Abstract
Coastal taipan (Oxyuranus scutellatus) envenoming causes life-threatening neuromuscular paralysis in humans. We studied the time period during which antivenom remains effective in preventing and arresting in vitro neuromuscular block caused by taipan venom and taipoxin. Venom showed predominant pre-synaptic neurotoxicity at 3 µg/mL and post-synaptic neurotoxicity at 10 µg/mL. Pre-synaptic neurotoxicity was prevented by addition of Australian polyvalent antivenom before the venom and taipoxin and, reversed when antivenom was added 5 min after venom and taipoxin. Antivenom only partially reversed the neurotoxicity when added 15 min after venom and had no significant effect when added 30 min after venom. In contrast, post-synaptic activity was fully reversed when antivenom was added 30 min after venom. The effect of antivenom on pre-synaptic neuromuscular block was reproduced by washing the bath at similar time intervals for 3 µg/mL, but not for 10 µg/mL. We found an approximate 10–15 min time window in which antivenom can prevent pre-synaptic neuromuscular block. This time window is likely to be longer in envenomed patients due to the delay in venom absorption. Similar effectiveness of antivenom and washing with 3 µg/mL venom suggests that antivenom most likely acts by neutralizing pre-synaptic toxins before they interfere with neurotransmission inside the motor nerve terminals.
Highlights
Snake envenoming is a major health issue in the tropics [1]
We aimed to investigate the time during which the Australian commercial polyvalent antivenom remains effective in preventing the occurrence and reversal of already existing pre- and post-synaptic in vitro neuromuscular block caused by coastal taipan venom and taipoxin
We investigated the effect of antivenom on venom-mediated pre- and post-synaptic neurotoxicity and showed that this could be mimicked by washing the neuromuscular preparation with the physiological salt solution, at least for the venom at 3 μg/mL
Summary
Snake envenoming is a major health issue in the tropics [1]. Neuromuscular paralysis is a common, life-threatening clinical effect of envenoming by some cobras (genus: Naja), kraits (genus: Bungarus), coral snakes (genera: Micrurus, Calliophis), some Australasian elapids (Oxyuranus, Acanthophis, and Notechis species), and some viperids (Crotalus, Daboia, Vipera species) in humans [3,4]. Neurotoxic snake venoms possess toxins acting pre- or post-synaptically at the neuromuscular junction, resulting in neuromuscular blockade. Pre-synaptic neurotoxins ( known as β-neurotoxins) are phospholipase A2 toxins which enter the motor nerve terminals and diminish vesicular recycling that results in a depletion of the synaptic vesicles. Motor nerve terminals are damaged structurally resulting in denervation of the muscles. Post-synaptic neurotoxins ( known as α-neurotoxins) are three-finger toxins that competitively antagonise the nicotinic acetylcholine receptors (nAChR) at the motor end-plate [9,10]
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