Death and Destruction

In my last blog I touched on death adder venom and its effects on the human body. This post will go into more detail about the types of venom, their effects and the processes involved in revering these deadly toxins. Although there will be examples of the species which carry a particular venom it is important to remember that venoms will contain more than one toxin.  

WARNING: I will post juicy pictures so if you are squeamish then maybe find another post to read this week.

Neurotoxic venom attacks the neuromuscular junction which causes paralysis of the voluntary muscles. Without treatment death can occur, caused by asphyxiation and respiratory failure. Other symptoms include slurred speech loss of vision, sweating, convulsions and episodes of unconsciousness. Many elapid venoms display highly neurotoxic side effects. Tiger snakes, Brown snakes, taipans and adders are some examples of Australian species with highly neurotoxic venom. Treatment for this is in the form of antivenin. Tiger snake antivenin is commonly used for a wide range of elapid species.

Rough scale snake bite

http://www.brisbanetimes.com.au/queensland/reptile-handler-bitten-by-pet-snake-denies-being-reckless-20140116-30w8v.html

29/4/14 20:46

Haemotoxins destroy red blood cells causing huge problems for the circulatory system. Internal bleeding and hemoraging also leads to multiple organ failure the victim may experience bruising at the bite site. Clotting of the blood is common as well as anticoagulant properties in some species. Some cases have reported victims uncontrollably bleeding from all of the body’s orifices. Antivenin can reversed some of these effects if medical attention is received shortly after a bite however amputation of effected digits or limbs is common in poorer countries where victims may not receive treatment for a couple of hours. Many viper species possess this venom as well as the black snake family here in Australia. Gaboon viper and the Eastern diamondback rattlesnakes are some of the most common cases.

Fasciotomy procedure. An attempt to relieve the massive swelling from Eastern Diamondback Rattlesnake bite. Not commonly practiced to to risk of infections and terrible scaring.

http://www.ebaumsworld.com/pictures/view/31375/

29/4/14 20:19

Cytotoxins are similar to hemotoxins however they are much more destructive at the bite site. They destroy cellular tissues and cause blood poisoning. Its is advised not to apply a pressure bandage as venom attacks the bite site so withholding it can cause more damage. Puff adders, Black mambas and African cobras commonly posses a cytotoxic venom as well as a strong neurotoxin.

Puff adder bite

http://www.capesnakes.org.za/forum/viewtopic.php?f=46&t=565

29/04/14 20:39

Myotoxins are a gruesome set of toxins which destroys muscle tissues. These toxins block the signals to the muscles and cause then to degenerate. Symptoms consist of numbness of the limbs, swelling of the tongue, painful breathing and at later stages necrosis of the limbs. Liver failure is common as the organ works overtime to rid the body of toxins created by the festering wound. The Fer de lance  of South America is well known for having a myotoxic venom.

Severe necrosis following a Fer de lance bite.

http://www.squidoo.com/dangerous-snakes-of-latin-america

29/04/14 19:58

Again it is important to remember that it is not as clean cut as this. Lots of species produce a cocktail of toxins which may leave the victim feeling a number of these effects. It can also depend on the individual bitten. Some people may handle venom better than others. There are cases of people going into anaphylactic shock and dying minutes after a bite. It’s probably best never to find out.

References:
Mirtschin, P, Davis, R 1992, Revised edition dangerous snakes of Australia, an illustrated guide to Australia's most venomous snakes, New Holland Publishers Ltd, UK.

Teixeira, C, Landucci, E, Antunes, E, Chacur, M, Cury, Y 2003,” Inflammatory effects of snake venom myotoxic phospholipases a2, Toxicon, vol.42, iss.8, pp.947-962.