The venomous snakes of Australia are members of the family Elapidae, of which the cobras are also members. In contrast to North American Crotalidae, the Elapidae possess a relatively unsophisticated venom delivery apparatus with nonretractile small- to medium-sized paired fangs that have grooved venom channels rather than hollow venom ducts. It is thought that the Elapidae exert voluntary control over the injection of venom, hence the occurrence of the "dry bite," without envenomation. 9

The venom of the Australian elapids contains several important components.9 Neurotoxins (tiger snake, taipan, and death adder) act at the neuromuscular junction and cause paralysis. Signs may become apparent 2 to 4 h after the bite and may include ptosis, partial ophthalmoplegia (diplopia), dysarthria, loss of facial expression, and loss of airway control as well as respiratory paralysis in severe cases. Myolysins are structurally related to the neurotoxins but instead produce rhabdomyolysis, which may result in muscle pain, weakness, myoglobinuria, renal failure, and hyperkalemia. The procoagulant toxins (brown snake, tiger snake, taipan) act as prothrombin converters, leading to fibrinogen consumption and resulting in a coagulopathy. Intracranial hemorrhage is a recognized complication. Renal impairment or failure may also result from snakebite. The mechanisms are poorly understood and may include hypotension, myoglobinuria, coagulopathy, and direct renal toxicity (the brown snake).10 Local tissue destruction is uncommon with any Australian species, although mild to moderate ecchymosis and swelling may occur.

The brown snakes are capable of inflicting bites that cause rapid collapse and death. 4 Brown snake venom has been found to cause severe cardiovascular depression in anesthetized dogs, and these effects may account for the sudden deaths described.

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