Botulism, the most potent toxin known, has been weaponized by several countries. In 1995, an Iraqi defector revealed Iraqi research into and deployment of over 100 munitions containing the toxin. Both aerosol delivery and food supply contamination are possible methods of attack. The toxin exerts its effect through entering presynaptic cholinergic neurons and blocking acetylcholine release. Failed acetylcholine transmission results throughout the nervous system. This causes a clinical picture that is physiologically the opposite of nerve agent intoxication (too much acetylcholine in synapses). Following an incubation period of 3 to 8 days (ingestion) or 24 to 36 h (inhalation), bulbar palsies, diplopia, ptosis, mydriasis, dysarthria, dysphonia, and dysphagia develop. A classic descending, symmetric skeletal muscle paralysis ensues. Death is usually related to respiratory failure. The diagnosis is clinical and is confirmed by cultures of food, stool, and gastric contents. ELISA nasal mucosa swabs may be helpful within 24 h of inhaled botulinum toxin exposure. Treatment is directed primarily at providing respiratory support. Antitoxin is available through the CDC or USAMRIID (see Table 181-1). The CDC-licensed antitoxin is trivalent (effective against three toxin types) and is a horse IgG product, with attendant risks of anaphylaxis and serum sickness. The USAMRIID product is heptavalent (effective against toxin types A through G), and although also equine derived, it is a FAB-fragment product with a theoretically lower risk of anaphylaxis and serum sickness. It is only available for use under an IND protocol. An investigational pentavalent vaccine also exists for high-risk groups.

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