Botulism in the United States: A Review
December 1, 1998
Botulism in the United States: A Review
disease update
Source: Shapiro RL, et al. Botulism in the United States: A clinical and epidemiologic review. Ann Intern Med 1998; 129:221-228.
Roughly 100 cases of botulism are reported annually to the Centers for Disease Control and Prevention (CDC), and, with new modes of transmission, including black tar heroin abuse and terrorist use of biological warfare, timely review of the subject seems appropriate.
Most cases result from toxins A, B, or E, but seven distinct forms of neurotoxin (A to G) are recognized, produced by (at least) three genetically distinguishable forms of Clostridium botulinum, a ubiquitous, anaerobic, gram-positive, spore-forming bacillus. Food preservation, which usually kills nonsporulating organisms, is ineffective against the heat-resistant spores that excrete exotoxin, which irreversibly binds to the presynaptic nerve terminal, inhibiting acetylcholine release and causing autonomic and voluntary muscle paralysis.
In foodborne botulism, following a gastrointestinal prodrome of nausea, vomiting, cramps, or diarrhea, neurologic symptoms set in, beginning with dry mouth, blurred vision, and diplopia, followed by dysphonia, dysarthria, dysphagia, and descending muscle weakness affecting the arms, respiratory muscles, and legs in a proximal to distal progression. Recovery requires weeks to months and correlates with formation of new neuromuscular synapses. Abscess wounds provide the anaerobic environment needed for spores to germinate and excrete neurotoxin in wound botulism, which produces a neurologic syndrome identical to foodborne botulism but without the gastrointestinal prodrome. Median time to onset of symptoms is seven days, compared to 18-36 hours with foodborne botulism. Infant botulism usually occurs during the first six months of life, most commonly during the second month, and presents with constipation, poor suck and swallow, weak cry, and descending paralysis. GI absorption of toxin is the presumed mechanism, but, in 85%, the source is unknown. In 15%, honey ingestion is implicated. The rare adult infectious botulism is the adult equivalent of infantile botulism and may result from gastrointestinal colonization with C. botulinum.
Diagnosis is suspected on clinical grounds and may be confirmed by detecting toxin in serum, stool, or food samples using the mouse innoculation test that can be performed by the CDC; the emergency 24-hour telephone number is (404) 639-2888. Stool cultures for C. botulinum are also considered diagnostic. Supportive measures (primarily mechanical ventilation) remain the mainstay of treatment, with gastric lavage if food exposure was recent and cathartics or enemas, in the absence of ileus, to remove unabsorbed toxin from the gastrointestinal tract. Surgical debridement and antibiotics are indicated for wound botulism.
Trivalent equine antitoxin contains antibodies to types A, B, and E and is administered intravenously (10 cc) to neutralize unbound toxin. When administered early, it prevents progression, shortens the need for ventilatory support, shortens hospital stay, and decreases mortality. Up to 9% of patients have a hypersensitivity reaction, and, consequently, equine antitoxin is not recommended for infantile botulism. As of June 1998, human botulism immune globulin is available in the United States solely for infantile botulism under an Investigational New Drug Protocol and may be obtained by calling the California Department of Health at (510) 540-2646. (Michael Rubin, MD, is Associate Professor of Neurology, New York Hospital-Cornell Medical Center.)
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