scombroid poisoning, with theother forms of fish poisoning being relativelyuncommon. It is unfortunate that there are sofew reliable statistical data available. Localpublic health authorities should encourage thereporting of outbreaks, since poisonous fish mayconstitute a serious public health and economicthreat in some regions.Recent biotoxicological surveys that have

'been conducted in the tropical Pacific give someidea as to the incidence of poisonous fishes inspecific localities.

LocalityPhoenix Islands (16) ---Johnston Island (16) -

Galapagos Islands (29) -

Cocos Island (30)--

Numberspeciestested93605733

Percent ofspeciesfoundtoxic29756767

Among important field studies (7, 8, 21-23),Hiyama's work (7) is particularly useful, mag-nificently illustrated, and contains a valuablereview of the poisonous fish problem in Saipanand the Marshall Islands. Only meager statis-tical data are contained in any of these reports,but they do aid in developing an appreciationof the scope of the problem in the regionsdiscussed.

Clinical Characteristics

Since the chemical characteristics of fishpoisons have not been defined, poisonous fishesmay be tentatively classified on the basis oftheir phylogenetic relationships and sympto-matology of the intoxications which they pro-duce (10, 24). Certain fish groups are clas-sified under more than one category. Althoughthe weaknesses of this somewhat artificial sys-tem are recognized, it appears to be the mostpractical classification at present. Forms ofichthyosarcotoxism caused by fishes may besubdivided into the following clinical cate-gories (see table).

Lamprey and Hagfish Poisoning

The slime and flesh of certain lampreys andhagfishes are reported to produce a gastroin-testinal upset (32). The clinical characteris-

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Diagnostic characteristics of the various types of ichthyosarcotoxism

Type of poisoning Causative fish Symptomatology

Lamprey or hagfish- Lampreys, hagfish (slime, Gastrointestinal upset(?). Precise symptomatologyflesh). unknown.

Elasmobranch-- Sharks, rays (liver, flesh)- Gastrointestinal symptoms predominate in mildcases; neurological symptoms in severe cases.Deaths reported, but case fatality rate unknown.

Chimaeroid -Chimaeroid or ratfish (flesh, Neurological symptoms(?). Precise symptomatologyviscera). unknown.

Gymnothorax or moray Moray eels (flesh, viscera)---- Violent neurotoxic symptoms with convulsions andeel. paralysis predominating. Case fatality rate about

10 percent or more.

Scombroid -Scombroid fishes-tuna, bo- Histamine-like reaction with nausea, vomiting,nito, skipjack, etc. (inade- flushing of the face, swelling of the lips, urticaria,quately preserved flesh). and pruritus. Symptoms subside usually within

12 hours. Antihistaminic drugs effective.

Puffer -Tetraodontoid or puffer-like Rapid onset and extremely violent neurotoxic symp-fishes (viscera). toms: paresthesias, motor paralysis, convulsions,

death by respiratory paralysis. Case fatality rateabout 61 percent.

Ciguatera -More than 300 species of Onset may be gradual or sudden. Symptoms mildtropical reef fish, including to severe. Gastrointestinal and neurotoxic. Pa-snapper, seabass, grouper, resthesias, extreme weakness, joint aches, myalgiabarracuda, wrasse, parrot- and paradoxical sensory disturbance predominate.fish, and surgeonfish. Case fatality rate about 7 percent.

Gempylid diarrhea- Gempylids, escolars (flesh)____ Diarrhea develops rapidly but is painless. No otheruntoward effects.

tics of the intoxication, termed lamprey andhagfish poisoning, have not been completelydefined.

Elasmobranch Poisoning

The most severe cases of elasmobranch poi-soning usually result from the ingestion of theliver of sharks and rays. The musculature ofsome elasmobranchs is also reported as mildlytoxic with the symptoms seldom more thanthat of a mild gastroenteritis with a predom-inating diarrhea. Ingestion of toxic liver re-sults in the onset, usually within a period of30 minutes, of nausea, vomiting, diarrhea, ab-dominal pain, headache, a rapid, weak pulse,malaise, cold sweats, oral paresthesia, a burningsensation of the tongue, throat, and esophagus.As time progresses, the neurological and othersymptoms become more pronounced, resultingin extreme weakness, trismus, muscular cramps,sensation of heaviness of the limbs, blepharo-spasm, dilatation of pupils, hiccups, visual dis-turbances, joint aches, delirium, ataxia, incon-

tinence, dysuria, respiratory distress, coma,and death. The recovery period, if the victimsrecover, varies from a day or two to severalweeks. The mortality rate is not known.

Chimaeroid Poisoning

The musculature and viscera of certain chi-maeroids or ratfish have been incriminated ascontaining a neurotoxin. This form of ich-thyosarcotoxism, if it occurs, would be termedchimaeroid poisoning. Only vague referenceshave appeared in the literature regarding thetoxicity of this group of fish, by Pellegrin in1899, and by Phisalix in 1922. Halstead andBunker reported in 1952 that the reproductiveorgans were toxic. Nothing is known aboutthe nature of the toxin, or its relationship toother forms of ichthyosarcotoxism.

Moray Eel Poisoning

The musculature and viscera of some of thetropical marine muraenid or moray eels con-

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tain a violent poison. The disease is termedgymnothorax or moray eel poisoning (25, 26).Symptoms of tingling and numbness about thelips, tongue, hands, and feet, with a feeling ofheaviness in the legs, usually develop withinseveral minutes to 8 hours after ingestion ofthe toxin. These symptoms may be followedby nausea, vomiting, diarrhea, abdominal pain,malaise, metallic taste, sore throat, laryngealparalysis, meningismus, laryngeal spasm,aphonia, excessive mucus production, foamingat the mouth, intense perspiration, increasedbody temperature, crying out as if in pain,conjunctivitis, paralysis of the respiratorymuscles, ataxia, general motor incoordination,trismus, violent clonic and toxic convulsions,abnormal deep and superficial reflexes, coma,and death. Sensory reactions to deep and su-perficial pain are usually normal. Character-istic signs of this form of intoxication ap-pear to be the absence of thoracic respirationwith pronounced abdominal breathing, profuseperspiration, violent convulsions, purposelessmovements, and the extended period of time

Moray eel, Gymnothoraa javanicus

in which areflexia is present. In some casesthe reflexes may be absent for a period of 2months or more. The case fatality rate is esti-mated to be about 10 percent, and death is be-lieved to be the result of respiratory paralysis.

Scombroid Poisoning

Some of the scombroids (tuna, skipjack, andbonito) may on rare occasions cause ciguatera,but usually they produce an entirely differentform of intoxication, termed scombroid poison-ing. This is the only type of fish poisoning inwhich bacteria appear to play an etiological rolein the formation of the toxin. If scombroidsare inadequately preserved, a toxic "histamine-like" substance is formed, possibly from thedecarboxylation of histidine, a normal constit-

uent of fish flesh. Kawabata and associateshave recently termed this substance "saurine"(33). Victims complain of fish having a"sharp or peppery" taste. The symptoms mostoften present are nausea, vomiting, flushing ofthe face, intense headache, epigastric pain,burning of the throat, difficulty in swallowing,thirst, pruritus, swelling of the lips, and urti-caria, which are typical of a histamine reaction.Symptoms generally subside within 12 hours.

Tuna, Neothunnus macropterus

For some unknown reason scombroid fish ap-pear to be more prone to producing intoxica-tions of this type than other fish. The mor-tality rate is unknown.

Puffer Poisoning

The most violent form of fish poisoning isproduced by tetraodontoid or puffer-likefishes. The disease is characterized by rapidlydeveloping, violent symptoms. The onset andsymptoms in puffer poisoning vary accordingto the person and the amount of poison in-gested. However, malaise, pallor, dizziness,paresthesias of the lips and tongue, and ataxiamost frequently develop within 10 to 45 min-utes after ingestion of the fish, but cases havebeen reported in which the symptoms did notdevelop for 3 hours or more. The paresthe-sias which the victim usually describes as a"tingling or prickling sensation" may subse-quently involve the fingers and toes, thenspread to other portions of the extremities, andgradually develop into severe numbness. Insome cases the numbness may involve the entirebody, in which instance the patients havestated that it felt as though their bodies were"floating." Hypersalivation, profuse sweat-ing, extreme weakness, precordial pain, head-ache, subnormal temperatures, decreased bloodpressure, and a rapid, weak pulse usually ap-pear early in the succession of symptoms.

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Gastrointestinal symptoms of nausea, vomit-ing, diarrhea, and epigastric pain are some-times present early in the disease, whereas inother cases they are totally lacking. Contra-dictory statements appear in the literaturerelative to pupillary changes, but these differ-ences can probably be resolved on the basis ofthe time at which the examination is made.Apparently the pupils are constricted duringthe initial stage and later become dilated. Asthe disease progresses the eyes become fixedand the pupillary and corneal reflexes are lost.

Shortly after the development of the pares-thesias, respiratory symptoms become a promi-nent part of the clinical picture. Respiratorydistress, increased rate of respiration, move-ments of the nostrils, and diminution in depthof respiration are generally observed. Respir-atory distress later becomes very pronounced,and the lips, extremities, and body become in-tensely cyanotic. Petechial hemorrhages in-volving extensive areas of the body, blistering,and subsequent desquamation have been re-ported. Severe hematemesis has also beenknown to occur. Muscular twitching, tremor,

Puffer, Arothron meleagris

and incoordination become progressively worseand finally terminate in an extensive muscularparalysis. The first areas to become para-lyzed are usually the throat and larynx, result-ing in aphonia, dysphagia, and later completeaphagia. The muscles of the extremities be-come paralyzed and the patient is unable tomove.As the end approaches, the eyes of the patient

become fixed and glassy, and convulsions mayoccur. The victims may become comatose, butin most instances they retain consciousness andtheir mental faculties remain acute until shortlybefore death. Death results from a progressiveascending paralysis involving the respiratorymuscles. On the basis of Japanese statistics,the case fatality rate is 61.5 percent. If death

occurs, it generally takes place within the first6 hours, or within 24 hours at the latest. Theprognosis is said to be good if the patient sur-vives for 24 hours.

Ciguatera

More than 300 species of marine fish havebeen incriminated as causative agents of thisform of ichthyosarcotoxism. Fish most com-monly involved are seabass or grouper, bar-racuda, snapper, parrotfish, wrasse, surgeon-fish, and various other types of reef fishes.The time of onset and symptomatology of

ciguatera varies greatly according to the per-son, species of fish, toxicity, and amount andportion of fish ingested. Tingling about thelips, tongue, and throat followed by numbnessmay develop immediately or at any time withina period of 30 hours after the ingestion of thetoxin. The usual time interval for the develop-ment of symptoms is from 1 to 6 hours. Theinitial symptoms in some instances consist ofnausea, vomiting, metallic taste, dryness of themouth, abdominal cramps, tenesmus, and diar-rhea, followed by perioral tingling and numb-ness. The muscles of the mouth, cheeks, andjaws may become drawn and spastic with a feel-ing of numbness. Generalized symptoms ofheadache, anxiety, malaise, prostration, dizzi-ness, pallor, cyanosis, insomnia, chilly sensa-tions, fever, profuse sweating, rapid weakpulse, weight loss, myalgia, and joint aches arefrequently present. Victims usually complainof a feeling of profound exhaustion and weak-ness. The feeling of weakness may becomeprogressively worse until the patient is unableto walk. Muscle pains are generally describedas a dull, heavy ache, or cramping sensation,but on occasion may be sharp, shooting, and af-fect particularly the arms and legs. Victimscomplain of their teeth feeling loose and pain-ful in their sockets.

Visual disturbances, consisting of blurring,temporary blindness, photophobia, and sco-toma, are common. Pupils are usually dilatedand the reflexes diminished. Frequently re-ported are skin disorders, which are generallyinitiated by an intense generalized pruritus,followed by erythema, maculopapular erup-tions, blisters, extensive areas of desquama-

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tion-particularly of the hands and feet-andoccasionally ulceration. There may also be aloss of hair and nails.In severe intoxications, the neurotoxic com-

ponents are especially pronounced. Paresthe-sias involve the extremities, and paradoxicalsensory disturbances may be present in whichthe victim interprets cold as a "tingling, burn-ing, dry-ice or electric-shock sensation," or hotobjects may give a feeling of cold. In regardto the paradoxical sensory disturbance, theclassical case usually cited is that in which anAmerican naval officer who was poisoned byeating an amberjack was later observed sub-consciously blowing on his ice cream, whichwas "burning" his tongue, in order to cool it.Ataxia and generalized motor incoordinationbecome progressively worse. The reflexes arediminished and muscular paralyses develop.There may be clonic and tonic convulsions,muscular twitchings, tremors, dysphonia, dys-phagia, coma, and death by respiratory paraly-sis. The limited morbidity statistics show acase fatality rate of about 7 percent. Deathmay occur within 10 minutes, but generally re-quires several days.In those instances in which the victim sur-

vives, recovery is slow and convalescence maybe very prolonged, with extreme weakness, sen-sory disturbances, and excessive weight loss be-ing the last symptoms to disappear. Whenpatients have survived severe intoxication, com-plete recovery has required a period of severalyears. Several workers have reported cases inwhich the symptoms persisted for as long as 25years. Individuals who have been severely in-toxicated have stated that during periods ofstress, fatigue, exposure, or poor nutrition,there is a recurrence of the myalgia and jointaches similar to those suffered during the origi-nal acute period of the disease (10).

Gempylid Diarrhea

Some of the gempylids or escolars contain anoil within their flesh and bone marrow whichhas a pronounced purgative effect when in-gested. Gnempylid diarrhea (27) developsrapidly, and is said to be without cramping orpain. Since there are no other untowardeffects, ingestion of the oil can hardly be con-

sidered as an intoxication in the usual sense ofthe word.

Treatment of Fish Poisoning

The treatment of fish poisoning is largelysymptomatic. There are no specific antidotes,and an attack does not impart immunity.Gastric lavage and catharsis should be insti-tuted at the earliest possible time. In many in-stances, 10 percent calcium gluconate givenintravenously has given prompt relief, whereasin others it has been ineffective. Paraldehydeand ether inhalations have been reported to beuseful in controlling the convulsions. Nik-ethamide or one of the other respiratory stimu-lants is advisable in cases of respiratory de-pression. In cases where excessive mucusproduction is a factor, aspiration and constantturning are essential. Atropine has been foundto make the mucus more viscid and difficult toaspirate, and is not recommended. Oxygen byinhalation and intravenous administration offluids supplemented with vitamins given par-enterally are usually beneficial. If laryngealspasm is present, intubation and tracheotomymay be necessary. In case of severe pain, opi-ates such as morphine, given in small divideddoses, will probably be required. Cool show-ers have been found to be effective in relievingsevere itching. Patients suffering from theparadoxical sensory disturbance should be givenfluids slightly warm or at room temperature, aswell as vitamin B complex supplements. Anti-histaminic drugs will be found to be useful inthe treatment of scombroid poisoning.

Prevention of Fish Poisoning

Scombroid fishes appear to be particularlysusceptible to putrefaction and the develop-ment of toxic substances. Geiger has shownthat the "histamine" content of the flesh of thePacific mackerel, Pneumatophorus diego, in-creases from 0.9 mg. per 100 gm. of tissue toabout 95 mg. per 100 gm. when kept at roomtemperature (200 to 25' C.) for about 10 hours(28, 33). In warmer climates scombroidsshould be promptly refrigerated or eaten soonafter capture. Toxic scombroid flesh cannot al-ways be detected by appearance. The toxin

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contenit may be very high with little or no evi-dence of putrefaction. Scombroid meat havinga sharp or peppery taste should be discarded.If the whole fish is available the gills should beexamined. Gills should be bright red and with-out evidence of off-odor. If there is the slight-est evidence of putrefaction discard the fish.

If one eliminates scaleless fish from the dietthere is no opportunity to come in contact witheither tetraodontoids or moray eels, since bothare without scales. In Japan, puffer fishesshould be purchased from a first-class author-ized restaurant having a licensed puffer cook.It is important that the individual preparing-the food has a thorough knowledge regardingthe fish and its toxicity. One can generallyhave this assurance by dealing only with thehigher class restaurants. It is advisable toeliminate all of the visceral organs and skinfrom the diet regardless of the species. Al-though the testes are usually nontoxic, it mustbe kept in mind that this organ is frequentlyconfused with the violently toxic ovaries, par-ticularly during the season of the year in whichthe reproductive organs are in the dormantstate.

Ordinary cooking does not inactivate thetoxin. It may still be present in lethal quan-tities even when passed through a steam retortin the commercial canning process. The poisoncan be inactivated chemically by cooking themeat in a strong solution of sodium bicarbon-ate, ordinary baking soda, for a prolonged pe-riod of time. This latter technique also de-stroys the flavor of the fish and renders ituseless for consumption.Our knowledge regarding the toxicity of most

species of tetraodontoid fishes, exclusive ofJapanese forms, is exceedingly meager. We doknow, however, that many of the tropical tetra-odontoid species have produced violent deathat one time or another. Unless a species is defi-nitely known to be nontoxic, which is ques-tionable even under the best of circumstances,all tropical forms should be eliminated fromthe diet.

If it is a question of survival-either eat thepuffer or die-and the edibility of the fish isunknown, it is recommended that the fish beeviscerated promptly, and only the muscula-ture be used. Moreover, the meat should be

cut or torn into small bits, and soaked in waterfor a minimum of 3 or 4 hours. buring thisperiod the flesh should be kneaded while in thewater, and the water changed at frequent inter-vals. The toxin is water-soluble and leachingwill effectively remove it.In dealing with potential ciguatera type of

fishes it should be kept in mind that the mostreliable methods of determining edibility in-volve the preparation of tissue extracts whichare injected intraperitoneally into mice, or feed-ing samples of the viscera and flesh to cats, ordogs, and observing the animals for the devel-opment of toxic symptoms. Viscera, that is,liver and intestines of tropical marine fishshould never be eaten. Also, the roe of mostmarine fish is potentially dangerous, and insome cases may produce rapid death. Fisheswhich are unusually large for their speciesshould be discarded, particularly barracuda(Sphyraena), jacks (Cranax), and grouper(Epinephelwm), during their reproductive sea-son. If one is living under survival conditionsand questionable fish must be eaten, it is advis-able to cut the fish into thin fillets and soakthem in several changes of water for at least30 minutes. This will serve to leach out thepoison which is readily water-soluble. Do notuse the rinse water for cooking purposes. If aquestionable species is cooked by boiling, thewater should always be discarded. Again itshould be pointed out that ordinary cookingprocedures do not attenuate ichthyosarcotoxins.

SummaryFish poisoning is a disease of antiquity.

Fishes are believed to become poisonous as aresult of their food habits-feeding on marinealgae. There is no evidence that plankton orradioactive substances are a factor in the pro-duction of the poisons. Poisonous fishes arelargely circumtropical in their distribution.Toxin content is greatest in puffers during theirreproductive season of the year, but this is prob-ably not true of most other fishes. The distri-bution of the toxin within the body of thefish is subject to considerable fluctuation, but ifthe fish is poisonous, some of the poison willbe present in the viscera in about 90 percent ofthe cases. Poisonous fishes cannot be detectedby their appearance.

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Fish poisoning should not be confused withbacterial food poisoning, with which it has noetiological connections. The overall incidenceof fish poisoning is not known. There areeight clinical types of ichthyosarcotoxism rec-ognized at present. With the exceptions ofgempylid diarrhea and scombroid poisoning,all other types of ichthyosarcotoxism are char-acterized by neurotoxic symptoms. The treat-ment of fish poisoning is symptomatic. Little isknown about the chemical and pharmacologicalproperties of fish poisons.

REFERENCES

(1) Gaillard, C.: Recherches sur les poissons repr&sentes dans quelques tombeaux Bgyptiens del'ancien empire. Mem. Inst. Frangais Arch.Orient. 51: 97-100 (1923).

(2) Autenreith, H. F.: Ueber das Gift der Fische.Tuibingen, C. F. Osiander, 1833, 287 pp.

(3) Gudger, E. W.: Poisonous fishes and fish poison-ing, with special reference to ciguatera in theWest Indies. Am. J. Trop. Med. 10: 43-55,January 1930.

(4) Baughman, J. L.: The marine fisheries of theMayas as given in Diego de Landa's "Relacion delas cosas de Yucatan" with notes on the prob-able identification of fishes. Texas J. Sc. 4:432-459, April 1952.

(5) Phisalix, M.: Animaux venimeux et venins.Paris, Masson et Cie., 1922, vol. 1, pp. 487-628.

(6) Gilman, R. L.: A review of fish poisoning in thePuerto Rico-Virgin Islands area. U. S. Nav.Med. Bull. 40: 19-27, January 1942.

(7) Hiyama, Y.: Report on the research on poison-ous fishes of the South Seas. Odawara, Japan,Nissan Fisheries Experiment Station, 1943, pp.1-137. Also English translation in U. S. Fishand Wildlife Service Spec. Scient. Rep. No.25. Washington, D. C., U. S. Government Print-ing Office, 1950, pp. 1-188.

(8) Arcisz, W.: Ciguatera, tropical fish poisoning.U. S. Fish and Wildlife Service Spec. Scient.Rep. No. 27. Washington, D. C., U. S. Gov-ernment Printing Office, 1950, pp. 1-23.

(9) Fish, C. J., and Cobb, M. C.: Noxious marine ani-mals of the central and western Pacific Ocean.U. S. Fish and Wildlife Service Res. Rep.No. 36. Washington, D. C., U. S. GovernmentPrinting Office, 1954, pp. 1-45.

(10) Halstead, B. W., and Lively, W. M.: Poisonousfishes and ichthyosarcotoxism. U. S. ArmedForces M. J. 5: 157-175, February 1954.

(11) Whitley, G. P., and Halstead, B. W.: An anno-tated bibliography of the poisonous and veno-mous fishes of Australia. Rec. Australian Mus.23: 211-227, September 1955.

(12) Ross, S. G.: Preliminary report on fish poison-ing at Fanning Island (Central Pacific). M.J. Australia 2: 617-621, Nov. 22, 1947.

(13) Halstead, B. W.: Current status of research onPacific poisonous fishes and ichthyosarcotoxism.In Symposium on venoms, edited by E. B. Buck-ley and Nandor Porges. American Associationfor the Advancement of Science Pub. No. 44.Washington, D. C., 1956, pp. 29-32.

(14) Kawabata, T., Halstead, B. W., and Judefind, T.F.: A report of a series of recent outbreaks ofunusual cephalopod and fish intoxications inJapan. Am. J. Trop. Med. & Hyg. 6: 935-939(1957).

(15) Halstead, B. W.: Ichthyotoxism. A neglectedmedical problem. M. Arts & Sc. 5: 115-121,Fourth Quarter, 1951.

(16) Halstead, B. W., and Bunker, N. C.: A survey ofthe poisonous fishes of the Phoenix Islands.Copeia 1954: 1-11, January.

(17) Dawson, E. Y., Aleem, A. A., and Halstead, B.W.: Marine algae from Palmyra Island withspecial reference to the feeding habits and toxi-cology of reef fishes. Allan Hancock Found.Pub. Occ. Pap. 17: 1-39 (1955).

(18) Habekost, R. C., Fraser, I. M., and Halstead, B.W.: Observations on toxic marine algae. J.Washington Acad. Sc. 45: 101-103, April 1955.

(19) Fukuda, T., and Tani, I.: Statische Beobachtunguiber die Fuguvergiftung. Japanese J. M. Sc.(IV. Pharm.) 10: 48-50 (1937).

(20) Fukuda, T.: Violent increase of cases of pufferpoisoning. Rinsho to Kenkyu 29: 5-12, Feb-ruary 1952.

(21) Steinbach, E.: Bericht uber die Gesundheitver-hialtnisse der Enigeborenen der Marshall-Inselnim Jahre 1893-94 und Bemerkung fiber Fisch-gift. Mitt. Forschung. Gelehrt. Deutsch.Schutzgeb. 8: 157-171 (1895).

(22) Matsuo, R.: Study of the poisonous fishes atJaluit Island. Nanyo Gunto Chihobyo ChosaRonbunshu 2: 309-326 (1934).

(23) Yasukawa, T.: Report of an investigation ofpoisonous fishes within the Jurisdiction of theSaipan branch of the Government-General.Tokyo, Imperial University Contagious DiseaseResearch Institute, 1935. Also English trans-lation in U. S. Fish and Wildlife Service Spec.Scient. Rep. No. 25. Washington, D. C., U. S.Government Printing Office, 1950, pp. 189-197.

(24) Halstead, B. W.: Some general considerations ofthe problem of poisonous fishes and ichthyosar-cotoxism. Copeia 1953: 31-33, January.

(25) Khlentzos, C. T.: Seventeen cases of poisoningdue to ingestion of an eel, Gymnothora, faavi-marginatus. Am. J. Trop. Med. 30: 785-793(1950).

(26) Ralls, R. J., and Halstead, B. W.: Moray eelpoisoning and a preliminary report on theaction of the toxin. Am. J. Trop. Med. & Hyg.4: 136-140, January 1955.

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(27) Gudger, E. W.: A new purgative, the oil of the"castor oil fish," Ruvettus. Boston M. & Surg.J. 192: 107-111, March 1925.

(28) Geiger, E.: Histamine content of unprocessedand canned fish. A tentative method of quanti-tative determination of spoilage. Food Res.9: 293-297 (1944).

(29) Halstead, B. W., and Schall, M. C.: A report onthe poisonous fishes captured during the Wood-row G. Krieger expedition to the GalapagosIslands. In Essays in the natural sciences inhonor of Captain Allan Hancock. Los Angeles,University of Southern California Press, 1955,pp. 147-172.

(30) Halstead, B. W., and Schall, M. C.: A report onthe poisonous fishes captured during the Wood-

row G. Krieger expedition to Cocos Island.Pacific Sc. 10: 103-109, January 1956.

(31) Courville, D. A., Halstead, B. W., and Hessel,D. W.: A review of the literature concerningthe chemistry of marine biotoxins. Chem.Rev. In press.

(32) Engelsen, H.: Om giftfisk og giftige fisk. Nord.hyg. tidskr. 3: 316-325 (1922).

(33) Kawabata, T., Ishizaka, K., and Miura, T.:Studies on the food poisoning associated withputrefaction of marine products. III. Physio-logical and pharmacological properties ofnewly isolated vagus-stimulant, named "sau-rine" (in Japanese). Bull. Japanese Soc.Scient. Fish. 21: 347-351 (1955).

"Model" Law to Cut Poison Deaths

The American Medical Association's Com-mittee on Toxicology has formulated a "model"law for the precautionary labeling of hazard-ous substances in commercial, household, andindustrial chemical products.The labeling would apply to hazardous sub-

stances defined as toxic, irritating, sensitizing,corrosive, flammable, explosive, or radioactiveunder customary or reasonably anticipatedconditions of handling or use.

"Model" text would require declaration ofhazardous ingredients and warning statementson the label and in the literature accompanyingchemical products.

Requirements of the model law are:* Labeling of all chemical products contain-

ing hazardous substances that are not nowregulated.

* Applications of the same labeling stand-ards to chemicals for domestic use and for ex-port. (This will refute the common com-plaint that inferior standards apply to foreigncustomers.)

* Prohibition of re-use of food and drug con-tainers bearing their original labels.

* Identification and warnings for stronglysensitizing chemicals which cause allergic orinflammatory reactions in living tissue oncontact.A significant departure in the new law is the

deletion of the word "poison." Referencestandards, based on animal tests, provide amore consistent and reliable index of poison-ous properties than did the former label, ac-cording to the committee, not only becausethere are variations in existing legal limits forpoison but also because there is a lack ofagreement among scientists on a definition ofthe term.

Inadequate labeling of potentially harmfulchemicals, the committee reports, has been amajor handicap to a successful attack on theproblem of accidental poisoning. Moreover.lack of information about hazardous ingredi-ents may complicate or delay treatment inemergency situations.The committee's work in formulating a

model law was endorsed by various organiza-tions such as the National Drug Trade Confer-ence, the American Public Health Association,the Cincinnati Academy of Medicine, and thePennsylvania Pharmaceutical Association.

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