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The emerging syndrome of envenoming by the New Guinea small-eyed snake Micropechis ikaheka
Authors:Warrell  DA; Hudson  BJ; Lalloo  DG; Trevett  AJ; Whitehead  P; Bamler  PR; Ranaivoson  M; Wiyono  A; Richie  TL; Fryauff  DJ; O'Shea  MT; Richards  AM; Theakston  RD
Affiliation:Centre for Tropical Medicine, University of Oxford, UK; Royal North Shore Hospital, St Leonards, NSW, Australia; Department of Medicine, University of Papua New Guinea, PNG; Bulollo Health Centre, PNG; Gaubin Lutheran Mission Hospital, Kar Kar Island, PNG; Intensive Care Unit, Provincial Hospital, Jayapura, Irian Jaya, Indonesia; US Naval Medical Research Unit No 2, Jakarta, Indonesia; Christensen Research Institute, Madang, PNG; Alistair Reid Venom Research Unit, Liverpool School of Tropical Medicine, UK; Correspondence to: Prof DA Warrell, Centre for Tropical Medicine, John Radcliffe Hospital, Headington, Oxford OX3 9DU, UK; Present address: Public Health Dept, Nottingham Health Authority, Forest Rise, Berkeley Avenue, Nottingham, UK
Abstract:The New Guinea small-eyed or Ikaheka snake, <it>Micropechis ikaheka</it>, which occurs throughout New Guinea and some adjacent islands, is feared by the indigenes. The first proven human fatality was in the 1950s and this species has since been implicated in many other cases of severe and fatal envenoming. Reliable attribution of envenoming to this species in victims unable to capture or kill the snake recently became possible by the use of enzyme immunoassay. Eleven cases of proven envenoming by <it>M. ikaheka</it>, with two fatalities, were identified in Papua New Guinea and Irian Jaya. Five patients showed no clinical signs of envenoming by other Australasian elapids: mild local swelling, local lymphadenopathy, neurotoxicity, general myalgia, spontaneous systemic bleeding, incoagulable blood and passage of dark urine (haemoglobinuria or myoglobinuria). Two patients developed hypotension and two died of respiratory paralysis 19 and 38 h after being bitten. <it>In vitro</it> studies indicate that the venom is rich in phospholipase A2, is indirectly haemolytic, anticoagulant and inhibits platelets, but is not procoagulant or fibrinolytic. It shows predominantly post-synaptic neurotoxic and myotoxic activity. Anecdotally, Commonwealth Serum Laboratories' (CSL) death adder antivenom has proved ineffective whereas CSL polyvalent antivenom may be beneficial. Anticholinesterase drugs might prove effective in improving neuromuscular transmission and should be tested in patients with neurotoxic envenoming.
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