The majority of venomous snakes have fangs at the front of their mouths which enable them to inject venom. This is produced by the venom glands, of which there are two, one on each side of the head behind the eye. Each gland is surrounded by muscle, which, on contraction, forces the venom out of the lumen of the gland, along the venom duct, which is positioned on either side of the upper jaw, and then down the canal or groove in the fang. Venomous snakes are divided into three major groups: elapids (fam ily Elapidae), sea snakes (family Hydrophiidae) and vipers (family Viperidae). There is also a small group of venomous colubrids (back-fanged snakes) which include the boomslang (Dispholidus typus) found in southern Africa and the red-neck keel-back snake (Rhabdophis sub-miniatus) in Southeast Asia. Elapids are landsnakes with short fixed fangs covered by a gum-fold, the vagina dentis. Sea snakes have very short fixed fangs and characteristic flattened tails; they are most common in Asian coastal waters. The Viperidae is divided into the true vipers (Vi-perinae) and the pit vipers (Crotalinae). These snakes have long, erectile fangs and triangular heads (Figure 21.1); their bodies are usually shorter and fatter than those of most elapids. The pit vipers possess a thermosen-sitive (loreal) pit between the eye and the nostril which is used for detecting warm-blooded prey in the dark; most snakes have diurnal hunting habits. The true vipers do not possess these loreal pits.
Viper bites are much more common than elapid bites, except in the Pacific Australasian area where vipers do not naturally occur. Sea snake bites used to be common among fishing folk of Asian and western Pacific coastal areas but, because of recent modernisation of fishing methods, they have become much rarer. In South and Central America, snakes of medical importance include Bothrops atrox (the Barba amarilla, often miscalled fer-de-lance, which probably causes more deaths in South and Central America than any other snake) and the tropical rattlesnake (Crotalus durissus). In Africa, the puff adder (Bitis arietans), cobras (mostly Naja species), mambas (four species of Dendroaspis) and the carpet or saw-scaled viper (Echis species) are common. Members of the genus Echis almost certainly cause more snakebite deaths than any other snake in the world, particularly in farmers. In parts of Asia, Russell's viper (Daboia russelii), the Malayan pit viper (Calloselasma rhodostoma), the saw-scaled viper (Echis carinatus), the sharp-nosed pit viper (Agkistrodon acutus), the Mamushi pit viper (A. halys), the Habu viper (Trimeresurus flavoviridis), cobras (mainly Naja species) and kraits (Bungarus caeruleus and B. multi-cinctus) are important. In Australasia, which has some of
Principles and Practice of Travel Medicine. Edited by Jane N. Zuckerman. © 2001 John Wiley & Sons Ltd.
the most venomous land snakes in the world, there are no vipers. One of the most important species in this region is probably the Papuan taipan (Oxyuranus scutellatus canni) which is the main cause of death due to snake bite in Papua New Guinea and probably also in Irian Jaya.
Snake bite is mainly a rural and occupational hazard and therefore affects men more than women; farmers, plantation workers, herdsmen and hunter gatherers are at greatest risk. Children also are frequently bitten due to their inquisitive nature; for example, they may play with snakes or put their hands down old rat holes or behind piles of stones or sticks where snakes may be lurking. Travellers and foreign visitors are entering rural areas of the tropics more frequently and this is resulting in more accidents. Most bites occur in the daytime and involve the foot, toe or lower leg as a result of accidentally disturbing a snake; however, some species of snake (e.g. kraits) may bite sleeping victims at night. Bites by sea snakes, although rare, may occur in holiday makers who swim in the sea or in rivers to which sea snakes have access.
Snake bite statistics based on hospital figures are misleading because in the rural tropics, where snake bite is common, victims rarely go to hospital, preferring treatment from traditional healers. In Bangladesh, for example, snake bite victims will visit the ohzas, in Sri Lanka the ayurvedic healers and in Ecuador the local shamans. In Nigeria, one such healer treats several hundred snake bite patients each year, his house being just a mile from one of the largest university teaching hospitals in Africa, which records only about five cases annually. It is unclear whether traditional therapy has benefits; most local healers do not wish to give away their secrets. The main problem when patients visit such healers is that the admission of patients to the hospital is delayed. This delay, in cases of severe envenoming, can result in a fatal outcome. Some years ago when sea snake bite was a problem in Asian coastal areas, less than 15% of those bitten sought treatment from the government medical services.
Enzyme-linked immunosorbent assay (ELISA) has been used, combined with information obtained from survey questionnaires, to reliably identify specific venom antibodies in the blood of individuals envenomed by snakes in the past (Theakston et al., 1977; Theakston, 1991). Such detailed rural survey procedures have revealed a higher incidence of snake bite, and a higher mortality from this cause, than previously suspected. This reinforces the fact that hospital figures grossly underestimate the real extent of the problem. On the basis of such findings in northern Nigeria, it is estimated that snake bite causes many thousands of deaths per annum in the West African savannah, mainly due to the carpet viper, Echis ocellatus (Pugh and Theakston, 1980). Likewise, in Amazonian Ecuador and Brazil, the incidence and mortality due to snake bite in the indigenous Indian populations, such as the Waorani in Ecuador and the Kaxinawa in northwest Brazil, is simply not recorded in the snake bite statistics of the country. It is estimated that almost 5% of Waorani Indians in northeastern Ecuador die annually from snake bite. A group of anthropologists reported that 45% of the population had experienced at least one snake bite and 95% of all adult males have been bitten once (Larrick et al., 1978). These risks also apply to travellers, especially in remote areas such as this which are now readily accessible by small aeroplane or by road following the opening up of many regions in the Amazon and other remote areas by oil and timber companies.
The incidence of snake bite in Sri Lanka, a popular holiday location, is currently one of the highest in the world, with 400 bites and six deaths per 100000 population per year. Here the most important species from the medical point of view is Russell's viper (D. russelii), which is common in the paddy fields during sowing and harvesting of rice (Phillips et al., 1988). At these times of the year, there is a massive increase in the incidence of snake bite corresponding to the period when the farmers are in the paddies. A similar problem exists in Burma (Myanmar) where bites by Russell's viper are reckoned to be the fifth most common cause of death. In areas of Thailand, bites by the Thai cobra (N. kaouthia) represent a major problem in many rice-growing and fish-farming regions (Virivan et al., 1986). Further south, in the rubber plantations of Thailand and Malaysia, bites by the Malayan pit viper (Calloselasma rhodostoma) are a major cause of morbidity with some associated mortality (Warrell et al., 1986).
Reliable observations suggest that more than half of all those sustaining bites escape with minor or no poisoning because little or no venom is injected. On the other hand, mortality can be high when adequate medical treatment is not given for serious envenoming. It can be as high as 50% following envenoming by sea snakes (which occurs in 20% of all sea snake bites) and 10-15% in cases of E. ocellatus envenoming in West Africa. Snake bite in its early stages is very unpredictable and all victims should
Table 21.1 Precautions that should be taken to avoid snake bites
♦ Cut the grass short around houses or camp sites
♦ Wear proper shoes or boots, and ideally long trousers, when walking in the dark or in undergrowth where snakes are known to occur
♦ Make a noise when walking in areas where snakes are common
♦ Use a torch when walking at night
♦ Avoid sleeping on the ground: snakes are attracted to the warmth of the human body
♦ Take care after heavy rain: flooding may force snakes into the open in a confined area
♦ Avoid snakes as far as possible. Do not attack or corner a snake
♦ Do not handle snakes, even if you think that they are nonvenomous
♦ Never put your hand down holes/burrows or behind wood piles without looking
♦ Pay attention to warnings by members of the local community
♦ Take care swimming in waters where sea snakes are known to be active be observed closely for at least 24 h to assess the severity of poisoning and to ensure rational treatment.
For the traveller, there are several measures that are invaluable for avoiding snake bite and these should be strictly adhered to in areas where venomous snakes are found. They are summarised in Table 21.1.
Pathophysiology of Snake Envenoming
The major important clinical effects of venom may be classified as follows:
1. Local effects: increased vascular permeability and/or direct cytolytic action leading to pain, swelling and/or tissue necrosis.
2. Systemic effects:
(e) Myotoxicity, cardiotoxicity and nephrotoxicity (less common).
Local effects. Many different venoms contain components such as proteases, haemorrhagins, hyaluronidase, cytotoxins and phospholipases. These act to increase vascular permeability, damage vascular endothelium and destroy skin and subcutaneous tissue, leading to swelling, bruising and necrosis of a bitten limb.
Shock or hypotension is a prominent feature of envenoming by some species, particularly vipers. Syncope is sometimes reported soon after the bite; this may be an auto-pharmacological effect in which venoms contain substances that cause release of endogenous kinins or histamines. Later or prolonged hypotension is usually due to loss of fluid from the circulation because of changes in vascular permeability or because of haemorrhage. Some venoms may also cause direct myocardial toxicity or lead to vasodilatation.
Bleeding. The rapid development of intense local haemorrhage and systemic bleeding is a feature of envenoming by a number of species. These effects are caused by venom haemorrhagic factors (haemorrhagins), potent zinc me-talloproteinases which degrade proteins of the extracellular endothelial matrix (with resulting haemorrhage) and which can also affect platelet function by inhibiting aggregation. Haemorrhagins are responsible for the frequently observed gingival haemorrhage, or bleeding from old wounds/sores, etc. In combination with a coagulopathy, they can lead to life-threatening bleeding into tissues such as the brain and the gut.
Coagulopathy. The venoms of many vipers and some elapids contain substances capable of activating clotting factors. These may act on the clotting cascade at a number of sites, activating prothrombin and/or factors X and V or converting fibrinogen directly to fibrin (thrombin-like enzyme). In small animals, the effect of such actions is to cause total intravascular coagulation of the whole circulation. In humans, envenomed patients often develop a consumption coagulopathy or a disseminated intravascu-lar coagulation (DIC)-like state, with low fibrinogen levels, prolonged prothrombin and activated partial thromboplastin times and elevated levels of fibrin(ogen) degradation products. Although some venoms contain substances that act as anticoagulants in vitro, these are rarely clinically significant. Thrombocytopenia may occur because of consumption of platelets, but may also be due to a direct effect of venoms on platelet numbers and function.
Neurotoxicity. This is a prominent and life-threatening effect of envenoming by many elapids. A vast number of individual neurotoxins have been described and isolated; venom from one species often contains a mixture of different neurotoxins. They can be divided broadly by their major site of action: presynaptic or postsynaptic. Pre-synaptic neurotoxins are predominately phospholipases A2, which tend to bind with poor reversibility to the motor endplate and damage the nerve terminal, preventing transmitter release. Recovery is by regrowth and resprouting of axons. Postsynaptic neurotoxins tend to bind reversibly to postsynaptic receptors, and hence are more amenable to treatment.
Renal failure. Acute tubular necrosis occurs following
Table 21.2 Main clinical features of snake bite
Effects of poisoning
Natural mortality Average (approximate) death (%) (time)
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