North American Coral Snake Envenomation

Anwar, Mehruba; Bernstein, Jeff

doi:10.1007/978-94-007-6288-6_75-1

Cited by 2 publications

(2 citation statements)

References 24 publications

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“…For instance, the single published account of a Sinomicrurus macclellandi bite indicated that the victim felt nothing until motor issues started developing 6 h after the bite and culminated in lethal respiratory paralysis after 8 h [ 72 ]. Similarly, bites from snakes of the genus Micrurus often exhibit few symptoms besides paralysis [ 73 , 74 , 75 ].…”

Section: Introductionmentioning

confidence: 99%

Electric Blue: Molecular Evolution of Three-Finger Toxins in the Long-Glanded Coral Snake Species Calliophis bivirgatus

Dashevsky

Rokyta

Frank

et al. 2021

Toxins

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The genus Calliophis is the most basal branch of the family Elapidae and several species in it have developed highly elongated venom glands. Recent research has shown that C. bivirgatus has evolved a seemingly unique toxin (calliotoxin) that produces spastic paralysis in their prey by acting on the voltage-gated sodium (NaV) channels. We assembled a transcriptome from C. bivirgatus to investigate the molecular characteristics of these toxins and the venom as a whole. We find strong confirmation that this genus produces the classic elapid eight-cysteine three-finger toxins, that δδ-elapitoxins (toxins that resemble calliotoxin) are responsible for a substantial portion of the venom composition, and that these toxins form a distinct clade within a larger, more diverse clade of C. bivirgatus three-finger toxins. This broader clade of C. bivirgatus toxins also contains the previously named maticotoxins and is somewhat closely related to cytotoxins from other elapids. However, the toxins from this clade that have been characterized are not themselves cytotoxic. No other toxins show clear relationships to toxins of known function from other species.

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Section: Introductionmentioning

confidence: 99%

Electric Blue: Molecular Evolution of Three-Finger Toxins in the Long-Glanded Coral Snake Species Calliophis bivirgatus

Dashevsky

Rokyta

Frank

et al. 2021

Toxins

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“…Systemic envenomation by coral snakes (Micrurus spp.) in humans is characterized by neurotoxicity (Bucaretchi et al, 2016a,b;Risk et al, 2016;Anwar and Bernstein, 2017;Corbett and Clark, 2017) and various studies have confirmed this neurotoxicity in vivo (Vital Brazil, 1965;Weis and McIssac, 1971;Vital Brazil et al, 1976/77;Vital Brazil and Fontana, 1983/84) and in vitro (Vital Brazil et al, 1976/77;Vital Brazil and Fontana, 1983/84;Goularte et al, 1995;Vital Brazil et al, 1995;Abreu et al, 2008, Camargo et al, 2011Renjifo et al, 2012;Carbajal-Saucedo et al, 2014;Yang et al, 2017). The results described here show that, in common with other Micrurus spp., M. l. lemniscatus venom caused irreversible blockade of neurotransmission in mammalian and avian neuromuscular preparations.…”

Section: Discussionmentioning

confidence: 99%

Neurotoxicity of Micrurus lemniscatus lemniscatus (South American coralsnake) venom in vertebrate neuromuscular preparations in vitro and neutralization by antivenom

et al. 2019

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We investigated the effect of South American coral snake (Micrurus lemniscatus lemniscatus) venom on neurotransmission in vertebrate nerve-muscle preparations in vitro. The venom showed calcium-dependent PLA2 activity and caused irreversible neuromuscular blockade (0.1-30 µg/ml) in chick biventer cervicis (BC) and mouse phrenic nerve-diaphragm (PND) preparations. In BC preparations, contractures to exogenous acetylcholine and carbachol (CCh), but not KCl, were abolished by venom concentrations ≥0.3 µg/ml; in PND preparations, the amplitude of the tetanic response was progressively attenuated, but with little tetanic fade. In low Ca 2+ physiological solution, venom (10 µg/ml) caused neuromuscular blockade in PND preparations within ~10 min that was reversible by washing; the addition of Ca 2+ immediately after the blockade temporarily restored the twitch responses, but did not prevent the progression to irreversible blockade. Venom (10 µg/ml) did not depolarize diaphragm muscle, prevent depolarization by CCh, or cause muscle contracture or histological damage. Venom (3 µg/ml) had a biphasic effect on the frequency of miniature end-plate potentials, but did not affect their amplitude; there was a progressive decrease in the amplitude of evoked end-plate potentials. The amplitude of compound action potentials in mouse sciatic nerve was unaffected by venom (10 µg/ml). Pre-incubation of venom with coral snake antivenom (Instituto Butantan) at the recommended antivenom:venom ratio did not neutralize the neuromuscular blockade in PND preparations, but total neutralization was achieved with a 10-fold greater volume of antivenom. The addition of antivenom after 50% and 80% blockade restored the twitch responses. These results show that M. l. lemniscatus venom causes potent, irreversible neuromuscular blockade, without myonecrosis. This blockade is apparently mediated by pre-and postsynaptic neurotoxins and can be reversed by coralsnake antivenom.

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North American Coral Snake Envenomation

Cited by 2 publications

References 24 publications

Electric Blue: Molecular Evolution of Three-Finger Toxins in the Long-Glanded Coral Snake Species Calliophis bivirgatus

Electric Blue: Molecular Evolution of Three-Finger Toxins in the Long-Glanded Coral Snake Species Calliophis bivirgatus

Neurotoxicity of Micrurus lemniscatus lemniscatus (South American coralsnake) venom in vertebrate neuromuscular preparations in vitro and neutralization by antivenom

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