Pathophysiology of Brown Snake Venom

Some Key Facts About Brown Snakes:
-Brown snakes are common throughout mainland Australia (ie. not in Tasmania)
-They are the most common cause of snakebites and snakebites death in Australia.
-Compared to other snakes, they produce little but very potent venom.
-Their bites are either painless or almost painless.
-Brown snake venom includes powerful presynaptic neurotoxins, procoagulants, cardiotoxins and nephrotoxins. There is no myolytic activity.
-Humans are mainly affected by the coagulants which make up 30% of total venom protein.

How do they work?
Neurotoxins
Neurotoxins act on neurons at the motor end plate. Most toxins act by interfering with membrane proteins such as voltage-dependent ion channels. They prevent action potential from occuring thus leading to paralysis and eventually death.
A toxin found in the Australian common brown snake is called the textilotoxin which inhibits the release of acetylcholine presynaptically and/or blocks the postsynaptic nicotinic ACh receptors. This can cause respiratory paralysis.

Procoagulants
Coagulopathy is the hallmark of brown snake envenoming. Procoagulants are prothrombin activators, converting prothrombin into thrombin and fibrinogen into fibrin. This results in consumptive coagulopathy where circulating fibrinogen, plasminogen and other clotting factors are depleted, producing breakdown products which can be detected in a blood test. Platelet count is not affected initially. Thus, the patient is at risk of haermorrhage and intracranial haematomas.

References
http://www.emedicine.com/emerg/byname/Snake-Envenomations--Brown.htm
http://www.toxinology.com/generic_static_files/cslavh_antivenom_brown.html
http://www.kingsnake.com/toxinology/old/snakes/Pseudonaja/Pseudonaja.html


~Michelle