Death Adder Group

• Common death adder Acanthophis antarticus
• Desert death adder Acanthophis pyrrhus
• Northern death adder Acanthophis praelongus

Death adders used to be widespread across mainland Australia, but today are only occasionally seen in the wild, though they are common in captivity. They are distinctive in appearance and habits. There are three major species in the genus Acanthopis: the Northern Death Adder (A. praelongus, also found in New Guinea), the Common Death Adder (A antarctic us) and the Desert Death Adder (A. pyrrhus). However, the taxonomy of Death Adders is not finalised and up to 12 species, including the Pilbara Death Adder (A. armstrong), have been proposed. Whilst, Death Adders superficially resembles a viper and hence their name, they are, like all Australian snakes elapids.

The distinctive appearance of these snakes means they are more likely to be correctly identified. In the past it was considered that a snakebite at night time was more likely to be due to A antarcticus than any other species. However, Death Adders bites are now uncommon and the largest case series published to date comes from New Guinea.

In the era pre-antivenom, death adders had a bad reputation, with a 50% fatality rate.

The venom contains potent post-synaptic neurotoxins, but no other toxins that appear important in human envenoming. Specifically, they do not possess procoagulants or potent myotoxins.

Human envenoming causes purely postsynaptic flaccid paralysis, while myolysis, defibrination coagulopathy, and secondary renal damage do not occur. The bite site is variable in appearance, from mild to moderate swelling and is often painful.

This information should be read in conjunction with the detailed background information on Australian snakebite.

Death adders are widely distributed but now relatively rare in the wild in Australia. They do not appear to adapt well to human land use. Consequently, bites by death adders in the wild are extremely rare. In contrast, they are common in captivity and bites to reptile keepers are moderately common. They have potent venom and prior to antivenom, used to kill 50% of all people bitten. Death from death adder bite is now very rare.

The death adders are squat snakes with a distinctive triangular head, narrow neck, relatively short, dumpy body and thin tail with distal lure. Colour varies from earthy grey to red with darker transverse bands.

They prefer habitats with leaf litter or other ground debris in which to hide, usually, but not exclusively, in sandy soils, including coastal dune country. The death adder is commonly active at night, and it is often reluctant to move away if humans approach; relying on being hidden in leaf litter. It is therefore possible to step on a death adder hidden in this way.

Death adder venom is powerful, but limited in action. In man, its effects are principally those of paralysis due to postsynaptic neurotoxins. This raises an interesting possibility in therapy, as postsynaptic paralysis is often reversible with either antivenom or acetylcholinesterase inhibitors (edrophonium, neostigmine). Death adders do not cause a defibrination type coagulopathy or myolysis, and renal failure is not reported.

Death adder bites are usually quite painful at the bite site, though swelling is usually only slight and there is a tendency to local secondary infection.

NOTE: Gives positive result in the death adder tube of the Venom Detection Kit.

Preferred antivenom is CSL Death Adder Antivenom. Acetylcholinesterase inhibitors may also be effective in reversing paralysis.

Shea GM. The distribution and identification of dangerously venomous Australian terrestrial snakes. Aust.Vet.J. 1999;77(12):791-8.
Sutherland SK, Tibballs J. Treatment of snake bite in Australia. In: Sutherland SK, Tibballs J, editors. Australian Animal Toxins. 2nd ed. Melbourne: Oxford University Press; 2001. p. 286-342.
White J. Clinical Toxicology of Snakebite in Australia and New Guinea. In: Meier J, White J, editors. Handbook of Clinical Toxicology of Animal Venoms and Poisons. 1st ed. New York: CRC Press; 1995. p. 595-618.