Oxyuranus microlepidotus (Inland taipan)
Taipan venom is overwhelmingly neurotoxic and the bite pathology is reflective of this with the nervous system being severely affected. Symptoms include vomiting, flaccid paralysis, and eventual respiratory paralysis. However, while the myotoxic and procoagulative proteins are present to a lesser degree, they still play a role in the bite pathology. Oxyuranus microlepidotus (Inland taipan, formerly known as the fierce snake or western taipan) is far and away the most toxic land snake in the world, with a lethal dose estimated to be fifty times that of the Indian cobra Naja naja. The venom has a potent neurotoxic mechanism that causes a significant loss of synaptic vesicles and other neuropathology's similar to that elicited by taipoxin from O. scutellatus. However, a specific neurological factor has not been isolated which can be held responsible for the acute potency of this venom. In addition, unlike the venom from scutellatus or the common tiger snake Notechis scutatus, this specie, like the eastern brown snake Pseudonaja textilis, has a procoagulant property that does not require the presence of the cofactors calcium, factor V or phospholipid in order to activate normal prothrombin or the decarboxylated form in a concentration-dependent manner.
Oxyuranus scutellatus canni (Papuan taipan) is far less venomous than the Inland taipan, having a lethality that is on par with that of the common taipan, over seven times that of the Indian cobra. The bite pathology from this subspecies is overwhelmingly neurotoxic, primarily acting upon neuronal synapse and causing a decrease in neuromuscular action potentials producing clinical neurotoxic symptoms such as electrocardiographic abnormalities (sinus bradycardia and septal T wave inversion), ptosis, ophthalmoplegia, bulbar paralysis, and peripheral muscular weakness. The hemotoxicity of the venom is manifested by haemostatic failure due to prothrombin activators acting in concert with other venom components. Studies of coagulopathy in patients with total defibrination revealed significant reduction of factors V and VII and reduction of factors II, IX, XI, XII, and XIIIA as well decrease of plasminogen and alpha 2-antiplasmin levels and elevated levels of fibrin(ogen) degradation products; all resulting in a clinical decrease of platelet levels.
Bites from the taipan Oxyuranus scutellatus scutellatus produces pathologies similar to that of the Papuan taipan, causing severe neurological disturbances; like Notechis scutatus, Oxyuranus scutellatus inhibits Ca2+-dependent K+ transport. In addition, the venom has been shown to cause spheroechinocytosis which may result in an increase in blood viscosity and contribute to the clinically seen spontaneous bleeding but with the majority of the bleeding effects coming from the procoagulants found in the venom. The venom factor VII activator is one of the venom proteins isolated that is responsible for some of the hematological disturbances seen in bites, with proteolytic cleavage of factor V into factor VIIa increased in the presence of calcium and phospholipid. The factor VII activating protein is also the prothrombin activating protein but the factor Va-like portion of the enzyme complex that activates prothrombin is distinct from the portion that activates factor VII.