Foodborne botulism is not an infection, but rather an intoxication, that is, the toxin is ingested with food. Infant botulism involves ingestion of spores and wound botulism results from infection of a wound.
Toxin. The very strong botulinum neurotoxin is a heat-labile protein. Seven toxigenic types are differentiated, each of which produces an immunologi-cally distinct form of botulinum toxin. Types A, B, and E cause poisoning in humans. The toxin is a metalloprotease that catalyzes the proteolysis of components of the neuroexocytosis apparatus in the motor end plates, resulting in flaccid paralysis of the musculature.
Pathogenesis and clinical picture. Classic botulism results from eating spoiled foods in which the toxin has been produced under anaerobic conditions by C. botulinum. The toxin is absorbed in the gastrointestinal tract, and then transported to the peripheral nervous system in the bloodstream.
Within a matter of hours or days paralysis symptoms occur, especially in the nerves of the head. Frequent symptoms include seeing double, difficulty swallowing and speaking, constipation, and dry mucosa. Lethality rates range from 25-70%, depending on the amount of toxin ingested. Death usually results from respiratory paralysis. Wound botulism results from wound infection by C. botulinum and is very rare. Infant botulism, first described in 1976, results from ingestion of spores with food (e.g., honey). Probably due to the conditions prevailing in the intestines of infants up to the age of six months, the spores are able to proliferate there and produce the toxin. The lethality of infant botulism is low (<1 %).
Diagnosis. Based on toxin detection by means of the mouse neutralization test.
Therapy. Urgent administration of a polyvalent antitoxin.
Epidemiology and prevention. Botulism is a rare disease. Exposure to the toxin is a food hygiene problem that can be avoided by taking appropriate precautions during food production. Aerosolized botulinum toxin has been used experimentally as a bioweapon.
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