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Death adder envenoming causes neurotoxicity not reversed by antivenom Australian Snakebite Project ASP-16

Johnston, Christopher I., O'Leary, Margaret A., Brown, Simon G. A., Currie, Bart J., Halkidis, Lambros, Whitaker, Richard, Close, Benjamin and Isbister, Geof K. (2012). Death adder envenoming causes neurotoxicity not reversed by antivenom Australian Snakebite Project ASP-16. PLoS Neglected Tropical Diseases,6(9):e1841.

Document type: Journal Article
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Title Death adder envenoming causes neurotoxicity not reversed by antivenom Australian Snakebite Project ASP-16
Author Johnston, Christopher I.
O'Leary, Margaret A.
Brown, Simon G. A.
Currie, Bart J.
Halkidis, Lambros
Whitaker, Richard
Close, Benjamin
Isbister, Geof K.
Journal Name PLoS Neglected Tropical Diseases
Publication Date 2012
Volume Number 6
Issue Number 9
ISSN 1935-2727   (check CDU catalogue  open catalogue search in new window)
Scopus ID 2-s2.0-84866929202
Start Page e1841
Total Pages 7
Place of Publication United states
Publisher Public Library of Science
HERDC Category C1 - Journal Article (DIISR)
Abstract 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.

Author Summary
Death adders are a genus of venomous snakes found in Australia, Papua New Guinea and Indonesia. Death adder envenoming is a rare but important health problem in Australasia. Definite death adder bites were recruited as part of the Australian Snakebite Project (ASP). Clinical effects, laboratory results and response to antivenom treatment were recorded for each case. Death adder envenoming was confirmed by enzyme immunoassay in blood collected from patients. The most important clinical effect was neurotoxicity, which was mild in most cases. One vial of antivenom was shown to be effective at binding circulating death adder venom. However, antivenom had little effect on the neurotoxicity that developed in envenomed patients and neurotoxicity took on average one day to resolve. This study supports the idea of presynaptic neurotoxicity in death adder envenoming which was previously thought to be due to post-synaptic neurotoxicity. The study calls into question the benefit of antivenom, with poor response shown in patients with both mild and severe envenoming.
DOI http://dx.doi.org/10.1371/journal.pntd.0001841   (check subscription with CDU E-Gateway service for CDU Staff and Students  check subscription with CDU E-Gateway in new window)


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