|Common Name(s)||Botulinum Toxins|
|Scientific Name(s)||Clostridium botulinum (bacterium that produces toxins)|
|Physical Attributes||Rod-shaped, Gram positive, anaerobic organisms; seven types A-G; toxins are proteins with molecular weights of approximately 150,000 and bind to presynaptic membrane of neurons|
|Mode(s) of Transmission||Three forms: foodborne (ingesting toxin), wound (spores enter into blood), and infant (ingesting spores); commonly contracted through contaminated canned foods and black-tar herion|
|Likely BW Form(s)||Aerosol|
|Pathology||Double vision, blurred vision, drooping eyelids, slurred speech, difficulty swallowing, dry mouth, and muscle weakness; infants with botulism appear lethargic, feed poorly, are constipated, and have a weak cry and poor muscle tone; paralysis|
|Vector/Dormant Form||None; spores in soil|
|Incubation Period||Usually 24 to 36 hours (anywhere between 6 hours to 10 days)|
|Fatality||60% without treatment; 30% with antitoxin and mechanical ventilation treatment|
|Vaccine||Pentavalent toxoid vaccine for types A, B, C, D, and E under IND status (as of 2007)|
|Treatment||Antitoxin; surgically; therapy|
Botulism is caused by intoxication with the any of the seven distinct neurotoxins produced by the bacillus, Clostridium botulinum. The toxins are proteins with molecular weights of approximately 150,000, which bind to the presynaptic membrane of neurons at peripheral cholinergic synapses to prevent release of acetylcholine and block neurotransmission. The blockade is most evident clinically in the cholinergic autonomic nervous system and at the neuromuscular junction.
In the United States an average of 110 cases of botulism are reported each year. Of these, approximately 25% are foodborne, 72% are infant botulism, and the rest are wound botulism. Outbreaks of foodborne botulism involving two or more persons occur most years and usually caused by eating contaminated home-canned foods. The number of cases of foodborne and infant botulism has changed little in recent years, but wound botulism has increased because of the use of black-tar heroin, especially in California.
A biological warfare attack with botulinum toxin delivered by aerosol would be expected to cause symptoms similar in most respects to those observed with food-borne botulism.
In pure form, the toxin is a white crystalline substance, that is readily dissolvable in water, but decays rapidly in the open air. Symptoms of inhalation botulism may begin as early as 24-36 hours following exposure or as late as several days. Initial signs and symptoms include ptosis, generalized weakness, lassitude, and dizziness. Diminished salivation with extreme dryness of the mouth and throat may cause complaints of a sore throat. Urinary retention or ileus may also occur. Motor symptoms usually are present early in the disease; cranial nerves are affected first with blurred vision, diplopia, ptosis, and photophobia. Development of respiratory failure may be abrupt. Mucous membranes of the mouth may be dry and crusted. Neurological examination shows flaccid muscle weakness of the palate, tongue, larynx, respiratory muscles, and extremities. Deep tendon reflexes vary from intact to absent.
The occurrence of an epidemic with large numbers of afebrile patients with progressive ocular, pharyngeal, respiratory, and muscular weakness and paralysis hints strongly at the diagnosis. Single cases may be confused with various neuromuscular disorders such as atypical Guillain-Barrè syndrome, myasthenia gravis, or tick paralysis. The edrophonium (tensilon) test may be transiently positive in botulism.
Respiratory failure secondary to paralysis of respiratory muscles is the most serious complication and, generally, the cause of death. Reported cases of botulism prior to 1950 had a mortality of 60%. With tracheotomy and ventilator assistance, fatalities should be <5%. Intensive and prolonged nursing care may be required for recovery (which may take several weeks or even months).
A pentavalent toxoid of Clostridium botulinum types A, B, C, D, and E is available under IND status. This product has been administered to several thousand volunteers and occupationally at-risk workers and induces serum antitoxin levels that correspond to protective levels in experimental animal systems. The currently recommended schedule (0, 2, and 12 weeks, then a 1 year booster) induces solidly protective antitoxin levels in greater than 90 percent of those vaccinated after 1 year.
|Join the GlobalSecurity.org mailing list|