Death Adder Envenoming Causes Neurotoxicity Not Reversed by Antivenom - Australian Snakebite Project (ASP-16)

Christopher Johnston, Margaret O'Leary, Simon Brown, Bart Currie, Lambros Halkidis, Richard Whitaker, Benjamin Close, Geoffrey Isbister, Yusuf Nagree, Fergus Ker, Shaun Greene, Michael Taylor, Conrad Macrokanis, Gary Wilke, Adam Coulson, Christopher Barnes, Robert Bonni, Michael Downe, I Whyte, Alan TankelRandall Greenberg, Mark Webb, Rod Ellis, David Spai, Graham Ireland, Melissa Gan, Kate Porges, Daniel Bitmead, Kenny Tay, Mark Miller, Paul Bailey, Ioana Vlad, Chris Gavaghan, Anna Holdgate, Kent McGregor, Todd Fraser, Andis Graudins, Peter Garrett, David Ward, Nicholas Buckley, Betty Chan, Colin Page, Andrew Parkin, Helen Mead, Peter Thompson, Greg Treston, Sam Alfred, Tanya Gray, Justin Yeung, David McCoubrie, Andrew Dawson, Mark Little, Alan Gault, Ovidiu Pascu, Nick Ryan, Katie Mills, Peter Miller, Shane Curran, Naren Gunja, Robert Dowsett, Julian White, Tony Ghent, Sarah Just, Vaughan Williams

    Research output: Contribution to journalArticlepeer-review

    19 Citations (Scopus)


    Background: Death adders (Acanthophis spp) are found in Australia, Papua New Guinea and parts of eastern Indonesia. This study aimed to investigate the clinical syndrome of death adder envenoming and response to antivenom treatment. Methodology/Principal Findings: Definite death adder bites were recruited from the Australian Snakebite Project (ASP) as defined by expert identification or detection of death adder venom in blood. Clinical effects and laboratory results were collected prospectively, including the time course of neurotoxicity and response to treatment. Enzyme immunoassay was used to measure venom concentrations. Twenty nine patients had definite death adder bites; median age 45 yr (5-74 yr); 25 were male. Envenoming occurred in 14 patients. Two further patients had allergic reactions without envenoming, both snake handlers with previous death adder bites. Of 14 envenomed patients, 12 developed neurotoxicity characterised by ptosis (12), diplopia (9), bulbar weakness (7), intercostal muscle weakness (2) and limb weakness (2). Intubation and mechanical ventilation were required for two patients for 17 and 83 hours. The median time to onset of neurotoxicity was 4 hours (0.5-15.5 hr). One patient bitten by a northern death adder developed myotoxicity and one patient only developed systemic symptoms without neurotoxicity. No patient developed venom induced consumption coagulopathy. Antivenom was administered to 13 patients, all receiving one vial initially. The median time for resolution of neurotoxicity post-antivenom was 21 hours (5-168). The median peak venom concentration in 13 envenomed patients with blood samples was 22 ng/mL (4.4-245 ng/mL). In eight patients where post-antivenom bloods were available, no venom was detected after one vial of antivenom. Conclusions/Significance: Death adder envenoming is characterised by neurotoxicity, which is mild in most cases. One vial of death adder antivenom was sufficient to bind all circulating venom. The persistent neurological effects despite antivenom, suggests that neurotoxicity is not reversed by antivenom.

    Original languageEnglish
    Article numbere1841
    Pages (from-to)e1841
    Number of pages8
    JournalPlos Neglected Tropical Diseases
    Issue number9
    Publication statusPublished - 1 Sept 2012


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