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  • Updated 02.02.2024
  • Released 12.07.1993
  • Expires For CME 02.02.2027




In this article, the author reviews the clinical manifestations, diagnostic tests, and management of patients who present with botulism: foodborne, wound, adult intestinal toxemia, iatrogenic (following medical or cosmetic administration), and inhalational botulism. Recent information on wound and foodborne botulism is presented, along with diagnostic evaluations and treatments. Antitoxin treatment recommendations are included.

Key points

• Botulinum toxin is one of the most potent neurotoxins in the world and is lethal in small doses.

• Botulinum toxin acts at the neuromuscular junction. It interferes with proteins involved in acetylcholine vesicle fusion at the presynaptic nerve terminal, impeding acetylcholine release into synapses of the peripheral nervous system.

• Most cases of foodborne botulism come from improperly home-canned foods whose preparation does not destroy C botulinum spores.

• Wound botulism occurs through skin infections, with an increased incidence in people who inject drugs.

• The definitive diagnosis of botulism is made by laboratory confirmation, along with supportive clinical and electrodiagnostic features.

• Frequent monitoring of respiratory function is critical – either by forced vital capacity or negative inspiratory force; consider elective intubation for forced vital capacity less than 30% of predicted.

• Laboratory confirmation is done by demonstrating the presence of botulinum toxin in serum, stool, or food, or by culturing Clostridium species from stool or a wound.

•The Centers for Disease Control and Prevention (CDC) recommend administration of botulinum antitoxin as soon as the diagnosis is suspected.

Historical note and terminology

Following an increase in outbreaks of sausage intoxication in the early 1800s, Kerner (a German physician and poet) described 230 cases, characterizing the clinical syndrome of botulism (63). Further clarification of botulism as an entity was reported in 1897, when van Ermengem described the clinical, toxicological, and bacteriological features of an outbreak of foodborne botulism. He demonstrated that botulism was not due to an infection, but to an intoxication produced by a gram-positive, rod-shaped bacterium he named Bacillus botulinus, later called Clostridium botulinum. In the 1970s, Midura and Arnon identified infants developing paralysis following C botulinum colonization of the gastrointestinal tract, with subsequent release of botulinum toxin into the gut (68). Wound botulism was historically described in connection to traumatic injury. Its association with drug injection use was first reported in 1982 in New York City.

Before 1950, mortality from botulism was approximately 60% (26). More recent data showed that of reported cases, 5% of patients died (Centers for Disease Control and Prevention 2019).

Although termed “botulinum neurotoxin” (BoNT), the toxin comes from six groups of bacteria: Clostridium botulinum I-IV, Clostridium baratii, and Clostridium butyricum (73). Botulinum toxin is a family of serologically related neurotoxins: types A, B, C1, D, E, F, G, and a variably classified H (30; 37).

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