Back to Infectious Diseases or Bioterror Introduction


Agent: Botulism is caused by the neurotoxin produced by the bacillus Clostridium botulinum, a spore-forming obligate anaerobe widely found in soil; and by other Clostridium sp. Botulinum toxin is the most lethal known natural poison. There are seven different botulinum toxins, designated A-G. Significantly, botulinum antitoxins are specific to type, i.e., type A anti-toxin does not neutralize type B, and so on (see treatment below). As a naturally occurring disease, botulism appears as a severe food poisoning resulting from ingesting the neurotoxin, wound infection with the toxin, and intestinal (formerly "infant botulism"). Botulism as a BW weapon is discussed below (Arnon, Schecter, Inglesby, Henderson, Bartlett, Ascher, Eitzen, Fine, Hauer, Layton, Lillibridge, Osterholm, O'Toole, Parker, Perl, Russell, Swerdlow, & Tonat, 2001; Chin, 2000; Schecter & Arnon, 2000).

Routes of Infection: As a bioterror weapon, botulism can be dispersed in aerosol form or dispensed in food. The aerosol (inhalation) form would create more casualties, but the food method would also be disruptive as patients with botulism require lengthy critical care/ventilator support. Indeed, even a single case of botulism, especially if there is no obvious source, raises the possibility of deliberate use. By two days post attack, aerosolized botulinum would likely be degraded to a level of little danger (recalling that botulinum is widely found in soil (Arnon et al, 2001; Chin, 2000).

Incubation: The usual incubation period is 12-36 hours and ranges from two hours up to eight days, depending upon several factors (especially the amount of toxin absorbed); with the shorter period associated with more severe disease (Chin, 2000).


Signs & Symptoms: Regardless of route of ingestion, all forms of botulism produce similar neurological signs (though GI distress may occur from naturally occurring food borne botulism). The severity of symptoms varies significantly. Initial presentation includes cranial nerve involvement, with bulbar palsies, ptosis, diplopia, blurred vision, photophobia, and decreased visual accommodation. The mouth may be dry with pharyngeal injection. Symptoms progress to dysarthria, dysphonia, and dysphagia with loss of gag reflex. Further progression includes a descending symmetric flaccid paralysis with loss of head control, hypotonia, generalized weakness, and diaphragmatic and respiratory muscle paralysis. Death results from airway obstruction and inadequate tidal volume. Sensorium remains intact and unless there is a secondary or unrelated infection patients are afebrile (Arnon et al, 2001: Cieslak & Eitzen, 2000). The classic triad of botulism (Arnon et al, 2001) is:

Diagnosis: Initial diagnosis is on clinical grounds and workup may include electromyogram. Confirmation is through laboratory testing at CDC or one of about 20 other laboratories. CDC furnishes instructions for obtaining samples.

Differential Diagnosis: A cluster of patients with the classic triad of botulism is highly suspicious. Major differentials include Guillain-Barre syndrome, myasthenia gravis, depressant intoxication, and other central nervous system disorders.

Treatment: Treatment includes passive immunization and supportive care. If botulinism is identified early, botulinum antitoxin decreases the progressive nerve damage and disease severity, but does not reverse extant damage, hence speed is essential. The trivalent antitoxin available from state and local health departments has antibodies effective against botulinum types A, B, and E. Iraq is known to have produced and likely still possess weaponized types A,B,E, and F (several strains of A and E) (Shoham, 2000). The military has a heptavalent antitoxin effective against types A-G. The antitoxins are equine, hence a test dose is required (see insert for updates) and desensitization necessary in a small percentage of patients. Contact CDC at 404.639.2206 during office hours and at 404.639.2888 at other times.

Supportive care is focused primarily on respiratory support. For isolated severe cases, critical care includes with mechanical ventilation, enteral or parenteral feeding, and prevention/treatment of secondary infections. With decreasing respiratory function, anticipatory intubation is indicated. Ventilation may be necessary for several months. If secondary respiratory infections develop, aminoglycosides and clindamycin are contraindicated due to exacerbation of neuromuscular blockade.

Obviously there are insufficient critical care beds and/or ventilators or trained staff for a major attack. In the absence of adequate support, positioning at reverse Trendelenburg at 20-25 degrees is recommended over Fowler's or supine. Food should be given in small amounts; be soft, semi-solid, or finely chopped; non-abrasive and moist; and liquids may be better tolerated through a straw (Arnon et al, 2001; Chin, 2000; Cieslak & Eitzen, 2000).

Protection: The botulinum toxin cannot be absorbed through intact skin, hence covering mouth, nose, and eyes provides some protection in the event of known presence of the toxin. Aerosolized toxin is significantly degraded after two days. Though effective, post-exposure prophylaxis is a problem because of a lack of sufficient doses of antitoxin and by the risk of reaction to the antitoxin. The toxin is destroyed by heat (85 degrees C for at least five minutes). Clothing and skin can be cleansed with soap and water and contaminated surfaces with hypochlorite bleach. Person-to-person transmission is not a danger.


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