Evaluation of the therapeutic window of commercial antivenoms against neurotoxicity induced by Bungarus ceylonicus and Bungarus caeruleus venoms in the chick-biventer cervicis model.

Krait (Genus: Bungarus) envenoming is characterised by progressive neuromuscular paralysis. In Sri Lanka, the absence of a species-specific antivenom for envenoming by the endemic Sri Lankan krait (Bungarus ceylonicus) necessitates reliance on Indian polyvalent antivenoms, despite limited evidence of their efficacy. This study investigated the time window during which commercial Indian (BHARAT, VINS) and Australian polyvalent (Seqirus) antivenoms can prevent neurotoxicity induced by Sri Lankan Krait (B. ceylonicus) and Common Krait (Bungarus caeruleus) venoms using the chick biventer cervicis nerve-muscle preparation. Venoms were added at concentrations producing either predominantly pre-synaptic or post-synaptic neurotoxicity, and antivenoms were added 30 or 90 min after venom exposure. When added after venom, all antivenoms showed a consistent, time-dependent decline in efficacy against pre-synaptic neurotoxicity, with only partial prevention when added after 30 min and complete failure when added after 90 min. In contrast, post-synaptic neurotoxicity remained more amenable to neutralization after a delay; BHARAT partially prevented post-synaptic effects of both venoms at 30 min, while VINS fully prevented post-synaptic neurotoxicity of B. caeruleus at the same time point. These findings support the hypothesis that pre-synaptic toxins rapidly enter motor nerve terminals, limiting antivenom access and reversibility, whereas the effects of post-synaptic toxins are more readily reversible due to their extracellular mode of action.