94 TRANSACTIONS OF THE ROYAL SOCIETY OF TROPICAL MEDICINE AND HYGIENE. Vol. 69. No. 1. 1975.

MEDICAL

HAZARDS MICHAEL

OF THE CORAL

REEF

SOROKIN

Consultant Physician, Lautoka Hospital, Lautoka, Fiji. Coral reefs are the homes of some of the most beautiful and flamboyant creatures alive and are a major tourist attraction for any country fortunate enough to possess them. Amidst the beauty, however, lurk dangers understandably not publicised by travel agents and tourist bureaux. This paper presents some aspects of the problem as seen in Fiji. The Fiji group consists of 2 main land massesand nearly 300 smaller islands and coral atolls straddling the 180” meridian at 15”-22”s. The volcanic land masseshave fringing and barrier reefs with an abundance of marine life. A population widely scattered o 7er the islands means that accurate recording of the prevalence of poisoning is difficult and this is aggravated because many victims do not seek medical help. This account therefore describes only some points of interest. MILLS (1956) writing from New Hebrides, summarized the known pattern of poisoning in the South Pacific and FLECKER (1957) was responsible for outstanding work on injuries and envenomings. Since then extensive knowledge has been gained (HALSTEAD, 1959, 1965-1967; BANNERand HELFRICH, 1964; BANNER, 1965; CLELAND and SOUTHCOTT, 1965) and reference to the publications quoted will supply a comprehensive bibliography. Envenomings The term refers to parenteral injection of toxin by a spine, barb or tentacle. Most dramatic of such poisonings is the sting of the box jelly-fish or sea-wasp (ChironexJEeckeri) which has caused fatalities off the Queensland coast (CLELAND and SOIJTHCOTT, 1965). Fortunately we have not had experience of this in Fiji. The sea-wasp is a coelenterate as is the coral polyp, and scratches sustained from live coral are notorious for producing prolonged sepsis (BYRNE, 1924; PRESTON, 1950). The precise nature of the injury produced is uncertain although it is generally thought to be a foreign body reaction. However, limited experiments here suggest that it is possible to enrich a culture medium (MacKonkey’s) which will not normally grow staphylococci easily, in such a way as to encourage profuse growth of inoculated Staphylococcus pyogenes by introducing material from live coral into the medium. Echinoderms (starfish and sea-urchins) are a common cause of trouble in Fiji waters but only the unusual cases present at hospital CASE 1. M.R. A 40 year old man slipped and fell on the reef while fishing, his right knee coming down onto a “Vulawalu” i.e. crown-of-thorns starfish, Acanthuster plunci-tie Fijian name means “eight months” (of pain). When he puhed the animal off some of the small spines broke off in the wound. Although the wound was extremely painful he put up with it for 10 days when he finally presented as a very sick man in obvious pain with cellulitis circumferentially involving the leg from mid-calf to groin. There were seven puncture wounds around the knee exuding pus. Staphylococcus pyogenes was cultured from the wound and he was successfully treated with surgical drainage and antibiotics, taking a fortnight for full recovery. CASE 2. V.T. A 32 year old woman was referred with a 10 year history of a lump in the foot (Fig. 1). She remembered standing on a spiny sea-urchin, probably Diadema setosum (Fig. 2) which did not worry her much at the time but a painful swelling gradually developed which burst spontaneously leaving a chronic sinus. This process repeated itself again and again until she was left with a large non-tender masswith numerous sinuses occasionally discharging a small amount of pus. There was no lymphadenopathy or fever and no radiological bony change. Histological examination of biopsy material showed patchy, inflammatory foci extending into the subcutaneous tissue with multinucleate giant cells surrounding irregular masses of what were thought to be aggregated cocci. However, there was no bacterial or fungal I wish to thank the Permanent Secretary for Health of Fiji for permission to publish, Professor A. H. Banner of Hawaii for information and for generous hospitality, and Dr. H. Alastair Reid of the Liverpool School of Tropical Medicine for suggesting publication and for encouraging advice.

MICHAEL

95

SOROKIN

growth on culture. She showed fairly good improvement following 6 weeks of treatment with tetracycline and sulphadimidine. The patchy distribution of foci was no doubt the result of inoculation of skin organisms into the deeper tissues by the spines of the sea-urchin: these then induced a granulomatous reaction and a chronic lesion simulating “Madura foot”.

FIG. 1. Case 2. Chronic granulomafous lesion on sole of foot sustained by standing on spiny sea-urchin.

f

FIG. 2. The spiny seaurchin Diadema setosum 1 moving towards the

I

shelter of a coral rock at low-tide.

The other main group of invertebrates causing envenoming are the cone-shells (members of the Conidae family of molluscs). Severe and even fatal poisonings are well-documented (FLECKER, 1936; SARRAMEGNA, 1965) but only one trivial case has presented to me in the past seven years. However, MALPRESS (1972) reported a case of sting from the RoIlus geographus causing local necrosis, paraesthesiae, diplopia and muscle weakness. The

“Deadly”

Stonefish

This drab, ugly sluggish creature looking so like a piece of the dead coral rock that is its habitat, has an evil reputation throughout the Indo-Pacific area. The two species .Synanceja horridu (syn. trachynis) and Spanceja vermcosa are found in tropical waters off the coasts of East Africa, Australia, New Guinea, the Phillipines and the South Pacific isles. So dreaded is the stonefish that the victim of a fish sting sustained in coral shallows understandably gets out of the water as quickly as possible without bothering to investigate

96

MEDICAL HAZARDS OF THE CORAL REEF

exactly what creature he has been involved with; as there are many other fish capable of inflicting painful stings, positive identification is thus not always possible. Occasionally the victim is certain. CASE 3. E.K. A 36 year old man was wading barefoot on the reef at low tide when he saw a “lewa matua” (local name for synance$z spp.) just as he was stepping on to it. Unable to arrest his tread he was stung on the instep by two spines. Within minutes the foot had become tense and extremely painful. When first seen an hour later he was crying with agonising pain. There were no other symptoms, however, and apart from tachycardia and sweating no signs of systemic involvement. In a dramatic description quoted by WIENER (1958) Dr. W. Armstrong made strong claims for the efficacy of local emetine hydrochloride, so 60 mg. in solution were infiltrated into the wound track of this patient but with no effect, and he was not made free of pain until the area had been anaesthetized with 2% lignocaine. Antibiotics were given but the limb became swollen and regional adenitis and pyrexia developed. The systemic signs settled within 2 days but oedema persisted for 3 weeks. The venom produces paralysis, pulmonary haemorrhage, oedema and respiratory failure in laboratory animals (WIENER, 1958); in the paper quoted, WIENER reported a case with disturbed vision, semiconsciousness and breathing difficulty. My experience is limited to 6 cases and in none have there been systemic effects other than tachycardia, pyrexia and rigors. FLECKER (1956) minimized the effects and WOOLFORD(1965) questioned whether many cases described were in fact of stone-fish poisoning. In a series of 81 cases from Singapore, PHOON and ALFRED (1965) found none showing significant systemic signs. Where descriptions of death due to stonefish poisoning exist they are second-hand (WIENER, 1958; SMITH, 1957) and death may have been due to secondary infection rather than to the direct effect of stonefish venom. Clinical features of any envenoming must be the net resultant of dosage, toxicity of the venom at the time, site of sting and body resistance. For instance REID (1962) states that 73% casesof unequivocal sea-snake bites had no poisoning at all; conversely 9% were fatal. Thus the clinical manifestations of stone-fish sting are likely to be variable and cases should be managed watchfully, but the term “deadly” is a melodramatic misnomer. That the sting causes excruciating pain is without question; indeed there is a credible belief that death may occur from drowning as the hapless victim thrashes about in agony. Locally, tissue necrosis occurs. Persistence of oedema maybe due to loss of vasomotor and venomotor tone as in these cases the limb is emptied readily on elevation and fills like a bag on lowering. The venom is heat labile and emergency relief of pain may be achieved by immersing the limb in very hot water (REID, 1973). Stonefish antivenene is available from the Commonwealth Serum Laboratories, Melbourne and is reported as effective even in casesseen late (TRINCA, 1967) but has the drawbacks inherent in horse-serum preparations. Poisoning In this context the term refers to poisoning by ingestion. Fish poisoning is by far the commonest form of poisoning in the islands and presents a not unimportant public health problem. 3 distinct forms of poisoning occur in Fiji, viz, clupeid, tetraodon and ciguatera poisoning. Clupeid poisoning is a seasonal form caused by ingestion of the sardine-like &pea venenosaand related species (“daniva”) but cases are very rare because its toxicity is well-known locally. Tetraodon or pufferfish poisoning is also uncommon which is surprising because many Fijians, like Japanese, regard the flesh of the puffer as a delicacy. SOUTHCOTT(1973) comments laconically that “even though in Japan there are restaurants which are licensed to cook and sell these fishes . . . every year a number of Japanese die from eating them.” Only one outbreak has been reported from Fiji (SOROKIN, 1967) in which there was 1 death. In 2 cases in this group improvement followed intravenous neostigmine, lending support to the claims for the efficacy of edrophonium and neostigmine used in a case described by TORDA et al. (1973). Ciguatera poisoning The commonest form of fish intoxication as well as the most fascinating is ciguatera poisoning. (A remarkable account is to be found in the journals of Captain Cook.) During the months of October-March 1971-1972, 102 cases were treated in this hospital’s out-patient department and 86 cases presented during the 1972-73 season. Fish which cause ciguatera poisoning are usually large reef carnivores and in recent years the main culprit in our area has been the 5”hyraena barracuda (local name “Ogo”). Previously most cases resulted

MICHAEL

SOROKIN

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from eating “damu” = Lutjanus bohar known as red snapper (U.S.A.) or red bass (Australia) but most people now avoid this fish and indeed sale of it is prohibited in some markets. A list of 15 fish reported as toxic in Fiji waters was compiled by BANNER and HELFRICH (1964) but the world-wide list runs to 10 pages (BAGNISet al., 1970). Even this list omits the Cybium commersuniimplicated by TONGE et al., (1967) in an outbreak in Queensland and I have had a case attributed to a “Kerekere-i-cula” which is thought to be a member of the Holocanthus genus, also not included in the list. Few species are always poisonous; some are seasonally dangerous; some may be poisonous one year and not the next; fish of the same species may be toxic on one side of the reef and not on the other; areas known to be “safe” may suddenly, mystifyingly produce cases of poisoning. The biology of ciguatera poisoning remains a fascinating puzzle. Profound muscle weakness, bradycardia and strange, “inverted” sensations (hot feeling cold, and vice versa) are some of the outstanding clinical manifestations, but there are many others. An excellent summary of the clinical features is given by BAGNIS (1968) and he suggests that the wide spectrum of symptoms and signs may result from the fact that a variety of toxins is involved. Gastro-intestinal upsets are common to all forms of ciguatera poisoning but certainly we have not recently had the high incidence of paraesthesiae and bizarre dysaesthesiae which were frequent when most cases were of “damu” poisoning. Conversely, now that most of our casescome from barracudas we have been struck by the frequency of patients with bradycardia and hypotension which respond to atropine. Ciguatoxin has been isolated (SCHEUER et al., 1967) and is fat-soluble but recently a second, water-soluble toxin has been found in association with it in surgeonfish (YASUMOTO et al., 1971). If indeed the clinical manifestations result from more than one toxin each with different pharmacological properties, rational therapy must await the elucidation of the nature of these toxins. Most casesof poisoning whether by ingestion or envenoming are treated by busy non-academic doctors in remote areas who do not normally publish their results-which is a pity because although there is considerable toxicological knowledge available in the literature more definite clinical facts are needed.

Summary An account is given of some aspects of poisonings sustained by coming into contact with animals of the coral reefs of the Fiji Islands. Poisonings can be grouped into those in which the toxin is introduced parenterally-envenomings, and those in which it is ingested. Illustrative case histories are presented of injuries from 2 echinoderms and of envenoming from the “deadly” stonefish. A therapeutic approach to puffer-fish poisoning is mentioned and the problem of ciguatera poisoning is outlined. REFERENCES BANNER, A. H. (1965).

-,

Hawaii med. J., 24, 353.

HELFRXH, P. (1964). The distribution of Ciguatera in the Tropical Pacific. Hawuii Marine Laboratory Technical Report No. 3.

BAGNIS, R. (1968). Hawaii med. J., 28, 25. -, BERGLUND, F., ELIAS, P. S., VANESCII, G. J., HALSTEAD, B. W. & KOJIMA, K. (1970). BUZZ.WZd Hlth

Org., 42, 69.

BYRNE,K. (1924). Med. 3. Aus., 2, 694. J. B. & SOUTHCOTT, R. V. (1965). National Health and Medical Research Council: Special Report Series No. 12 Canberra. FLECKER, H. (1936). Med. 3. Aus., 1, 464. (1956). Ibid., 2, 371. (1957). Ibid., 2, 556. HALSTEAD, B. W. (1959). Dangerous Marine Animals. Cambridge, Maryland: Cornell Maritime Press. (1965), (1966), (1967). Poisonous and venomous Marine Animals. Vols. I-III. Washington, D.C.: U.S. CLELAND,

MALPRESS,

Government Printing Office. W. A. (1972). F;ii Sch. Med. J., 7, 150.

MILLS, A, R. (1956). 3. trop. Med. Hyg., 59, 99. PHOON, W. 0. & ALFRED, E. A. (1965). Singapore med. J., 6, 158. PRESTON, F. S. (1950). Br. med. J., 1, 642. REID, H. A. (1962). Ibid., 2, 576. (1973). Toxins of Animal and PZunt origin (Ed. de Vries, A. and Kochva, E.) Vol. III, p. 961. London: Gordon and Breach. SARRAMAGNA, R. (1965). South Pacific Commission Technical Paper No. 144. Noumeu, New Caledonia. SCHEUER, P. J., T AKAHASHI, W., TSUTSUMI, J. & YOSHIDA, T. (1967). Science, 155, 1267. SMITH, J. L. B. (1957). Copeia, 3, 249. SOUTHCOTT, R. V. (1973). Supplement to Impulse, 12, 17. EmDntrude: Winthrop Laboratories, N.S.W. SOROKIN, M. (1967). Fii; Sch. med. J., 2, 9.

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TONGE, J. I., BATTEY, Y., & FORBES,J. J. (1967). Med. J. Aus., 2, 1088. TORDA, T. A., SINCLAIR, E., ULYATT, D. B. (1973). Ibid., 1, 599. TRINCA, J. C. (1967). In Symposium on some Queensland Marine Species of Pharmacological Interest. Brisbane (quoted by Southcott, R. V. vide supra). WIENER, S. (1958). Med.J. Aus., 2, 218. WOOLFORD, H. (1965). Ibid., 1, 368. YASUMOTO, T., HASHIMOTO, Y., BAGNIS, R., RANDALL, J. E. & BANNER, A. H. (1971). Bull. Jap. Sot. scient.

Fish., 37, 724.

Medical hazards of the coral reef.

An account is given of some aspects of poisonings sustained by coming into contact with animals of the coral reefs of the Fiji Islands. Poisonings can...
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