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Envenomation and Consumption of Poisonous Seafood

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Envenomation and Consumption of Poisonous Seafood EDITORIAL 103 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.73.2.103 on 1 August 2002. Downloaded from Natural toxins destruction of the nerve terminal and ................................................................................... the terminal parts of the motor axon. Many of the presynaptically active neuro- toxic phospholipases are also potent Envenomation and consumption of myotoxins, and therefore the victims of envenoming bites by some snakes (for poisonous seafood example, sea snakes, Australian elapids, Berg adders, South American rattle- A Goonetilleke, J B Harris snakes) may be weak as a result of both neurotoxic and myotoxic damage. ................................................................................... The varied aetiology of neurotoxic involvement in snake envenomation in- Effects of naturally occurring toxins on the human nervous fluences the treatment and management system and available treatments are discussed of individual snakebites. Elapid snakes will always inoculate postsynaptically xposure to natural toxins is becom- cobras) can emit a fine spray of venom active neurotoxins. Severely envenomed ing more commonplace because of from the tips of their fangs and thereby victims will need ventilatory support. Egreater worldwide travel, increasing “spit” the venom for a distance of several The dissociation of neurotoxins from metres into the eyes of their prey. The AChR is probably accelerated by anti- captivity of exotic animals in private and 7 institutional collections, and an expan- vipers and pit vipers (families Viperidae venom and possibly by anticholineste- sion in the trade in tropical seafood. and Crotalidae) are relatively bulky rases. If ventilatory support is main- Although the effects of natural toxins are snakes with large heads and fangs that tained and appropriate treatment with often trivial, some may result in neuro- fold into the roof of the mouth at rest— antivenom and possibly anticholineste- rases is available, recovery will be rapid logical emergencies. A good understand- envenomation always causes defibrina- and uneventful. If appropriate antiven- ing of the origin and management of tion, extensive soft tissue haemorrhages, oms are unavailable respiratory support neurotoxic poisoning is therefore impor- and bleeding from gums, old wounds for 24 hours will usually allow full recov- tant for the neurologist interested in and orifices. In contrast the snakes of the ery. Venoms of most elapid snakes (for tropical medicine. The true incidence of family Elapidae (for example, kraits, example, cobras and coral snakes) typi- neurotoxic poisonings is impossible to mambas, cobras) and of the related fam- ily Hydrophiidae (sea snakes) have short cally contain only postsynaptically active ascertain because of underreporting. It neurotoxins. If the victim exhibits neuro- has been suggested that each year there fixed fangs and inoculate a venom that is characteristically neurotoxic; an enveno- toxic signs but shows little or no may be up to 1000 deaths in the Mahar- response to the relevant antivenoms or ashtra state of India 1 and 600 deaths in mation by these snakes, though often associated with defibrination, is rarely anticholinesterases it is likely that the Sri Lanka resulting from snake bites, and venom contains presynaptically active 1000 to 2000 deaths in Mexico after associated with significant haemorrhage or local tissue damage. This distinction neurotoxins; the victim will therefore scorpion stings. Tick paralysis has been need ventilatory support and conserva- estimated to cause the death of 10 000 may be misleading, as envenoming bites 2 by some viperids and crotalids (for tive management for several days until calves each year. There are thought to be damage to the neuromuscular systems around 50 000 human victims of ciguat- example, the Berg adder, Bitis atropos of 3 Southern Africa, and the South Ameri- are repaired. Myotoxicity may be recog- era poisoning each year. can rattlesnake, Crotalus durissus terrifi- nised by the presence of muscle pains, This editorial briefly outlines some of cus) inflict an envenoming bite that pro- especially on movement, and myoglo- the effects of naturally occurring toxins 8 duces significant neurotoxic signs; an binuria. Such patients need careful on the human nervous system. We http://jnnp.bmj.com/ envenoming bite by the Asian monocel- management to prevent acute renal fail- suggest that a general awareness of the lated cobra, Naja kaouthia, is responsible ure caused by the release of myoglobin circumstances in which exposure to for very severe and disfiguring local from the damaged muscle. Envenoming natural toxins may occur and of the superficial necrosis. bites by the South American rattlesnake, expression of poisoning in the form of The neurotoxic signs (for example, Australian tiger snake, Australian king clinical features will improve the preven- ptosis, ophthalmoplegia, dysphoria, in- brown (mulga) snake, the taipans of tion, detection, and management of ability to protrude the tongue or smile, Australia and Papua New Guinea and these potentially fatal conditions. Three generalised weakness) can be caused by sea snakes are particularly liable to cause recent texts discussing some of these the actions of three major groups of muscle damage. on October 1, 2021 by guest. Protected copyright. issues are available to the interested toxin. Postsynaptically active neurotox- Two groups of elapid snakes, the kraits 4–6 reader. ins bind to the α-subunit of the acetyl- and mambas, are worthy of special men- choline receptor (AChR) at the neuro- tion. Kraits are nocturnal, snake-eating ENVENOMATION muscular junction, causing what is animals. Envenoming bites may be so Snakes somewhat loosely called a curare-like innocuous as to fail to arouse a sleeping Venoms enable snakes to immobilise and neuromuscular paralysis. These toxins victim, and it is uncommon for the initiate the digestion of their prey. The are found in the venoms of all elapid and offending snake to be seen. A victim who venom is usually introduced into the vic- hydrophid snakes. Presynaptically active sleeps in the open or in a simple rural tim through a pair of fangs. Inspection of neurotoxins are found in the venoms of shelter anywhere in South East Asia and the bite site may show one or two fang many elapid snakes, especially the elapid who awakes with morning weakness, puncture marks, single or multiple snakes of Australia and Papua New loin pain, and a metallic taste in the scratch marks where fangs were dragged Guinea, the kraits of South East Asia, mouth has possibly been bitten by a across the skin, or a mixture of puncture and in the venoms of some vipers and krait. The difficulty of identifying a marks and scratches. The presence of crotalids (for example, Berg adder, South biting snake, and the fact that the onset multiple puncture marks at different American rattlesnake, Russell’s viper of of serious weakness may be slow can sites and in different orientations is sug- southern India and Sri Lanka). The tox- mean that victims often delay seeking gestive of multiple bites and a potentially ins are active phospholipases. They bind medical attention. This can be a signifi- serious envenomation. Some snakes (for to motor nerve terminals, causing the cant problem. Envenoming bites by example, African and Asian spitting depletion of synaptic vesicles and the kraits are difficult to manage because the www.jnnp.com 104 EDITORIAL J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.73.2.103 on 1 August 2002. Downloaded from Table 1 Envenomation Envenoming species Location Features Snakes Elapidae Cobras, kraits, mambas, coral Africa, Asia, Australasia Local effects unusual.* Early neurotoxic effects, especially snakes, Australasian venomous blurred vision and ptosis. Some Australasian elapids† cause snakes haemostatic effects, rhabdomyolysis and renal failure Viperidae/Crotalidae Vipers, adders, rattlesnakes, Africa, Asia, Europe, N and S Severe local and haemostatic effects (especially gingival moccasins America bleeding) common. Hypertension and shock (especially N American rattlesnakes). Renal failure commonest cause of death. Neurotoxic effects unusual‡ Colubridae Comprise & all known species of Africa, Asia, Australasia, Europe, Envenomation may develop slowly over many days, varying snake S America from local swelling to repeated vomiting, abdominal pain, headache, haemostatic effects and renal failure Atractaspididae Burrowing asps or stiletto snakes Africa, Middle East Local effects. Violent gastrointestinal (nausea, vomiting, diarrhoea) and respiratory (dyspnoea, respiratory failure) effects Hydrophiidae Sea snakes Pacific and Indian oceans Initial headaches, thick feeling of tongue. Flaccid paralysis and rhabdomyolysis later Spiders Latrodectus Black widow or redback spiders Asia, Australasia, Europe, N Painful needle-like bite, may lead to painful local America lymphadenopathy within 30 minutes. Painful muscle spasms§ and rigidity throughout body. Autonomic effects Phoneutria Wandering or banana spiders S America Painful bite leading to burning sensation, spreading proximally in limb. Autonomic effects, temporary blindness, respiratory distress Atrax Funnel web spiders Australasia Painful bite. Neurotoxic symptoms (perioral numbness, spasms of tongue) may occur within 10 minutes. Autonomic effects, muscle spasms, dyspnoea, and coma Scorpions Buthus N Africa, S Europe, Middle East Painful sting. Cardiac dysrythmias, thirst, urinary retention,
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