B Jane Distad MD (

Dr. Distad of University of Washington has no relevant financial relationships to disclose.

Christina M Marra MD, editor. (

Dr. Marra of the University of Washington School of Medicine has no relevant financial relationships to disclose.

Originally released December 7, 1993; last updated January 26, 2021; expires January 26, 2024


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. New 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, thereby blocking release into cholinergic 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 demonstrating the presence of botulinum toxin in serum, stool, or suspected food, or isolation of C botulinum from a wound, 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

Botulism as a clinical 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 (Midura and Arnon 1976). 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% (Dembek et al 2007).

Although termed “botulinum neurotoxin” (BoNT), the toxin comes from 6 groups of bacteria: Clostridium botulinum I-IV, Clostridium baratii, and Clostridium butyricum (Peck 2009). Botulinum toxin is a family of serologically related neurotoxins: types A, B, C1, D, E, F, G, and a variably classified H (Dover et al 2014; Hackett et al 2018).

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