Pseudechis (Latin = false-adder)
Black snakes

Pseudechis australis (Mulga)

The venom of Pseudechis australis (Mulga) differs markedly from that of other Australian elapids in that the primary toxins are not neurotoxic but rather myotoxic, producing severe muscle damage and necrosis, which are evidenced by an increase in serum creatine kinase as well as histological observations, and that the venom is strongly anticoagulative but without fibrinolysis. The pathology disruption of neuromuscular function produced by PLA2s in the venom, characterised by pronounced morphological damage to muscle fibres, motor nerve terminals and cytoplasmic organelles.

P. colletti (Collet's snake) bites produce myoglobinuria and has a relatively high direct haemolytic activity, with hemolysis due to phospholipase B hydrolysis of phosphatidylcholine. Like P. australis, the myolytic effects can be diagnosed not only through histopathological studies but also by testing for a sharp increase in serum creatine kinase, an increase which is more commonly seen in species of Crotalus (Rattlesnakes) but has been recorded in a death from Notechis scutatus envenomation. The primary structures of the two phospholipase As responsible for myoglobinuria has been shown to have strong homology with that of a similarly acting enzyme from the beaked sea snake Enhydrina schistosa.. The phospholipase A2 isolated from this specie has been shown to induce myodegeneration and necrosis in with subsequent myoglobinuria and myoglobinuric nephropathy. The haemolytic phospholipase B is a 35 kDa homodimer and is strongly haemolytic towards human and rabbit erythrocytes, but not for bovine or ovine erythrocytes, and is partially responsible for the myoglobinuria seen in bites from this specie

The procoagulant property of the red-bellied black snake P. porphyriacus venom is, like Notechis scutatus, due to calcium, factor V and phospholipid dependent activation or normal prothrombin, in contrast to the venoms of Pseudonaja textilis and Oxyuranus microlepidotus which do not require co-factors to activate both normal prothrombin or the decarboxylated form. The pseudexins are the primary toxic phospholipase A2s in porphyriacus venom; pseudexin A and B isozymes are virtually identical to each other and possessing similar toxicity, pseudexin C, however, is not as closely related or toxic but all are immunologically similar to other snake venom PLA2s.

The Papuan black snake P. papuanus causes neurotoxic, hemotoxicity, and mild procoagulopathy; the clinical pathology is remarkably similar to that of the Papuan taipan: mild defibrination and depletion of other clotting factors with elevated fibrin(ogen) degradation products and other evidence of fibrinolysis, prolongation of prothrombin time, and thrombocytopenia. A lethal 15 kDa, neutral PLA2 isolated from the venom has been shown to decimate platelet aggregation and is responsible for the clinically seen haemostatic disruptions.

Pseudechis australis and butleri bites are treated with black snake antivenom while the other species are treated with tiger snake antivenom.

Species

Scientific name	Common name	Translation of latin name
Pseudechis australis	Mulga/ King brown	southern false-adder
Pseudechis butleri	Speckled mulga/ Butler's snakes	Butler's false-adder, after W.H. Butler, Australian naturalist
Pseudechis colletti	Collett's snake	Collett's false-adder, after R. Collett, once director of the Oslo Museum
Pseudechis guttatus	Spotted black snake	spotted false-adder
Pseudechis papuanus	Papuan black snake	Papuan false-adder
Pseudechis porphyriacus	Red-bellied black snake	russet (or purple) false-adder

Publications on Pseudechis
last updated 1-98, next expected update 3-98

Additional photos - will be archived by February 12, 1998

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