A farmer in rural India is bitten by a snake. On examination: bilateral ptosis, ophthalmoplegia, and difficulty swallowing without significant local swelling or tissue necrosis. This clinical picture is MOST consistent with envenomation by which snake, and what is the toxin mechanism?

• A Russell's viper (Daboia russelii) — phospholipase A2 causing local necrosis
• B Common krait (Bungarus caeruleus) — presynaptic and postsynaptic neurotoxins causing neuromuscular blockade ✓
• C Saw-scaled viper (Echis carinatus) — thrombin-like enzyme causing consumptive coagulopathy
• D King cobra (Ophiophagus hannah) — cardiotoxins causing direct myocardial depression

Explanation

The clinical presentation of bilateral ptosis, ophthalmoplegia, bulbar palsy, and absent local tissue damage (no swelling, no necrosis) is the hallmark of neurotoxic envenomation by elapids, specifically the common krait. Krait venom contains beta-bungarotoxin (presynaptic — prevents acetylcholine release) and alpha-bungarotoxin (postsynaptic — competitive nicotinic receptor blockade). This pure descending flaccid paralysis without haematotoxicity distinguishes krait from viper envenomation. Russell's viper (A) causes haemotoxicity and local tissue necrosis. Saw-scaled viper (C) causes coagulopathy with viperin. King cobra (D) can cause neurotoxicity but also significant local effects.

Reference: The Essentials of Forensic Medicine and Toxicology (Narayan Reddy), 34th ed.

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Written and medically reviewed by the StethoPrep medical team.