Monday 16 May 2016

Antivenom

Australia is notorious for is venomous creatures in particular the venomous snakes. Taipans, brown snakes, tiger snakes and death adders strike fear into the hearts of many people. Despite these species harbouring some incredibly toxic venoms, snake bites in Australia resulting in fatalities is now a rare incidence. Why so?

Desert death adder (Acanthophis pyrrhus) a species with a strong postsynaptic toxin component.
Production of high quality and relatively easily sourced antivenom, education of the public and quality medical care all are essential in reducing fatalities (White & Meier, 1995).

Antivenom comes in two forms;
Polyvalent antivenoms are a fantastic idea conceptually. The idea of having a wide-ranging effective antivenom to cover most if not all species would truly change the medicinal treatment of bites. This level of effectiveness however, has not been reached (White & Meier, 1995). Polyvalents are often used as a last alternative as reactions, often worse than the response to the venom, are common (White & Meier, 1995). Many other side effects are common and effectively counteracting all components of the venom is far from certain.

Monovalent antivenoms are highly specific and are produced to counteract the venom from one species. These serums may still cause reaction but are far less common. Due to their specific nature they also target most if not all of the venom component. These factors make monovalent a much safer option to treat a patient with a known envenomation (White & Meier, 1995).
Red-headed krait (Bungarus flaviceps baluensis) a species with strong presynaptic neurotoxin components.
Most dangerous Australian snake’s venom is dominated by postsynaptic neurotoxins. Neurotoxins are classed into postsynaptic and presynaptic depending on what area of the neuron is impacted (White & Meier, 1995). Bites from presynaptic neurotoxins often take a long time to manifest with few symptoms initially, however, after a certain length of time the neuron is permanently damaged and antivenom is no longer effective (White & Meier, 1995). Postsynaptic neurotoxins work oppositely with a fast onset of symptoms but reacts much more effectively to antivenom even hours after the envenomation (White & Meier, 1995).

References
White, J. and Meier, J., 1(995). Handbook of clinical toxicology of animal venoms and poisons (Vol. 236). CRC Press.

Images by Nick Weigner

1 comment:

  1. So, you’re saying that, if I get bitten by a snake, I should hope it’s got postsynaptic neurotoxin? What kinds of reactions to anti-venoms are seen because, while I don’t want to get bitten by a snake, I’d prefer to at least know what I’m up against with the potential reactions to anti-venoms :)

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