Platypus venom
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The Platypus is one of the only mammals to produce venom. The male has a pair of spurs on the hind limbs through which it can deliver a painful but non-fatal cocktail of poisons.
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[edit] Spur and crural gland
Venom is produced in the crural glands of the male, which are kidney-shaped alveolar glands located in the upper thigh connected by a thin-walled duct to a calcaneus spur on each hind limb. Female platypuses, in common with echidnas, have rudimentary spur buds which do not develop (dropping off before the end of their first year) and lack functional crural glands.[1] The spur is attached to a small bone which allows articulation; the spur can move at a right angle to the limb allowing a greater range of attack than a fixed spur would allow.[2] The spur normally lies flat against the limb but is raised when required.[3]
[edit] Venom
The crural gland produces a cocktail of venom, composed of over 250 different chemicals but with four major toxins. Of the four, three are defensin-like proteins (DLPs) unique to the Platypus. The different chemicals in the poison have a range of effects from lowering blood pressure to causing pain and increasing blood flow around the wound.[2] Coagulating effects have been seen during experiments on laboratory animals, but this has not been observed consistently. Unlike snake venom, there are appears to be no necrotic component in the Platypus' venom - although some muscle wastage has been observed in cases of envenomation in humans, it is likely that this is due to the inability to use the limb while the effects of the venom persist.[3] It is unknown whether the pain caused is a result of the associated oedema around the wound or whether the venom has a component which acts directly on the pain receptors.
Although the makeup of platypus venom has a broadly similar range of effects to that of snake venom, it appears to have a different function from those poisons produced by non-mammalian species: its effects are non-life threatening but nevertheless powerful enough to seriously impair the victim. It is not used as a method of disabling or killing prey, and although it acts a defensive mechanism, only males produce venom. Since production rises during the breeding season it is theorized that it is used as an offensive weapon to assert dominance and control territory during this period.[2]
[edit] Effect on humans
Although powerful enough to kill smaller animals,[2] the venom is not lethal to humans, but does produce excruciating pain; so intense that the victim may be incapacitated. Swelling rapidly develops around the entry wound and gradually spreads outwards. Information obtained from case studies and anecdotal evidence show that the pain develops into a long-lasting hyperalgesia that can persist for months but usually lasts from a few days to a few weeks.[3][4] Anecdotal evidence suggests that the intense pain subsides quickly, but a clinical report from 1992 showed that the severe pain was persistent and did not respond to morphine. There have been no reported human fatalities.[3]
[edit] Uses
Because of the possible direct effect on pain receptors and its observed resistance to morphine the components of platypus venom are being investigated as a potential source for pain killers for conditions with chronic pain. They are also being studied as treatment for high blood pressure.[5]
[edit] See also
[edit] Notes
- ^ J.R.Grant. Fauna of Australia chap.16 vol.1b. Australian Biological Resources Study (ABRS). Retrieved on 13 December 2006.
- ^ a b c d Gerritsen, Vivienne Baillie (2002-12). "Platypus poison". Protein Spotlight (29). Retrieved on 13 December.
- ^ a b c d The venom of the platypus (Ornithorhynchus anatinus). Retrieved on 13 December 2006.
- ^ G. M. de Plater, P. J. Milburn and R. L. Martin (2001-3). "Venom From the Platypus, Ornithorhynchus anatinus, Induces a Calcium-Dependent Current in Cultured Dorsal Root Ganglion Cells". Journal of Neurophysiology 85 (3): 1340-1345.
- ^ Deborah Smith (2003-02-17). Platypus poison may kill pain. Sydney Morning Herald. Retrieved on 13 December 2006.