Two Cases of Severe Food-Borne Botulism: Could High-Dose Methylcobalamin Accelerate Recovery?

Botulinum neurotoxins (BoNTs) are zinc-dependent endopeptidases that cleave presynaptic SNARE proteins and arrest acetylcholine release, producing flaccid paralysis with protracted recovery. We report two cases of a mother and son who developed severe food-borne botulism after eating Fesikh (traditional salted fish) with rapidly progressive descending paralysis requiring ventilation, prominent dysautonomia (hypotension responsive to fluids, bradycardia, dry mucosae, constipation with abdominal distension, as well as urinary retention), and intact consciousness. Both received trivalent antitoxin on day 2; the son was extubated on day 10, and the mother on day 16. Persistent bladder atony, fatigue, weakness, and poor concentration improved with structured physiotherapy accompanied by intramuscular methylcobalamin, which was initiated on day 1 of admission and subsequently transitioned to an eight-week course of oral methylcobalamin (500 µg daily) during the post-extubation rehabilitation phase. We discuss mechanistic plausibility and hypothesize that higher-dose methylcobalamin might accelerate neuromuscular recovery by stabilizing mitochondria, attenuating caspase-mediated apoptosis, and promoting axonal regeneration and sprouting.