The venom is produced in a gland which is situated behind the eye. The venom gland is surrounded by muscles which can contract and compress the venom gland. The venom is thus forced from the gland through a duct to the fang which is either canalized or grooved. Snake venom is not a single component, but is a highly complex mixture of a variety of components with varying actions, which can work together having different toxicities. Geographical variation of the venom of the same species is well known. This is especially evident in Russell’s viper where the clinical picture varies from monosystemic to multisystemic manifestation. In general, venom contains low molecular weight polypeptides, enzymes such as proteases, phospholipses, esterases, hyaluronidases, nucleotidases and lecithinases and biologically active amines such as serotonin. Haemotoxins are very complex having procoagulant enzymes that stimulate blood clotting but result in incoagulable blood due to consumption coagulopathy. Haemorrhagins (zinc metalloproteinases) damage the endothelial lining of blood vessels causing spontaneous bleeding and direct red cell damage that produces intravascular haemolysis.
Neurotoxin causes paralysis of muscles by blocking the neuromuscular junction. These could be either post-synaptic (Elapidae) or pre-synaptic (Elapidae and some Viperidae). Phospholipase A2 is the principal component in the pre-synaptic neurotoxins that damage nerve endings, initially releasing acetylcholine transmitter, then interfering with the release. Post-synaptic neurotoxin polypeptide compete with acetylcholine for receptors in the neuromuscular junction and lead to curare-like paralysis. Some components of the neurotoxins have either direct or indirect action on the brain causing alteration of the level of consciousness. Haemolytic and myolytic phospholipase A2 produce rhabdomyolysis and myoglobinuria causing secondary renal failure and red cell membrane damage leading to haemolysis.
Local tissue injury occurs at the site of bite due to proteases, hyaluronidases and other enzymatic effects of the venom. There are many more toxins and a description of these are beyond the scope of this book.
Quantity of venom injected at a bite varies irrespective of the size of the snake. The snake may be able to control whether or not venom is injected and does not exhaust the store of venom even after several strikes. Bites by young or small snake should not be ignored as it could produce fatal envenoming.