Tiger snake (Notechis spp) envenoming: Australian Snakebite Project (ASP‐13)

O’Leary, Margaret A.; Elliott, Matthew; Brown, Simon G A

doi:10.5694/mja11.11300

Cited by 56 publications

(48 citation statements)

References 24 publications

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“…This is well supported by clinical observations that neurotoxic snake envenoming almost exclusively results in flaccid paralysis [4,5,6,7,8,9,10,11,12] which is due to the blockade of neurotransmission at the neuromuscular junction by venom neurotoxins [13,14,15,16]. Neuromuscular paralysis in snake envenoming varies from mild to life threatening, depending on the degree of envenoming (i.e., quantity of injected venom reaching the circulation), the composition of the venom and potentially early therapeutic interventions.…”

Section: Neuromuscular Paralysis In Snake Envenomingsupporting

confidence: 60%

“…Recovery of function by re-innervation takes 3 to 5 days after exposure to the toxin, and by 7 days, re-innervation is complete [13]. Many snake venoms that are known to cause severe paralysis in humans, such as Indian krait ( B. caeruleus ) [4], Malayan krait ( B. candidus ) [6], Chinese banded krait ( B. multicinctus ) [48], coastal taipan ( O. scutellatus ) [49] and tiger snake ( N. scutatus ) [11] venoms, contain potent pre-synaptic neurotoxins (Supplementary Table S1). A detailed account of these toxins is available in the review by Harris and Scott-Davey [16].…”

Section: Neuromuscular Junction: the Primary Target Sitementioning

confidence: 99%

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Antivenom for Neuromuscular Paralysis Resulting From Snake Envenoming

Silva

Hodgson

2017

Toxins

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Antivenom therapy is currently the standard practice for treating neuromuscular dysfunction in snake envenoming. We reviewed the clinical and experimental evidence-base for the efficacy and effectiveness of antivenom in snakebite neurotoxicity. The main site of snake neurotoxins is the neuromuscular junction, and the majority are either: (1) pre-synaptic neurotoxins irreversibly damaging the presynaptic terminal; or (2) post-synaptic neurotoxins that bind to the nicotinic acetylcholine receptor. Pre-clinical tests of antivenom efficacy for neurotoxicity include rodent lethality tests, which are problematic, and in vitro pharmacological tests such as nerve-muscle preparation studies, that appear to provide more clinically meaningful information. We searched MEDLINE (from 1946) and EMBASE (from 1947) until March 2017 for clinical studies. The search yielded no randomised placebo-controlled trials of antivenom for neuromuscular dysfunction. There were several randomised and non-randomised comparative trials that compared two or more doses of the same or different antivenom, and numerous cohort studies and case reports. The majority of studies available had deficiencies including poor case definition, poor study design, small sample size or no objective measures of paralysis. A number of studies demonstrated the efficacy of antivenom in human envenoming by clearing circulating venom. Studies of snakes with primarily pre-synaptic neurotoxins, such as kraits (Bungarus spp.) and taipans (Oxyuranus spp.) suggest that antivenom does not reverse established neurotoxicity, but early administration may be associated with decreased severity or prevent neurotoxicity. Small studies of snakes with mainly post-synaptic neurotoxins, including some cobra species (Naja spp.), provide preliminary evidence that neurotoxicity may be reversed with antivenom, but placebo controlled studies with objective outcome measures are required to confirm this.

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Section: Neuromuscular Paralysis In Snake Envenomingsupporting

confidence: 60%

Section: Neuromuscular Junction: the Primary Target Sitementioning

confidence: 99%

Antivenom for Neuromuscular Paralysis Resulting From Snake Envenoming

Silva

Hodgson

2017

Toxins

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“…Peak CK concentrations were abnormally high in less than 17% of patients, and even in these cases there were only modest elevations with the median and maximum being 666 and 1066 U/l, respectively. In comparison, the reported median peak CK values following envenoming by mulga snakes and tiger snakes in Australia were 3100 U/l [20] and 4749 U/l [19], with severe myotoxicity being associated with CK values over 100,000 U/L. This means that myotoxicity in Russell’s viper envenoming is uncommon and mild when it occurs compared to other myotoxic snakes.…”

Section: Discussionmentioning

confidence: 99%

“…Local muscle necrosis is a component of the local necrotic effects [12,13]. Systemic myotoxicity has been reported following envenoming by some vipers [14,15], sea snakes [16–18], Australasian elapids [19,20] and some Asian kraits [21,22]. Systemic myotoxicity ranges in severity.…”

Section: Introductionmentioning

confidence: 99%

Clinical and Pharmacological Investigation of Myotoxicity in Sri Lankan Russell’s Viper (Daboia russelii) Envenoming

et al. 2016

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BackgroundSri Lankan Russell’s viper (Daboia russelii) envenoming is reported to cause myotoxicity and neurotoxicity, which are different to the effects of envenoming by most other populations of Russell’s vipers. This study aimed to investigate evidence of myotoxicity in Russell’s viper envenoming, response to antivenom and the toxins responsible for myotoxicity.Methodology and FindingsClinical features of myotoxicity were assessed in authenticated Russell’s viper bite patients admitted to a Sri Lankan teaching hospital. Toxins were isolated using high-performance liquid chromatography. In-vitro myotoxicity of the venom and toxins was investigated in chick biventer nerve-muscle preparations. Of 245 enrolled patients, 177 (72.2%) had local myalgia and 173 (70.6%) had local muscle tenderness. Generalized myalgia and muscle tenderness were present in 35 (14.2%) and 29 (11.8%) patients, respectively. Thirty-seven patients had high (>300 U/l) serum creatine kinase (CK) concentrations in samples 24h post-bite (median: 666 U/l; maximum: 1066 U/l). Peak venom and 24h CK concentrations were not associated (Spearman’s correlation; p = 0.48). The 24h CK concentrations differed in patients without myotoxicity (median 58 U/l), compared to those with local (137 U/l) and generalised signs/symptoms of myotoxicity (107 U/l; p = 0.049). Venom caused concentration-dependent inhibition of direct twitches in the chick biventer cervicis nerve-muscle preparation, without completely abolishing direct twitches after 3 h even at 80 μg/ml. Indian polyvalent antivenom did not prevent in-vitro myotoxicity at recommended concentrations. Two phospholipase A2 toxins with molecular weights of 13kDa, U1-viperitoxin-Dr1a (19.2% of venom) and U1-viperitoxin-Dr1b (22.7% of venom), concentration dependently inhibited direct twitches in the chick biventer cervicis nerve-muscle preparation. At 3 μM, U1-viperitoxin-Dr1a abolished twitches, while U1-viperitoxin-Dr1b caused 70% inhibition of twitch force after 3h. Removal of both toxins from whole venom resulted in no in-vitro myotoxicity.ConclusionThe study shows that myotoxicity in Sri Lankan Russell’s viper envenoming is mild and non-life threatening, and due to two PLA2 toxins with weak myotoxic properties.

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“…1,4 Updated recommendations 2013 advocate single vial of relevant snake monovalent or polyvalent antivenom in snakebite cases for all five major groups of Australian snakes. Larger or repeated antivenom doses do not quicken recovery or improvement of laboratory parameters.…”

mentioning

confidence: 99%