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The Inland Taipan

The Inland Taipan

The Oxyuranus microlepidotus (inland taipan) is a member of the family Elapidae (elapid snakes), and belongs to the Genus Oxyuranus. The back, sides and tail are of a buff brown colour, and it's eyes are of average size, with a blackish brown iris. It is found only in the central, and central western desert regions of Australia.

Although the inland taipan has the most lethal venom of any snake in the world, it is placid and shy. However, if cornered and/or provoked, it holds it's body in low, flat, S-shaped curves with it's head pointed straight at the disturber. It usually makes a single bite, or a few fast ones.

The venom of the inland taipan is primarily neurotoxic. However, while the myotoxic and procoagulative proteins are present to a lesser degree, they too contribute to the bite pathology.


The neurotoxins contained in the inland taipan's venom are as follow:

*Taipoxin - presynaptic neurotoxin, phospholipase A2 based, moderately acidic sialo-glycoprotein, MW 45,600, as a ternary complex 1:1:1 with a , b , g subunits. a and b subunits are 120 amino acids long, with 7 disulphide bridges. g subunit has 135 amino acids and 8disulphide bridges. Only the very basic (pI >10) g-subunit has lethal neurotoxicity. LD50 of complete molecule is 2 mg/kg (IV mouse). 17% of venom.

*Paradoxin - presynaptic neurotoxin, phospholipase A2 based, essentially identical to taipoxin. It accounts for 12% of crude venom, is a sialo-glycoprotein with three subunits and has an LD50 of 2 mg/kg (IV mouse). Amino acid analysis of paradoxin and taipoxin, both in whole form and as subunits, shows close homology.

*O. scutellatus fraction III - minimal data. Presumed postsynaptic neurotoxin. LD50 100 mg/kg (IV mouse). 47% of venom.*O. scutellatus fraction IV - minimal data. Presumed postsynaptic neurotoxin. LD50 100 mg/kg (IV mouse). MW approximately 8,000. 10% of venom.


Composition of this mixture may not be uniform throughout all populations of taipans.

The presynaptic constituents are much more potent than those which are postsynaptic. They work by affecting the terminal axon. On reaching the neuromuscular junction the presynaptic neurotoxin must bind to the terminal axon membrane, damage the membrane, and then exert its toxin effects. Initially this may cause release of acetylcholine (Ach), with some muscle twitching, rarely noticed clinically, before destroying vesicles and blocking further Ach release. This process takes from 60 to 80 minutes. Following the process, the neuromuscular block becomes detectable, and quickly becomes complete paralysis....

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