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Botulism begins with cranial nerve palsies and develops into descending symmetrical motor paralysis, which may involve the respiratory muscles. No fever or other signs of infection occur. The time course depends on the amount of toxin present and whether it was ingested preformed in food or produced endogenously in the intestinal tract or a wound.
Spores of C. botulinum are found in soil, pond, and lake sediments in many parts of the world, including the United States. If spores contaminate food, they may convert to the vegetative state, multiply, and produce toxin in storage under proper conditions. This may occur with no change in food taste, color, or odor. The alkaline conditions provided by vegetables, such as green beans, and mushrooms and fish support the growth of C. botu-linum, and the acidic conditions provided by foods such as canned fruit do not support thegrowth of the bacterium. Botulism most often occurs after ingestion of home-canned products that have not been heated at temperatures sufficient to kill C. botulinum spores, although inadequately sterilized commercial fish products have also been implicated. Be-cause the toxin is heat labile, food must be ingested uncooked or after insufficient cook-ing. Botulism often occurs in small family outbreaks in the case of home-prepared foods or less often as isolated cases connected to commercial products. Infant and wound botu-lism results when the toxin is produced endogenously, beginning with environmental spores that are either ingested or contaminate wounds.
Food-borne botulism is an intoxication, not an infection. The ingested preformed toxin is absorbed in the intestinal tract and reaches its neuromuscular junction target via the blood-stream. Once bound there, its inhibition of acetylcholine release causes paralysis due to lack of neuromuscular transmission. The specific disease manifestations depend on the specific nerves to which the circulating toxin binds. Cardiac arrhythmias and blood pressure insta-bility are believed to be due to effects of the toxin on the autonomic nervous system. As with tetanus, the damage to the synapse once the toxin has bound is permanent and recovery requires the sprouting of the presynaptic axons and formation of new synapses.
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