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Chapter: Medical Microbiology: An Introduction to Infectious Diseases: Clostridium, Peptostreptococcus, Bacteroides, and Other Anaerobes

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Botulism : Clinical Aspects

Food-borne botulism usually starts 12 to 36 hours after ingestion of the toxin.

BOTULISM : CLINICAL   ASPECTS

MANIFESTATIONS

Food-borne botulism usually starts 12 to 36 hours after ingestion of the toxin. The first signs are nausea, dry mouth, and, in some cases, diarrhea. Cranial nerve signs, including blurred vision, pupillary dilatation, and nystagmus, occur later. Symmetrical paralysis begins with the ocular, laryngeal, and respiratory muscles and spreads to the trunk and extremities. The most serious finding is complete respiratory paralysis. Mortality is 10 to 20%.

Infant Botulism

A syndrome associated with C. botulinum that occurs in infants between the ages of 3 weeks and 8 months is now the most commonly diagnosed form of botulism. The or-ganism is apparently introduced on weaning or with dietary supplements, especially honey, and multiplies in the infant’s colon, with absorption of small amounts of toxin. The infant shows constipation, poor muscle tone, lethargy, and feeding problems and may have ophthalmic and other paralyses similar to those in adult botulism. Infant botulism may mimic sudden infant death syndrome. The benefits of antitoxin and antimicrobic agents have not been clearly established.

Wound Botulism

Very rarely, wounds infected with other organisms may allow C. botulinum to grow. Wound botulism in parenteral users of cocaine and maxillary sinus botulism in intranasal users of cocaine has been reported. Disease similar to that from food poisoning may de-velop, or it may begin with weakness localized to the injured extremity. Botulism without an obvious food or wound source is occasionally reported in individuals beyond infancy. It is possible that some such cases result from ingestion of spores of C. botulinum with subsequent in vivo production of toxin in a manner similar to that in infant botulism.

DIAGNOSIS

The toxin can be demonstrated in blood, intestinal contents, or remaining food, but these tests require inoculation of mice and are performed only in reference laboratories.C. bot-ulinum may also be isolated from stool or from foodstuffs suspected of responsibility forbotulism.

TREATMENT AND PREVENTION

The availability of intensive supportive measures, particularly mechanical ventilation, is the single most important determinant of clinical outcome. With proper ventilatory sup-port, mortality should be less then 10%. The administration of large doses of horse C. botulinum antitoxin is thought to be useful in neutralizing free toxin. Frequent hyper-sensitivity reactions related to the equine origin of this preparation makes it unsuitable for use in infants. Antimicrobial agents are given only to patients with wound botulism.

 Adequate pressure cooking or autoclaving in the canning process kills spores, and heating food at 100°C for 10 minutes before eating destroys the toxin. Food from dam-aged cans or those that present evidence of positive inside pressure should not even be tasted because of the extreme toxicity of the C. botulinum toxin.

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