The assessment of biohazards in the workplace has been concentrated on agricultural workers, health-care workers and laboratory personnel, who are at considerable risk of adverse health effects. A detailed compilation of biohazards by Dutkiewicz et al. (1988) shows how widespread the risks can be to workers in many other occupations as well (table 38.1).
Cultivating and harvesting
Breeding and tending animals
Abattoirs, food packaging plants
Storage facilities: grain silos, tobacco and other processing
Processing animal hair and leather
Wood processing: sawmills, papermills, cork factories
Laboratory animal care
Patient care: medical, dental
Pharmaceutical and herbal products
Clinical and research laboratories
Sewage and compost facilities
Industrial waste disposal systems
Source: Dutkiewicz et al. 1988.
Dutkiewicz et al. (1988) further taxonomically classified the micro-organisms and plants (table 38.2), as well as animals (table 38.3), which might possibly present biohazards in work settings.
Non-sporing gram- positive rods and coryne-bacteria
Yeast-like geophilic fungi
Parasites of wheat
Other lower plants
1 Infection-zoonosis: Causes infection or invasion usually contracted from vertebrate animals (zoonosis).
2 (e) Endotoxin.
3 (m) Mycotoxin.
Source: Dutkiewicz et al. 1988.
Invertebrates other than arthropods
1 Infection-zoonosis: Causes infection or invasion contracted from vertebrate animals.
2 Vector of pathogenic viruses, bacteria or parasites.
3 Toxic B produces toxin or venom transmitted by bite or sting.
Source: Dutkiewicz et al. 1988.
Micro-organisms are a large and diverse group of organisms that exist as single cells or cell clusters (Brock and Madigan 1988). Microbial cells are thus distinct from the cells of animals and plants, which are unable to live alone in nature but can exist only as parts of multicellular organisms.
Very few areas on the surface of this planet do not support microbial life, because micro-organisms have an astounding range of metabolic and energy-yielding abilities and many can exist under conditions that are lethal to other life forms.
Four broad classes of micro-organisms that can interact with humans are bacteria, fungi, viruses and protozoa. They are hazardous to workers due to their wide distribution in the working environment. The most important micro-organisms of occupational hazard are listed in table 38.2 and table 38.3 .
There are three major sources of such microbes:
1. those arising from microbial decomposition of various substrates associated with particular occupations (e.g., mouldy hay leading to hypersensitivity pneumonitis)
2. those associated with certain types of environments (e.g., bacteria in water supplies)
3. those stemming from infective individuals harbouring a particular pathogen (e.g., tuberculosis).
Ambient air may be contaminated with or carry significant levels of a variety of potentially harmful micro-organisms (Burrell 1991). Modern buildings, especially those designed for commercial and administrative purposes, constitute a unique ecological niche with their own biochemical environment, fauna and flora (Sterling et al. 1991). The potential adverse effects on workers are described elsewhere in this Encyclopaedia.
Water has been recognized as an important vehicle for extra-intestinal infection. A variety of pathogens are acquired through occupational, recreational and even therapeutic contact with water (Pitlik et al. 1987). The nature of non-enteric water-borne disease is often determined by the ecology of aquatic pathogens. Such infections are of basically two types: superficial, involving damaged or previously intact mucosae and skin; and systemic, often serious infections that may occur in the setting of depressed immunity. A broad spectrum of aquatic organisms, including viruses, bacteria, fungi, algae and parasites may invade the host through such extra-intestinal routes as the conjunctivae, respiratory mucosae, skin and genitalia.
Although zoonotic spread of infectious disease continues to occur in laboratory animals used in biomedical research, reported outbreaks have been minimized with the advent of rigorous veterinary and husbandry procedures, the use of commercially reared animals and the institution of appropriate personnel health programmes (Fox and Lipman 1991). Maintaining animals in modern facilities with appropriate safeguards against the introduction of vermin and biological vectors is also important in preventing zoonotic disease in personnel. Nevertheless, established zoonotic agents, newly discovered micro-organisms or new animal species not previously recognized as carriers of zoonotic micro-organisms are encountered, and the potential for spread of infectious disease from animals to humans still exists.
Active dialogue between veterinarians and physicians regarding the potential of zoonotic disease, the species of animals that are involved, and the methods of diagnosis, is an indispensable component of a successful preventive health programme.
Medical and laboratory staff and other health-care workers, including related professions, are exposed to infection by micro-organisms if the appropriate preventive measures are not taken. Hospital workers are exposed to many biological hazards, including human immunodeficiency virus (HIV), hepatitis B, herpes viruses, rubella and tuberculosis (Hewitt 1993).
Work in the agricultural sector is associated with a wide variety of occupational hazards. Exposure to organic dust, and to airborne micro-organisms and their toxins, may lead to respiratory disorders (Zejda et al. 1993). These include chronic bronchitis, asthma, hypersensitivity pneumonitis, organic dust toxic syndrome and chronic obstructive pulmonary disease. Dutkiewicz and his colleagues (1988) studied samples of silage for the identification of potential agents causing symptoms of organic and toxic syndrome. Very high levels of total aerobic bacteria and fungi were found. Aspergillus fumigatus predominated among the fungi, whereas bacillus and gram-negative organisms (Pseudomonas, Alcaligenes, Citrobacter and Klebsiella species) and actinomycetes prevailed among the bacteria. These results show that contact with aerosolized silage carries the risk of exposure to high concentrations of micro-organisms, of which A. fumigatus and endotoxin-producing bacteria are the most probable disease agents.
Short-term exposures to certain wood dusts may result in asthma, conjunctivitis, rhinitis or allergic dermatitis. Some thermophilic micro-organisms found in wood are human pathogens, and inhalation of ascomycete spores from stored wood chips has been implicated in human illnesses (Jacjels 1985).
Examples illustrative of specific working conditions follow:
1. The fungus Penicillium camemberti var. candidum is used in the production of some types of cheese. The high frequency of precipitating antibodies of this fungus in the workers’ blood samples, together with the clinical causes of the airway symptoms, indicate an aetiological relationship between airway symptoms and heavy exposure to this fungus (Dahl et al. 1994).
2. Micro-organisms (bacteria and fungi) and endotoxins are potential agents of occupational hazard in a potato processing plant (Dutkiewicz 1994). The presence of precipitins to microbial antigens was significantly correlated with the occurrence of the work-related respiratory and general symptoms that were found in 45.9% of the examined workers.
3. Museum and library personnel are exposed to moulds (e.g., Aspergillus, Penicillium) which, under certain conditions, contaminate books (Kolmodin-Hedman et al. 1986). Symptoms experienced are attacks of fever, chill, nausea and cough.
4. Ocular infections can result from the use of industrial microscope eyepieces on multiple shifts. Staphylococcus aureus has been identified among the micro-organism cultures (Olcerst 1987).
An understanding of the principles of epidemiology and the spread of infectious disease is essential in the methods used in the control of the causing organism.
Preliminary and periodic medical examinations of workers should be carried out in order to detect biological occupational diseases. There are general principles for conducting medical examinations in order to detect adverse health effects of workplace exposure, including biological hazards. Specific procedures are to be found elsewhere in this Encyclopaedia. For example, in Sweden the Farmers’ Federation initiated a programme of preventive occupational health services for farmers (Hoglund 1990). The main goal of the Farmers’ Preventive Health Service (FPHS) is to prevent work-related injuries and illnesses and to provide clinical services to farmers for occupational medical problems.
For some infectious disease outbreaks, appropriate preventive measures may be difficult to put in place until the disease is identified. Outbreaks of the viral Crimean-Congo haemorrhagic fever (CCHF) which demonstrated this problem were reported among hospital staff in the United Arab Emirates (Dubai), Pakistan and South Africa (Van Eeden et al. 1985).
In hot and temperate zones, snakebites may constitute a definite hazard for certain categories of workers: agricultural workers, woodcutters, building and civil engineering workers, fishermen, mushroom gatherers, snake charmers, zoo attendants and laboratory workers employed in the preparation of antivenom serums. The vast majority of snakes are harmless to humans, although a number are capable of inflicting serious injury with their venomous bites; dangerous species are found among both the terrestrial snakes (Colubridae and Viperidae) and aquatic snakes (Hydrophiidae) (Rioux and Juminer 1983).
According to the World Health Organization (WHO 1995), snakebites are estimated to cause 30,000 deaths per year in Asia and about 1,000 deaths each in Africa and South America. More detailed statistics are available from certain countries. Over 63,000 snakebites and scorpion stings with over 300 deaths are reported yearly in Mexico. In Brazil, about 20,000 snakebites and 7,000 to 8,000 scorpion stings occur annually, with a case-fatality rate of 1.5% for snake bites and between 0.3% and 1% for scorpion stings. A study in Ouagadougou, Burkina Faso, showed 7.5 snakebites per 100,000 population in peri-urban areas and up to over 69 per 100,000 in more remote areas, where case-fatality rates reached 3%.
Snakebites are a problem also in developed parts of the world. Each year about 45,000 snakebites are reported in the United States, where the availability of health care has reduced the number of deaths to 9–15 per year. In Australia, where some of the world’s most venomous snakes exist, the annual number of snakebites is estimated at between 300 and 500, with an average of two deaths.
Environmental changes, particularly deforestation, may have caused the disappearance of many snake species in Brazil. However, the number of reported cases of snakebites did not decrease as other and sometimes more dangerous species proliferated in some of the deforested areas (WHO 1995).
There are only two species of venomous lizards, both members of the genus Heloderma: H. suspectum (Gila monster) and H. horridum (beaded lizard). Venom similar to that of the Viperidae penetrates wounds inflicted by the anterior curved teeth, but bites in humans are uncommon and recovery is generally rapid (Rioux and Juminer 1983).
Snakes do not usually attack humans unless they feel menaced, are disturbed or are trodden on. In regions infested with venomous snakes, workers should wear foot and leg protection and be provided with monovalent or polyvalent antivenom serum. It is recommended that persons working in a danger area at a distance of over half-an-hour’s travel from the nearest first-aid post should carry an antivenom kit containing a sterilized syringe. However, it should be explained to workers that bites even from the most venomous snakes are seldom fatal, since the amount of venom injected is usually small. Certain snake charmers achieve immunization by repeated injections of venom, but no scientific method of human immunization has yet been developed (Rioux and Juminer 1983).
International Standards and Biological Hazards
Many national occupational standards include biological hazards in their definition of harmful or toxic substances. However, in most regulatory frameworks, biological hazards are chiefly restricted to micro-organisms or infectious agents. Several US Occupational Safety and Health Administration (OSHA) regulations include provisions on biological hazards. The most specific are those concerning hepatitis B vaccine vaccination and blood-borne pathogens; biological hazards are also covered in regulations with a broader scope (e.g., those on hazard communication, the specifications for accident prevention signs and tags, and the regulation on training curriculum guidelines).
Although not the subject of specific regulations, the recognition and avoidance of hazards relating to animal, insect or plant life is addressed in other OSHA regulations concerning specific work settingsfor example, the regulation on telecommunications, the one on temporary labour camps and the one on pulpwood logging (the latter including guidelines concerning snake-bite first-aid kits).
One of the most comprehensive standards regulating biological hazards in the workplace is European Directive No. 90/679. It defines biological agents as “micro-organisms, including those which have been genetically modified, cell cultures and human endoparasites, which may be able to provoke any infection, allergy or toxicity,” and classifies biological agents into four groups according to their level of risk of infection. The Directive covers the determination and assessment of risks and employers’ obligations in terms of the replacement or reduction of risks (through engineering control measures, industrial hygiene, collective and personal protection measures and so on), information (for workers, workers’ representatives and the competent authorities), health surveillance, vaccination and record-keeping. The Annexes provide detailed information on containment measures for different “containment levels” according to the nature of the activities, the assessment of risk to workers and the nature of the biological agent concerned.
Adapted from 3rd edition, Encyclopaedia of Occupational Health and Safety.
Aquatic animals dangerous to humans are to be found among practically all of the divisions (phyla). Workers may come into contact with these animals in the course of various activities including surface and underwater fishing, the installation and handling of equipment in connection with the exploitation of petroleum under the sea, underwater construction, and scientific research, and thus be exposed to health risks. Most of the dangerous species inhabit warm or temperate waters.
Porifera. The common sponge belongs to this phylum. Fishermen who handle sponges, including helmet and scuba divers, and other underwater swimmers, may contract contact dermatitis with skin irritation, vesicles or blisters. The “sponge diver’s sickness” of the Mediterranean region is caused by the tentacles of a small coelenterate (Sagartia rosea) that is a parasite of the sponge. A form of dermatitis known as “red moss” is found among North American oyster fishers resulting from contact with a scarlet sponge found on the shell of the oysters. Cases of type 4 allergy have been reported. The poison secreted by the sponge Suberitus ficus contains histamine and antibiotic substances.
Coelenterata. These are represented by many families of the class known as Hydrozoa, which includes the Millepora or coral (stinging coral, fire coral), the Physalia (Physalia physalis, sea wasp, Portuguese man-of-war), the Scyphozoa (jellyfish) and the Actiniaria (stinging anemone), all of which are found in all parts of the ocean. Common to all these animals is their ability to produce an urticaria by the injection of a strong poison that is retained in a special cell (the cnidoblast) containing a hollow thread, which explodes outwards when the tentacle is touched, and penetrates the person’s skin. The various substances contained in this structure are responsible for such symptoms as severe itching, congestion of the liver, pain, and depression of the central nervous system; these substances have been identified as thalassium, congestine, equinotoxin (which contains 5-hydroxytryptamine and tetramine) and hypnotoxin, respectively. Effects on the individual depend upon the extent of the contact made with the tentacles and hence on the number of microscopic punctures, which may amount to many thousands, up to the point where they may cause the death of the victim within a few minutes. In view of the fact that these animals are dispersed so widely throughout the world, many incidents of this nature occur but the number of fatalities is relatively small. Effects on the skin are characterized by intense itching and the formation of papules having a bright red, mottled appearance, developing into pustules and ulceration. Intense pain similar to electric shock may be felt. Other symptoms include difficulty in breathing, generalized anxiety and cardiac upset, collapse, nausea and vomiting, loss of consciousness, and primary shock.
Echinoderma. This group includes the starfishes and sea urchins, both of which possess poisonous organs (pedicellariae), but are not dangerous to humans. The spine of the sea urchin can penetrate the skin, leaving a fragment deeply imbedded; this can give rise to a secondary infection followed by pustules and persistent granuloma, which can be very troublesome if the wounds are close to tendons or ligaments. Among the sea urchins, only the Acanthaster planci seems to have a poisonous spine, which can give rise to general disturbances such as vomiting, paralysis and numbness.
Mollusca. Among the animals belonging to this phylum are the cone shells, and these can be dangerous. They live on a sandy sea-bottom and appear to have a poisonous structure consisting of a radula with needle-like teeth, which can strike at the victim if the shell is handled incautiously with the bare hand. The poison acts on the neuromuscular and central nervous systems. Penetration of the skin by the point of a tooth is followed by temporary ischaemia, cyanosis, numbness, pain, and paraesthesia as the poison spreads gradually through the body. Subsequent effects include paralysis of the voluntary muscles, lack of coordination, double vision and general confusion. Death can follow as a result of respiratory paralysis and circulatory collapse. Some 30 cases have been reported, of which 8 were fatal.
Platyhelminthes. These include the Eirythoe complanata and the Hermodice caruncolata, known as “bristle worms”. They are covered with numerous bristle-like appendages, or setae, containing a poison (nereistotoxin) with a neurotoxic and local irritant effect.
Polyzoa (Bryozoa). These are made up of a group of animals which form plant-like colonies resembling gelatinous moss, which frequently encrust rocks or shells. One variety, known as Alcyonidium, can cause an urticarious dermatitis on the arms and face of fishermen who have to clean this moss off their nets. It can also give rise to an allergic eczema.
Selachiis (Chondrichthyes). Animals belonging to this phylum include the sharks and sting-rays. The sharks live in fairly shallow water, where they search for prey and may attack people. Many varieties have one or two large, poisonous spines in front of the dorsal fin, which contain a weak poison that has not been identified; these can cause a wound giving rise to immediate and intense pain with reddening of the flesh, swelling and oedema. A far greater danger from these animals is their bite, which, because of several rows of sharp pointed teeth, causes severe laceration and tearing of the flesh leading to immediate shock, acute anaemia and drowning of the victim. The danger that sharks represent is a much-discussed subject, each variety seeming to be particularly aggressive. There seems no doubt that their behaviour is unpredictable, although it is said that they are attracted by movement and by the light colour of a swimmer, as well as by blood and by vibrations resulting from a fish or other prey that has just been caught. Sting-rays have large, flat bodies with a long tail having one or more strong spines or saws, which can be poisonous. The poison contains serotonine, 5-nucleotidase and phosphodiesterase, and can cause generalized vasoconstriction and cardio-respiratory arrest. Sting-rays live in the sandy regions of coastal waters, where they are well hidden, making it easy for bathers to step on one without seeing it. The ray reacts by bringing over its tail with the projecting spine, impaling the spike keep into the flesh of the victim. This may cause piercing wounds in a limb or even penetration of an internal organ such as the peritoneum, lung, heart or liver, particularly in the case of children. The wound can also give rise to great pain, swelling, lymphatic oedema and various general symptoms such as primary shock and cardio-circulatory collapse. Injury to an internal organ may lead to death in a few hours. Sting-ray incidents are among the most frequent, there being some 750 every year in the United States alone. They can also be dangerous for fishermen, who should immediately cut off the tail as soon as the fish is brought aboard. Various species of rays such as the torpedo and the narcine possess electric organs on their back, which, when stimulated by touch alone, can produce electric shocks ranging from 8 up to 220 volts; this may be enough to stun and temporarily disable the victim, but recovery is usually without complications.
Osteichthyes. Many fishes of this phylum have dorsal, pectoral, caudal and anal spines which are connected with a poison system and whose primary purpose is defence. If the fish is disturbed or stepped upon or handled by a fisherman, it will erect the spines, which can pierce the skin and inject the poison. Not infrequently they will attack a diver seeking fish, or if they are disturbed by accidental contact. Numerous incidents of this kind are reported because of the widespread distribution of fish of this phylum, which includes the catfish, which are also found in fresh water (South America, West Africa and the Great Lakes), the scorpion fish (Scorpaenidae), the weever fish (Trachinus), the toadfish, the surgeon fish and others. Wounds from these fishes are generally painful, particularly in the case of the catfish and the weever fish, causing reddening or pallor, swelling, cyanosis, numbness, lymphatic oedema and haemorrhagic suffusion in the surrounding flesh. There is a possibility of gangrene or phlegmonous infection and peripheral neuritis on the same side as the wound.
Other symptoms include faintness, nausea, collapse, primary shock, asthma and loss of consciousness. They all represent a serious danger for underwater workers. A neurotoxic and haemotoxic poison has been identified in the catfish, and in the case of the weever fish a number of substances have been isolated such as 5-hydroxytryptamine, histamine and catecholamine. Some catfishes and stargazers that live in fresh water, as well as the electric eel (Electrophorus), have electric organs (see under Selachii above).
Hydrophiidae. This group (sea snakes) is to be found mostly in the seas around Indonesia and Malaysia; some 50 species have been reported, including Pelaniis platurus, Enhydrina schistosa and Hydrus platurus. The venom of these snakes is very similar to that of the cobra, but is 20 to 50 times as poisonous; it is made up of a basic protein of low molecular weight (erubotoxin) which affects the neuromuscular junction blocking the acetylcholine and provoking myolysis. Fortunately sea snakes are generally docile and bite only when stepped on, squeezed or dealt a hard blow; furthermore, they inject little or no venom from their teeth. Fishermen are among those most exposed to this hazard and account for 90% of all reported incidents, which result either from stepping on the snake on the sea bottom or from encountering them among their catch. Snakes are probably responsible for thousands of the occupational accidents attributed to aquatic animals, but few of these are serious, while only a small percentage of the serious accidents turn out to be fatal. Symptoms are mostly slight and not painful. Effects are usually felt within two hours, starting with muscular pain, difficulty with neck movement, lack of dexterity, and trismus, and sometimes including nausea and vomiting. Within a few hours myoglobinuria (the presence of complex proteins in urine) will be seen. Death can ensue from paralysis of the respiratory muscles, from renal insufficiency due to tubular necrosis, or from cardiac arrest due to hyperkalaemia.
Every effort should be made to avoid all contact with the spines of these animals when they are being handled, unless strong gloves are worn, and the greatest care should be taken when wading or walking on a sandy sea bottom. The wet suit worn by skin divers offers protection against the jellyfish and the various Coelenterata as well as against snakebite. The more dangerous and aggressive animals should not be molested, and zones where there are jellyfish should be avoided, as they are difficult to see. If a sea snake is caught on a line, the line should be cut and the snake allowed to go. If sharks are encountered, there are a number of principles that should be observed. People should keep their feet and legs out of the water, and the boat should be gently brought to shore and kept still; a swimmer should not stay in the water with a dying fish or with one that is bleeding; a shark’s attention should not be attracted by the use of bright colours, jewellery, or by making a noise or explosion, by showing a bright light, or by waving the hands towards it. A diver should never dive alone.
Adapted from 3rd edition, Encyclopaedia of Occupational Health and Safety.
Annually millions of scorpion stings and anaphylactic reactions to insect stings may occur worldwide, causing tens of thousands of deaths in humans each year. Between 30,000 and 45,000 cases of scorpion stings are reported annually in Tunisia, causing between 35 and 100 deaths, mostly among children. Envenomation (toxic effects) is an occupational hazard for populations involved in agriculture and forestry in these regions.
Among the animals that can inflict injury on humans by the action of their venom are invertebrates, such as Arachnida (spiders, scorpions and sun spiders), Acarina (ticks and mites), Chilopoda (centipedes) and Hexapoda (bees, wasps, butterflies, and midges).
All species are venomous, but in practice only a few types produce injury in humans. Spider poisoning may be of two types:
1. Cutaneous poisoning, in which the bite is followed after a few hours by oedema centred around a cyanotic mark, and then by a blister; extensive local necrosis may ensue, and healing may be slow and difficult in cases of bites from spiders of the Lycosa genus (e.g., the tarantula).
2. Nerve poisoning due to the exclusively neurotoxic venom of the mygales (Latrodectus ctenus), which produces serious injury, with early onset, tetany, tremors, paralysis of the extremities and, possibly, fatal shock; this type of poisoning is relatively common amongst forestry and agricultural workers and is particularly severe in children: in the Amazonas, the venom of the “black widow” spider (Latrodectus mactans) is used for poison arrows.
Prevention. In areas where there is a danger of venomous spiders, sleeping accommodation should be provided with mosquito nets and workers should be equipped with footwear and working clothes that give adequate protection.
These arachnids have a sharp poison claw on the end of the abdomen with which they can inflict a painful sting, the seriousness of which varies according to the species, the amount of venom injected and the season (the most dangerous season being at the end of the scorpions’ hibernation period). In the Mediterranean region, South America and Mexico, the scorpion is responsible for more deaths than poisonous snakes. Many species are nocturnal and are less aggressive during the day. The most dangerous species (Buthidae) is found in arid and tropical regions; their venom is neurotropic and highly toxic. In all cases, the scorpion sting immediately produces intense local signs (acute pain, inflammation) followed by general manifestations such as tendency to fainting, salivation, sneezing, lachrymation and diarrhoea. The course in young children is often fatal. The most dangerous species are found amongst the genera Androctonus (sub-Saharan Africa), Centrurus (Mexico) and Tituus (Brazil). The scorpion will not spontaneously attack humans, and stings only when it considers itself endangered, as when trapped in a dark corner or when boots or clothes in which it has taken refuge are shaken or put on. Scorpions are highly sensitive to halogenated pesticides (e.g., DDT).
This order of arachnid is found chiefly in steppe and sub-desert zones such as the Sahara, Andes, Asia Minor, Mexico and Texas, and is non-venomous; nevertheless, sun spiders are extremely aggressive, may be as large as 10 cm across and have a fearsome appearance. In exceptional cases, the wounds they inflict may prove serious due to their multiplicity. Solpugids are nocturnal predators and may attack a sleeping individual.
Ticks are blood-sucking arachnids at all stages of their life cycle, and the “saliva” they inject through their feeding organs may have a toxic effect. Poisoning may be severe, although mainly in children (tick paralysis), and may be accompanied by reflex suppression. In exceptional cases death may ensue due to bulbar paralysis (in particular where a tick has attached itself to the scalp). Mites are haematophagic only at the larval stage, and their bite produces pruritic inflammation of the skin. The incidence of mite bites is high in tropical regions.
Treatment. Ticks should be detached after they are anaesthetized with a drop of benzene, ethyl ether or xylene. Prevention is based on the use of organophosphorus pesticide pest repellents.
Centipedes differ from millipedes (Diplopoda) in that they have only one pair of legs per body segment and that the appendages of the first body segment are poison fangs. The most dangerous species are encountered in the Philippines. Centipede venom has only a localized effect (painful oedema).
Treatment. Bites should be treated with topical applications of dilute ammonia, permanganate or hypochlorite lotions. Antihistamines may also be administered.
Insects may inject venom via the mouthparts (Simuliidaeblack flies, Culicidaemosquitoes, Phlebotomussandflies) or via the sting (bees, wasps, hornets, carnivorous ants). They may cause rash with their hairs (caterpillars, butterflies), or they may produce blisters by their haemolymph (Cantharidaeblister flies and Staphylinidaerove beetles). Black fly bites produce necrotic lesions, sometimes with general disorders; mosquito bites produce diffuse pruriginous lesions. The stings of Hymenoptera (bees, etc.) produce intense local pain with erythema, oedema and, sometimes, necrosis. General accidents may result from sensitization or multiplicity of stings (shivering, nausea, dyspnoea, chilling of the extremities). Stings on the face or the tongue are particularly serious and may cause death by asphyxiation due to glottal oedema. Caterpillars and butterflies may cause generalized pruriginous skin lesions of an urticarial or oedematous type (Quincke’s oedema), sometimes accompanied by conjunctivitis. Superimposed infection is not infrequent. The venom from blister flies produces vesicular or bullous skin lesions (Poederus). There is also the danger of visceral complications (toxic nephritis). Certain insects such as Hymenoptera and caterpillars are found in all parts of the world; other suborders are more localized, however. Dangerous butterflies are found mainly in Guyana and the Central African Republic; blister flies are found in Japan, South America and Kenya; black flies live in the intertropical regions and in central Europe; sandflies are found in the Middle East.
Prevention. First level prevention includes mosquito nets and repellent and/or insecticide application. Workers who are severely exposed to insect bites can be desensitized in cases of allergy by the administration of increasingly large doses of insect body extract.
Adapted from The Oxford Textbook of Medicine, edited by DJ Weatherall, JGG Ledingham and DA Warrell (2nd edition, 1987), pp. 6.66-6.77. By permission of Oxford University Press.
A proportion of patients bitten by venomous snakes (between <10% to >60%), depending on the species, will develop minimal or no signs of toxic symptoms (envenoming) despite having puncture marks which indicate that the snake’s fangs have penetrated the skin.
Fear and effects of treatment, as well as the snake’s venom, contribute to the symptoms and signs. Even patients who are not envenomed may feel flushed, dizzy and breathless, with constriction of the chest, palpitations, sweating and acroparaesthesiae. Tight tourniquets may produce congested and ischaemic limbs; local incisions at the site of the bite may cause bleeding and sensory loss; and herbal medicines often induce vomiting.
The earliest symptoms directly attributable to the bite are local pain and bleeding from the fang punctures, followed by pain, tenderness, swelling and bruising extending up the limb, lymphangitis and tender enlargement of regional lymph nodes. Early syncope, vomiting, colic, diarrhoea, angio-oedema and wheezing may occur in patients bitten by European Vipera, Daboia russelii, Bothrops sp, Australian Elapids and Atractaspis engaddensis. Nausea and vomiting are common symptoms of severe envenoming.
There is local swelling, bleeding from the fang marks and sometimes (Rhabophis tigrinus) fainting. Later vomiting, colicky abdominal pain and headache, and widespread systemic bleeding with extensive ecchymoses (bruising), incoagulable blood, intravascular haemolysis and kidney failure may develop. Envenoming may develop slowly over several days.
Local effects include pain, swelling, blistering, necrosis and tender enlargement of local lymph nodes. Violent gastro-intestinal symptoms (nausea, vomiting and diarrhoea), anaphylaxis (dyspnoea, respiratory failure, shock) and ECG changes (a-v block, ST, T-wave changes) have been described in patients envenomed by A. engaddensis.
Bites by kraits, mambas, coral snakes and some cobras (e.g., Naja haje and N. nivea) produce minimal local effects, whereas bites by African spitting cobras (N. nigricollis, N. mossambica, etc.) and Asian cobras (N. naja, N. kaouthia, N. sumatrana, etc.) cause tender local swelling which may be extensive, blistering and superficial necrosis.
Early symptoms of neurotoxicity before there are objective neurological signs include vomiting, “heaviness” of the eyelids, blurred vision, fasciculations, paraesthesiae around the mouth, hyperacusis, headache, dizziness, vertigo, hypersalivation, congested conjunctivae and “gooseflesh”. Paralysis starts as ptosis and external ophthalmoplegia appearing as early as 15 minutes after the bite, but sometimes delayed for ten hours or more. Later the face, palate, jaws, tongue, vocal cords, neck muscles and muscles of deglutition become progressively paralysed. Respiratory failure may be precipitated by upper airway obstruction at this stage, or later after paralysis of intercostal muscles, diaphragm and accessory muscles of respiration. Neurotoxic effects are completely reversible, either acutely in response to antivenom or anticholinesterases (e.g., following bites by Asian cobras, some Latin American coral snakesMicrurus, and Australian death addersAcanthophis) or they may wear off spontaneously in one to seven days.
Envenoming by Australian snakes causes early vomiting, headache and syncopal attacks, neurotoxicity, haemostatic disturbances and, with some species, ECG changes, generalized rhabdomyolysis and kidney failure. Painful enlargement of regional lymph nodes suggests impending systemic envenoming, but local signs are usually absent or mild except after bites by Pseudechis sp.
Patients “spat” at by spitting elapids experience intense pain in the eye, conjunctivitis, blepharospasm, palpebral oedema and leucorrhoea. Corneal erosions are detectable in more than half the patients spat at by N. nigricollis. Rarely, venom is absorbed into the anterior chamber, causing hypopyon and anterior uveitis. Secondary infection of corneal abrasions may lead to permanent blinding opacities or panophthalmitis.
Local envenoming is relatively severe. Swelling may become detectable within 15 minutes but is sometimes delayed for several hours. It spreads rapidly and may involve the whole limb and adjacent trunk. There is associated pain and tenderness in regional lymph nodes. Bruising, blistering and necrosis may appear during the next few days. Necrosis is particularly frequent and severe following bites by some rattlesnakes, lance-headed vipers (genus Bothrops), Asian pit vipers and African vipers (genera Echis and Bitis). When the envenomed tissue is contained in a tight fascial compartment such as the pulp space of the fingers or toes or the anterior tibial compartment, ischaemia may result. If there is no swelling two hours after a viper bite it is usually safe to assume that there has been no envenoming. However, fatal envenoming by a few species can occur in the absence of local signs (e.g., Crotalus durissus terrificus, C. scutulatus and Burmese Russell’s viper).
Blood pressure abnormalities are a consistent feature of envenoming by Viperidae. Persistent bleeding from fang puncture wounds, venepuncture or injection sites, other new and partially healed wounds and post partum, suggests that the blood is incoagulable. Spontaneous systemic haemorrhage is most often detected in the gums, but may also be seen as epistaxis, haematemesis, cutaneous ecchymoses, haemoptysis, subconjunctival, retroperitoneal and intracranial haemorrhages. Patients envenomed by the Burmese Russell’s viper may bleed into the anterior pituitary gland (Sheehan’s syndrome).
Hypotension and shock are common in patients bitten by some of the North American rattlesnakes (e.g., C. adamanteus, C. atrox and C. scutulatus), Bothrops, Daboia and Vipera species (e.g., V. palaestinae and V. berus). The central venous pressure is usually low and the pulse rate rapid, suggesting hypovolaemia, for which the usual cause is extravasation of fluid into the bitten limb. Patients envenomed by Burmese Russell’s vipers show evidence of generally increased vascular permeability. Direct involvement of the heart muscle is suggested by an abnormal ECG or cardiac arrhythmia. Patients envenomed by some species of the genera Vipera and Bothrops may experience transient recurrent fainting attacks associated with features of an autopharmacological or anaphylactic reaction such as vomiting, sweating, colic, diarrhoea, shock and angio-oedema, appearing as early as five minutes or as late as many hours after the bite.
Renal (kidney) failure is the major cause of death in patients envenomed by Russell’s vipers who may become oliguric within a few hours of the bite and have loin pain suggesting renal ischaemia. Renal failure is also a feature of envenoming by Bothrops species and C. d. terrificus.
Neurotoxicity, resembling that seen in patients bitten by Elapidae, is seen after bites by C. d. terrificus, Gloydius blomhoffii, Bitis atropos and Sri Lankan D. russelii pulchella. There may be evidence of generalized rhabdomyolysis. Progression to respiratory or generalized paralysis is unusual.
The peripheral neutrophil count is raised to 20,000 cells per microlitre or more in severely envenomed patients. Initial haemo-concentration, resulting from extravasation of plasma (Crotalus species and Burmese D. russelii), is followed by anaemia caused by bleeding or, more rarely, haemolysis. Thrombocytopenia is common following bites by pit vipers (e.g., C. rhodostoma, Crotalus viridis helleri) and some Viperidae (e.g., Bitis arietans and D. russelii), but is unusual after bites by Echis species. A useful test for venom-induced defibrin(ogen)ation is the simple whole blood clotting test. A few millilitres of venous blood is placed in a new, clean, dry, glass test tube, left undisturbed for 20 minutes at ambient temperature, and then tipped to see if it has clotted or not. Incoagulable blood indicates systemic envenoming and may be diagnostic of a particular species (for example Echis species in Africa). Patients with generalized rhabdomyolysis show a steep rise in serum creatine kinase, myoglobin and potassium. Black or brown urine suggests generalized rhabdomyolysis or intravascular haemolysis. Concentrations of serum enzymes such as creatine phosphokinase and aspartate aminotransferase are moderately raised in patients with severe local envenoming, probably because of local muscle damage at the site of the bite. Urine should be examined for blood/haemoglobin, myoglobin and protein and for microscopic haematuria and red cell casts.
Patients should be moved to the nearest medical facility as quickly and comfortably as possible, avoiding movement of the bitten limb, which should be immobilized with a splint or sling.
Most traditional first-aid methods are potentially harmful and should not be used. Local incisions and suction may introduce infection, damage tissues and cause persistent bleeding, and are unlikely to remove much venom from the wound. The vacuum extractor method is of unproven benefit in human patients and could damage soft tissues. Potassium permanganate and cryotherapy potentiate local necrosis. Electric shock is potentially dangerous and has not proved beneficial. Tourniquets and compression bands can cause gangrene, fibrinolysis, peripheral nerve palsies and increased local envenoming in the occluded limb.
The pressure immobilization method involves firm but not tight bandaging of the entire bitten limb with a crepe bandage 4-5 m long by 10 cm wide starting over the site of the bite and incorporating a splint. In animals, this method was effective in preventing systemic uptake of Australian elapid and other venoms, but in humans it has not been subjected to clinical trials. Pressure immobilization is recommended for bites by snakes with neurotoxic venoms (e.g., Elapidae, Hydrophiidae) but not when local swelling and necrosis may be a problem (e.g., Viperidae).
Pursuing, capturing or killing the snake should not be encouraged, but if the snake has been killed already it should be taken with the patient to hospital. It must not be touched with bare hands, as reflex bites may occur even after the snake is apparently dead.
Patients being transported to hospital should be laid on their side to prevent aspiration of vomit. Persistent vomiting is treated with chlorpromazine by intravenous injection (25 to 50 mg for adults, 1 mg/kg body weight for children). Syncope, shock, angio-oedema and other anaphylactic (autopharmacological) symptoms are treated with 0.1% adrenaline by subcutaneous injection (0.5 ml for adults, 0.01 ml/kg body weight for children), and an antihistamine such as chlorpheniramine maleate is given by slow intravenous injection (10 mg for adults, 0.2 mg/kg body weight for children). Patients with incoagulable blood develop large haematomas after intramuscular and subcutaneous injections; the intravenous route should be used whenever possible. Respiratory distress and cyanosis are treated by establishing an airway, giving oxygen and, if necessary, assisted ventilation. If the patient is unconscious and no femoral or carotid pulses can be detected, cardiopulmonary resuscitation (CPR) should be started immediately.
In most cases of snakebite there are uncertainties about the species responsible and the quantity and composition of venom injected. Ideally, therefore, patients should be admitted to hospital for at least 24 hours of observation. Local swelling is usually detectable within 15 minutes of significant pit viper envenoming and within two hours of envenoming by most other snakes. Bites by kraits (Bungarus), coral snakes (Micrurus, Micruroides), some other elapids and sea snakes may cause no local envenoming. Fang marks are sometimes invisible. Pain and tender enlargement of lymph nodes draining the bitten area is an early sign of envenoming by Viperidae, some Elapidae and Australasian elapids. All the patient’s tooth sockets should be examined meticulously, as this is usually the first site at which spontaneous bleeding can be detected clinically; other common sites are nose, eyes (conjunctivae), skin and gastro-intestinal tract. Bleeding from venipuncture sites and other wounds implies incoagulable blood. Hypotension and shock are important signs of hypovolaemia or cardiotoxicity, seen particularly in patients bitten by North American rattlesnakes and some Viperidae (e.g., V berus, D russelii, V palaestinae). Ptosis (e.g., drooping of the eyelid) is the earliest sign of neurotoxic envenoming. Respiratory muscle power should be assessed objectivelyfor example, by measuring vital capacity. Trismus, generalized muscle tenderness and brownish-black urine suggests rhabdomyolysis (Hydrophiidae). If a procoagulant venom is suspected, coagulability of whole blood should be checked at the bedside using the 20-minute whole blood clotting test.
Blood pressure, pulse rate, respiratory rate, level of consciousness, presence/absence of ptosis, extent of local swelling and any new symptoms must be recorded at frequent intervals.
The most important decision is whether or not to give antivenom, as this is the only specific antidote. There is now convincing evidence that in patients with severe envenoming, the benefits of this treatment far outweigh the risk of antivenom reactions (see below).
Antivenom is indicated if there are signs of systemic envenoming such as:
1. haemostatic abnormalities such as spontaneous systemic bleeding, incoagulable blood or profound thrombocytopenia (<50/1 X 10-9)
3. hypotension and shock, abnormal ECG or other evidence of cardiovascular dysfunction
4. impaired consciousness of any cause
5. generalized rhabdomyolysis.
Supporting evidence of severe envenoming is a neutrophil leucocytosis, elevated serum enzymes such as creatine kinase and aminotransferases, haemoconcentration, severe anaemia, myoglobinuria, haemoglobinuria, methaemoglobinuria, hypoxaemia or acidosis.
In the absence of systemic envenoming, local swelling involving more than half the bitten limb, extensive blistering or bruising, bites on digits and rapid progression of swelling are indications for antivenom, especially in patients bitten by species whose venoms are known to cause local necrosis (e.g., Viperidae, Asian cobras and African spitting cobras).
Some developed countries have the financial and technical resources for a wider range of indications:
United States and Canada: After bites by the most dangerous rattlesnakes (C. atrox, C. adamanteus, C. viridis, C. horridus and C. scutulatus) early antivenom therapy is recommended before systemic envenoming is evident. Rapid spread of local swelling is considered to be an indication for antivenom, as is immediate pain or any other symptom or sign of envenoming after bites by coral snakes (Micruroides euryxanthus and Micrurus fulvius).
Australia: Antivenom is recommended for patients with proved or suspected snakebite if there are tender regional lymph nodes or other evidence of systemic spread of venom, and in anyone effectively bitten by an identified highly venomous species.
Europe: (Adder: Vipera berus and other European Vipera): Antivenom is indicated to prevent morbidity and reduce the length of convalescence in patients with moderately severe envenoming as well as to save the lives of severely envenomed patients. Indications are:
1. fall in blood pressure (systolic to less than 80 mmHg, or by more than 50 mmHg from the normal or admission value) with or without signs of shock
2. other signs of systemic envenoming (see above), including spontaneous bleeding, coagulopathy, pulmonary oedema or haemorrhage (shown by chest radiograph), ECG abnormalities and a definite peripheral leucocytosis (more than 15,000/ml) and elevated serum creatine kinase
3. severe local envenomingswelling of more than half the bitten limb developing within 48 hours of the biteeven in the absence of systemic envenoming
4. in adults, swelling extending beyond the wrist after bites on the hand or beyond the ankle after bites on the foot within four hours of the bite.
Patients bitten by European Vipera who show any evidence of envenoming should be admitted to hospital for observation for at least 24 hours. Antivenom should be given whenever there is evidence of systemic envenoming(1) or (2) aboveeven if its appearance is delayed for several days after the bite.
It is important to realize that most antivenom reactions are not caused by acquired Type I, IgE-mediated hypersensitivity but by complement activation by IgG aggregates or Fc fragments. Skin and conjunctival tests do not predict early (anaphylactic) or late (serum sickness type) antivenom reactions but delay treatment and may sensitize the patient. They should not be used.
Patients with a history of reactions to equine antiserum suffer an increased incidence and severity of reactions when given equine antivenom. Atopic subjects have no increased risk of reactions, but if they develop a reaction it is likely to be severe. In such cases, reactions may be prevented or ameliorated by pretreatment with subcutaneous adrenaline, antihistamine and hydrocortisone, or by continuous intravenous infusion of adrenaline during antivenom administration. Rapid desensitization is not recommended.
Antivenom should be given only if its stated range of specificity includes the species responsible for the bite. Opaque solutions should be discarded, as precipitation of protein indicates loss of activity and increased risk of reactions. Monospecific (monovalent) antivenom is ideal if the biting species is known. Polyspecific (polyvalent) antivenoms are used in many countries because it is difficult to identify the snake responsible. Polyspecific antivenoms may be just as effective as monospecific ones but contain less specific venom-neutralizing activity per unit weight of immunoglobulin. Apart from the venoms used for immunizing the animal in which the antivenom has been produced, other venoms may be covered by paraspecific neutralization (e.g., Hydrophiidae venoms by tiger snakeNotechis scutatusantivenom).
Antivenom treatment is indicated as long as signs of systemic envenoming persist (i.e., for several days) but ideally it should be given as soon as these signs appear. The intravenous route is the most effective. Infusion of antivenom diluted in approximately 5 ml of isotonic fluid/kg body weight is easier to control than intravenous “push” injection of undiluted antivenom given at the rate of about 4 ml/min, but there is no difference in the incidence or severity of antivenom reactions in patients treated by these two methods.
Manufacturers’ recommendations are based on mouse protection tests and may be misleading. Clinical trials are needed to establish appropriate starting doses of major antivenoms. In most countries the dose of antivenom is empirical. Children must be given the same dose as adults.
Marked symptomatic improvement may be seen soon after antivenom has been injected. In shocked patients, the blood pressure may rise and consciousness return (C. rhodostoma, V. berus, Bitis arietans). Neurotoxic signs may improve within 30 minutes (Acanthophis sp, N. kaouthia), but this usually takes several hours. Spontaneous systemic bleeding usually stops within 15 to 30 minutes, and blood coagulability is restored within six hours of antivenom, provided that a neutralizing dose has been given. More antivenom should be given if severe signs of envenoming persist after one to two hours or if blood coagulability is not restored within about six hours. Systemic envenoming may recur hours or days after an initially good response to antivenom. This is explained by continuing absorption of venom from the injection site and the clearance of antivenom from the bloodstream. The apparent serum half-lives of equine F(ab’)2 antivenoms in envenomed patients range from 26 to 95 hours. Envenomed patients should therefore be assessed daily for at least three or four days.
· Early (anaphylactic) reactions develop within 10 to 180 minutes of starting antivenom in 3 to 84% of patients. The incidence increases with dose and decreases when more highly refined antivenom is used and administration is by intramuscular rather than intravenous injection. The symptoms are itching, urticaria, cough, nausea, vomiting, other manifestations of autonomic nervous system stimulation, fever, tachycardia, bronchospasm and shock. Very few of these reactions can be attributed to acquired Type I IgE-mediated hypersensitivity.
· Pyrogenic reactions result from contamination of the antivenom with endotoxins. Fever, rigors, vasodilatation and a fall in blood pressure develop one to two hours after treatment. In children, febrile convulsions may be precipitated.
· Late reactions of serum sickness (immune complex) type may develop 5 to 24 (mean 7) days after antivenom. The incidence of those reactions and the speed of their development increases with the dose of antivenom. Clinical features include fever, itching, urticaria, arthralgia (including the temporomandibular joint), lymphadenopathy, periarticular swellings, mononeuritis multiplex, albuminuria and, rarely, encephalopathy.
Adrenaline (epinephrine) is the effective treatment for early reactions; 0.5 to 1.0 ml of 0.1% (1 in 1000, 1 mg/ml) is given by subcutaneous injection to adults (children 0.01 ml/kg) at the first signs of a reaction. The dose may be repeated if the reaction is not controlled. An antihistamine H1 antagonist, such as chlorpheniramine maleate (10 mg for adults, 0.2 mg/kg for children) should be given by intravenous injection to combat the effects of histamine release during the reaction. Pyrogenic reactions are treated by cooling the patient and giving antipyretics (paracetamol). Late reactions respond to an oral antihistamine such as chlorpheniramine (2 mg every six hours for adults, 0.25 mg/kg/day in divided doses for children) or to oral prednisolone (5 mg every six hours for five to seven days for adults, 0.7 mg/kg/day in divided doses for children).
Bulbar and respiratory paralysis may lead to death from aspiration, airway obstruction or respiratory failure. A clear airway must be maintained and, if respiratory distress develops, a cuffed endotracheal tube should be inserted or tracheostomy performed. Anticholinesterases have a variable but potentially useful effect in patients with neurotoxic envenoming, especially when post-synaptic neurotoxins are involved. The “Tensilon test” should be done in all cases of severe neurotoxic envenoming as with suspected myasthenia gravis. Atropine sulphate (0.6 mg for adults, 50 mg/kg body weight for children) is given by intravenous injection (to block muscarinic effects of acetylcholine) followed by an intravenous injection of edrophonium chloride (10 mg for adults, 0.25 mg/kg for children). Patients who respond convincingly can be maintained on neostigmine methyl sulphate (50 to 100 mg/kg body weight) and atropine, every four hours or by continuous infusion.
If the jugular or central venous pressure is low or there is other clinical evidence of hypovolaemia or exsanguination, a plasma expander, preferably fresh whole blood or fresh frozen plasma, should be infused. If there is persistent or profound hypotension or evidence of increased capillary permeability (e.g., facial and conjunctival oedema, serous effusions, haemoconcentration, hypoalbuminaemia) a selective vasoconstrictor such as dopamine (starting dose 2.5 to 5 mg/kg body weight/min by infusion into a central vein) should be used.
Urine output, serum creatinine, urea and electrolytes should be measured each day in patients with severe envenoming and in those bitten by species known to cause renal failure (e.g., D. russelii, C. d. terrificus, Bothrops species, sea snakes). If urine output drops below 400 ml in 24 hours, urethral and central venous catheters should be inserted. If urine flow fails to increase after cautious rehydration and diuretics (e.g., frusemide up to 1000 mg by intravenous infusion), dopamine (2.5 mg/kg body weight/min by intravenous infusion) should be tried and the patient placed on strict fluid balance. If these measures are ineffective, peritoneal or haemodialysis or haemofiltration are usually required.
Bites by some species (e.g., Bothrops sp, C. rhodostoma) seem particularly likely to be complicated by local infections caused by bacteria in the snake’s venom or on its fangs. These should be prevented with penicillin, chloramphenicol or erythromycin and a booster dose of tetanus toxoid, especially if the wound has been incised or tampered with in any way. An aminoglycoside such as gentamicin and metronidazole should be added if there is evidence of local necrosis.
Bullae can be drained with a fine needle. The bitten limb should be nursed in the most comfortable position. Once definite signs of necrosis have appeared (blackened anaesthetic area with putrid odour or signs of sloughing), surgical debridement, immediate split skin grafting and broad-spectrum antimicrobial cover are indicated. Increased pressure within tight fascial compartments such as the digital pulp spaces and anterior tibial compartment may cause ischaemic damage. This complication is most likely after bites by North American rattlesnakes such as C. adamanteus, Calloselasma rhodostoma, Trimeresurus flavoviridis, Bothrops sp and Bitis arietans. The signs are excessive pain, weakness of the compartmental muscles and pain when they are passively stretched, hypaesthesia of areas of skin supplied by nerves running through the compartment, and obvious tenseness of the compartment. Detection of arterial pulses (e.g., by Doppler ultrasound) does not exclude intracompartmental ischaemia. Intracompartmental pressures exceeding 45 mmHg are associated with a high risk of ischaemic necrosis. In these circumstances, fasciotomy may be considered but must not be attempted until blood coagulability and a platelet count of more than 50,000/ml have been restored. Early adequate antivenom treatment will prevent the development of intracompartmental syndromes in most cases.
Once specific antivenom has been given to neutralize venom procoagulants, restoration of coagulability and platelet function may be accelerated by giving fresh whole blood, fresh frozen plasma, cryoprecipitates (containing fibrinogen, factor VIII, fibronectin and some factors V and XIII) or platelet concentrates. Heparin must not be used. Corticosterioids have no place in the treatment of envenoming.
When cobra venom is “spat” into the eyes, first aid consists of irrigation with generous volumes of water or any other bland liquid which is available. Adrenaline drops (0.1 per cent) may relieve the pain. Unless a corneal abrasion can be excluded by fluorescein staining or slit lamp examination, treatment should be the same as for any corneal injury: a topical antimicrobial such as tetracycline or chloramphenicol should be applied. Instillation of diluted antivenom is not currently recommended.