Botulism pathogenesis

Gastrointestinal colonization in adults or children by clostridial bacteria does not typically take place except under circumstances where the normal flora has been altered by antibiotic treatment (Cheiington, 1998). Botulism results from in vivo production of toxin, analogous to the pathogenesis of infant botulism (McCroskey and Hatheway, 1988 Chia et al, 1986). Support for this form of botulism is provided by demonstration of prolonged excretion of toxin and C. botulinum in stool and/or by the demonstration of C. botulinum spores but not preformed toxin in suspected foods. 

BoNTs are a group of immunologically distinct but closely related bacterial proteins that act as potent inhibitors of synaptic transmission in skeletal muscle. Inhibition of ACh release from the presynaptic terminal of the neuromuscular junction (NMJ) is thought to be the sole mechanism involved in the toxins lethal action (Sellin, 1985 Simpson, 1986) and therefore the cause of botulism. The pathogenesis of intoxication is not completely understood but is generally thought to involve a multistep process to interrupt normal vesicular release of ACh Ifom the presynaptic motor nerve... 

The administration of heterologous antitoxin was one of the first therapeutic approaches developed for botuhsm patients and remains the most effective when initiated in the early stages of intoxication. The primary limitation of antitoxin treatment was established in some of the earhest published reports on experimental botuhsm. One of these reports evaluated the pathogenesis of oral intoxication and the efficacy of antitoxin therapy in monkeys (Back and Wood, 1928). Antitoxin treatment was not effective when administered after symptoms of botulism were already apparent, despite the fact that circulating toxin could still be detected in many of the animals. 

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