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Adding up the toxins


 
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Benjamin Blacklow has just completed his doctoral thesis at the University of Technology Sydney. In particular, he was investigating the different components of the venom in death adders and the consequences of their injection.     
Death adders resemble vipers in that they have large triangular shaped heads, thin necks and stout bodies. They also possess a spiny tail resembling a rattle which is used to lure prey, while the death adder remains mostly hidden under leaves.
Benjamin's research was looking at the toxins in the venom of death adders which inhabit Indonesia, Papua New Guinea and Australia. Widely distributed, death adders are found in every state in Australia. The common death adder is found primarily along the eastern and western coasts, while the desert death adder is found in most of inland Australia and Northern death adder is found along the northern coast. Death adders are active mostly at night and will only attack humans if disturbed and threatened.
While death adders do not present a significant risk in most of Australia, death adder envenomation is of serious concern in the Madang region of Papua New Guinea and Northern Australia. There are various pathological reactions to a death adder envenomation, including localised swelling and pain. However, it is the neurotoxins within the venom which are of greatest concern in treatment. While the neurotoxins can cause difficulty in speech and movement, it is the paralysis of respiratory muscles that is the principal danger to victims.
Death adder venom has two different types of neurotoxins which attack respiratory muscles, one acting rapidly and another much more slowly. What is of interest is that the slow acting neurotoxin cause irreversible damage to nerve terminals, sometimes presenting difficulty in the treatment of death adder bites. These venom components also change between and within species, depending on where they live. Some regional variats of death adders actually appear to lack these slow, irreversible neurotoxins.
When an individual has been bitten, it is possible that the patient was not actually envenomated. As such, antivenoms are not typically administered until a patient shows the effects of the neurotoxins. This is a safeguard against potential serum poisoning and anaphylactic shock which can result from the use of antivenom. A great deal of energy is required for the snake to produce venom protein. As such, snakes such as death adders can bite without injecting venom, as a form of warning to stay away, without spending any valuable venom.
This research highlights the need to be aware of the slow acting neurotoxins which can potentially cause permanent damage to nerve terminals when envenomation has taken place. Actual bites are best treated with the pressure immobilisation technique. As soon as safely possible, a crepe bandage should be applied around the affected area, as tightly as you would bind a sprained ankle. If a person was bitten on the leg, for instance, the area from the foot up would then be bandaged. A splint would then be finally applied so that the limb remains immobilised, slowing the progress of the venom through the lymphatic vessels.
Death adder venom is more complex than previously thought and Benjamin's research sheds light on the clinical observation that in some patients, the antivenom is less effective against the neurotoxic actions of the venom.

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