Abstract
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.
Highlights
Snake bite is a significant public health issue in the tropics [1]
In a recent clinical and neurophysiological investigation of neuromuscular paralysis in Sri Lankan Russell’s viper envenoming, we showed that the paralysis is mild, non-life threatening with no long term effects [6]
We have recently shown that the pre-synaptic neurotoxicity of the Sri Lankan Russell’s viper venom is primarily due to one of the S-type phospholipase A2 (PLA2) toxins, which we named U1-viperitoxin-Dr1a [33]
Summary
Coagulopathy, neuromuscular paralysis, acute kidney injury and local effects are the most important clinical syndromes of snake envenoming [2]. Russell’s viper bites cause a large number of envenomings across Asia, and are more medically important than any other snake in the region [3,4]. Both species of Russell’s vipers, i.e. D_russelii (found in Sri Lanka, India, Pakistan, Nepal, Bangladesh) and D. siamensis (found in some parts of southeast and east Asia such as Cambodia, Myanmar, Thailand, Taiwan, South China and, some parts of Indonesia including East Java), commonly cause venom-induced consumption coagulopathy, acute kidney injury and mild local effects throughout their distribution [3,5]. This study aimed to investigate evidence of myotoxicity in Russell’s viper envenoming, response to antivenom and the toxins responsible for myotoxicity
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