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 Tankel; Randall 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

doi:10.1371/journal.pntd.0001841

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

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19 Citations (Scopus)

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.

Original language	English
Article number	e1841
Pages (from-to)	e1841
Number of pages	8
Journal	Plos Neglected Tropical Diseases
Volume	6
Issue number	9
DOIs	https://doi.org/10.1371/journal.pntd.0001841
Publication status	Published - 1 Sept 2012

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10.1371/journal.pntd.0001841

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Johnston, C., O'Leary, M., Brown, S., Currie, B., Halkidis, L., Whitaker, R., Close, B., Isbister, G., Nagree, Y., Ker, F., Greene, S., Taylor, M., Macrokanis, C., Wilke, G., Coulson, A., Barnes, C., Bonni, R., Downe, M., Whyte, I., ... Williams, V. (2012). Death Adder Envenoming Causes Neurotoxicity Not Reversed by Antivenom - Australian Snakebite Project (ASP-16). Plos Neglected Tropical Diseases, 6(9), e1841. [e1841]. https://doi.org/10.1371/journal.pntd.0001841

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

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

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language = "English",

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Johnston, C, O'Leary, M, Brown, S, Currie, B, Halkidis, L, Whitaker, R, Close, B, Isbister, G, Nagree, Y, Ker, F, Greene, S, Taylor, M, Macrokanis, C, Wilke, G, Coulson, A, Barnes, C, Bonni, R, Downe, M, Whyte, I, Tankel, A, Greenberg, R, Webb, M, Ellis, R, Spai, D, Ireland, G, Gan, M, Porges, K, Bitmead, D, Tay, K, Miller, M, Bailey, P, Vlad, I, Gavaghan, C, Holdgate, A, McGregor, K, Fraser, T, Graudins, A, Garrett, P, Ward, D, Buckley, N, Chan, B, Page, C, Parkin, A, Mead, H, Thompson, P, Treston, G, Alfred, S, Gray, T, Yeung, J, McCoubrie, D, Dawson, A, Little, M, Gault, A, Pascu, O, Ryan, N, Mills, K, Miller, P, Curran, S, Gunja, N, Dowsett, R, White, J, Ghent, T, Just, S & Williams, V 2012, 'Death Adder Envenoming Causes Neurotoxicity Not Reversed by Antivenom - Australian Snakebite Project (ASP-16)', Plos Neglected Tropical Diseases, vol. 6, no. 9, e1841, pp. e1841. https://doi.org/10.1371/journal.pntd.0001841

TY - JOUR

T1 - Death Adder Envenoming Causes Neurotoxicity Not Reversed by Antivenom - Australian Snakebite Project (ASP-16)

AU - Johnston, Christopher

AU - O'Leary, Margaret

AU - Brown, Simon

AU - Currie, Bart

AU - Halkidis, Lambros

AU - Whitaker, Richard

AU - Close, Benjamin

AU - Isbister, Geoffrey

AU - Nagree, Yusuf

AU - Ker, Fergus

AU - Greene, Shaun

AU - Taylor, Michael

AU - Macrokanis, Conrad

AU - Wilke, Gary

AU - Coulson, Adam

AU - Barnes, Christopher

AU - Bonni, Robert

AU - Downe, Michael

AU - Whyte, I

AU - Tankel, Alan

AU - Greenberg, Randall

AU - Webb, Mark

AU - Ellis, Rod

AU - Spai, David

AU - Ireland, Graham

AU - Gan, Melissa

AU - Porges, Kate

AU - Bitmead, Daniel

AU - Tay, Kenny

AU - Miller, Mark

AU - Bailey, Paul

AU - Vlad, Ioana

AU - Gavaghan, Chris

AU - Holdgate, Anna

AU - McGregor, Kent

AU - Fraser, Todd

AU - Graudins, Andis

AU - Garrett, Peter

AU - Ward, David

AU - Buckley, Nicholas

AU - Chan, Betty

AU - Page, Colin

AU - Parkin, Andrew

AU - Mead, Helen

AU - Thompson, Peter

AU - Treston, Greg

AU - Alfred, Sam

AU - Gray, Tanya

AU - Yeung, Justin

AU - McCoubrie, David

AU - Dawson, Andrew

AU - Little, Mark

AU - Gault, Alan

AU - Pascu, Ovidiu

AU - Ryan, Nick

AU - Mills, Katie

AU - Miller, Peter

AU - Curran, Shane

AU - Gunja, Naren

AU - Dowsett, Robert

AU - White, Julian

AU - Ghent, Tony

AU - Just, Sarah

AU - Williams, Vaughan

PY - 2012/9/1

Y1 - 2012/9/1

N2 - 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.

AB - 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.

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U2 - 10.1371/journal.pntd.0001841

DO - 10.1371/journal.pntd.0001841

M3 - Article

SN - 1935-2735

VL - 6

SP - e1841

JO - Plos Neglected Tropical Diseases

JF - Plos Neglected Tropical Diseases

IS - 9

M1 - e1841

ER -

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

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