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Bites and stings from animals, venomous and non-venomous, cause an unknown number of injuries per year, butstatistics from a few key groups of venomous animals indicate that there are millions of cases annually, with at least125,000 deaths. While in most cases of venomous animal injury, the primary problem is direct venom toxicity effects,there may also be significant local tissue injury and non-venomous animals will principally cause direct trauma.Because of the global magnitude of human injury, morbidity and mortality from venomous animal bites and stings, thisarea will be dealt with in some detail, even though it encompasses more than just primary physical trauma.
Venomous animals
Venomous animals are found in most groups or classes of the Animal Kingdom and in most habitats, both terrestrialand marine, reflecting the selective advantage venom may bestow, in both acquiring prey and deterring predators. Inthis section of the chapter, the types of animals, the types of venoms, clinical effects and general comments onmanagement will be covered. This is followed by a more detailed look at individual types of animals and their effectson humans.Overview of venomous animalsOf the approximately 26 Phyla of animals, at least 6 contain species that use venom or internal poison, as either puredefense, or both for offence and defense (Figure 1). A few groups, however, account for the vast majority of cases of human envenoming or poisoning by animals:• Venomous snakes – >125,000 deaths/year.• Scorpions – approximately 5,000 deaths/year.• Stinging insects – hundreds of deaths/year due to anaphylactic reactions to venom.• Puffer fish – several hundred deaths/year.• Jellyfish – possibly scores of deaths/year.• Spiders – perhaps 10-50 deaths/year.• Stinging fish – perhaps 1-10 deaths/year.• Venomous molluscs – perhaps 1-10 deaths/year.Taxonomy considerationsFundamental to the understanding of trauma from venomous animals is a knowledge of the taxonomy of theseanimals, for without a reliable way of identifying an animal, it will not be possible to accurately record cause andeffect, essential in elucidating epidemiology, etiology, pathophysiology, and clinical management. It is beyond thescope of this chapter to detail the taxonomy of all venomous animals. A simplified scheme is outlined in Figure 1.Overview of venomsVenoms are nearly always complex mixtures of varied biologically active substances (toxins) which may workindependently or synergystically and each of which may have one or more quite distinct target sites and actions. Inmany venoms a single component or group of closely related components may be responsible for most or all major effects in envenomed humans, but in other venoms, particularly snake venoms, a multitude of diverse componentsmay each cause distinct major effects, resulting in a complex, multisystem disease process. 
 
Venoms have evolved principally because they benefit the venomous animal, giving it some competitive advantageover related non-venomous species. In many species the venom has evolved from digestive juices, especiallyenzymes, the venom gland being a highly evolved digestive gland. It is not surprising therefore that many venomousanimals use their venom principally to aid digestion, explaining many of the rather unpleasant effects on envenomedhumans. At some point in evolution some venomous animals have evolved venom with rather different effects,designed to assist acquiring prey or as a defense against predators. It is this latter group of venom toxins that oftencause the major systemic effects of envenoming in humans. Often these toxins may have evolved from digestiveenzymes, but their principal action is not related to enzymic activity. Indeed, there may be no significant residualenzymic activity, despite considerable sequence homology with the original enzyme. Classic examples of this are thephospholipase A2 (PLA2) toxins that are so prominent in snake venoms and have evolved into potent toxins such asneurotoxins, myotoxins, procoagulants, anticoagulants, platelet-active toxins and necrotoxins. There are many methods of classifying venom components and types of toxins. The method used herein is based onclinical effect. A single toxin may be active within several categories. NeurotoxinsNeurotoxins are classic venom components causing potentially lethal envenoming in humans. There are many types,widely distributed amongst venomous animals. Some cause flaccid paralysis, others cause hyperstimulation of portions of the nervous system. Paralysing neurotoxinsPresynaptic neuromuscular junction neurotoxinsThese toxins act at the neuromuscular junction (NMJ) in humans, damaging the terminal axon, resulting in a brief period of neurotransmitter release, followed by cessation of all neurotransmitter release, resulting in irreversibleparalysis. This manifests clinically as progressive flaccid paralysis. Antivenom therapy cannot reverse such paralysis,which may persist for days, weeks or occasionally months, but if given at the earliest sign of paralysis, may preventprogression to widespread severe paralysis. As these toxins affect the skeletal NMJ, they affect skeletal muscle only,including respiration, but not cardiac or smooth muscle. They have evolved from PLA2 toxins, but some are complexmulticomponent molecules without residual enzymatic activity. These toxins are particularly found in some snakevenoms. Postsynaptic neuromuscular junction neurotoxinsLike the presynaptic neurotoxins, these toxins act principally at the skeletal muscle NMJ, causing progressive flaccidparalysis, but act extracellularly by reversibly binding to the acetylcholine receptor on the muscle end plate. Their effect is therefore reversible with sufficient antivenom therapy and may also be at least partially overcome by the useof anticholinesterases, such as neostigmine, though this often requires ongoing dosing. These toxins are alsoparticularly found in some snake venoms. 
 
Presynaptic and postsynaptic synergystic neuromuscular junction neurotoxinsThese toxins are found in African mamba snake venoms. The dendrotoxins act presynaptically to increase release of the neurotransmitter, acetylcholine, flooding the NMJ and causing overstimulation of the muscle. This action issynergystically compounded by the second set of toxins in mamba venoms, the fasciculins, which act asanticholinesterases, preventing removal of the acetylcholine, thus increasing the neurotransmitter concentration andadding to the flooding effect, resulting in muscle fasciculation and effective paralysis of skeletal muscle. Sodium channel neurotoxinsThere are a variety of these toxins, the best known of which is tetrodotoxin (TTX), found in such diverse animals asthe Australian blue ringed octopus (in its saliva) and the flesh of puffer fish (fugu). A small molecule, TTX causesrapid, reversible short-lived flaccid paralysis of skeletal muscle principally by blocking nerve transmission, throughaction on the sodium channels of axons. Potassium channel neurotoxinsA variety of channel blocking toxins exist in venoms, most notably in some scorpion venoms and cone shell venoms.A variety of potassium channels may be affected, the usual clinical effect being flaccid paralysis, though hypertonicparalysis may also occur. Excitatory neurotoxinsA number of excitatory neurotoxins have been reported from venoms, especially arthropod venoms such as fromspiders and scorpions. These toxins may target diverse parts of the human nervous system, often as an unfortunatebiproduct of toxicity designed to immobilise prey species, mostly other arthropods. A good example is the Australianfunnel web spider, the principal toxin of which will affect arthropod prey, but not most mammals, an unfortunateexception being humans, who are exquisitely susceptible to this venom. Some of these toxins affect neuronal ionchannels, though mechanisms of action are still uncertain in many cases. Autonomic neurotoxinsA number of neurotoxins from venoms may affect part or all of the autonomic system, either primarily or secondarily.This includes neurotoxins from the previously mentioned classes, especially the excitatory and ion channel toxins. MyotoxinsThere are two principal types of myotoxic action in venoms; local, at the bite/sting area and systemic. The latter is of most clinical significance. Systemic myolysins are particularly important in some snake venoms, which in humansmay result in potentially lethal myolysis of skeletal muscle. These latter myotoxins are PLA2 toxins and in somecases are the same toxin as presynaptic neurotoxins (an example is notexin from Australian tiger snake venom),mediating myotoxicity through a part of the molecule distinct from the neurotoxic active site. Myotoxins cause
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