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  • Updated 04.05.2024
  • Released 07.12.1994
  • Expires For CME 04.05.2027

Infant botulism



Infant botulism is serious bacterial infection that results from ingestion of Clostridium botulinum spores that colonize the intestinal tract, releasing botulinum toxin resulting in progressive neuromuscular weakness (constipation, bulbar dysfunction, flaccid descending paralysis, and respiratory failure). Treatment includes urgent administration of botulinum immune globulin (BabyBIG®), which has been shown to shorten the course of the disorder as measured by the duration of mechanical ventilation, hospitalization, and tube feedings. If you suspect your patient has botulism, notify your state public health department. BabyBIG® can be obtained from the California Department of Health Services (phone 510-231-7600). Supportive care is also emphasized given potential complications, including respiratory failure. Most infants recover without sequelae. In this article, the author discusses the clinical manifestations, diagnosis, and therapy of infant botulism.

Key points

• Infant botulism presents with a progression of symptoms: constipation; cranial nerve palsies (weak cry, poor feeding, ptosis); flaccid descending paralysis; and possible respiratory failure.

• Symptoms result from ingestion of Clostridium botulinum spores that colonize the intestinal tract and produce botulism toxin (most commonly A and B).

• Botulism toxin binds irreversibly to presynaptic terminals, preventing release of acetylcholine and, thus, preventing muscle contraction.

• Treatment includes urgent administration of botulism immune globulin (BabyBIG®) as well as supportive care.

• BabyBIG® can be obtained from the California Department of Health Services (phone 510-231-7600).

Historical note and terminology

Human botulism has three major forms: (1) food-borne botulism, caused by ingesting preformed botulinum toxin; (2) wound botulism, due to direct infection with the bacterium Clostridium botulinum; and (3) infant botulism, caused by ingestion of C botulinum spores and subsequent production of the toxin within the infant gastrointestinal tract (67). Additionally, iatrogenic botulism secondary to clinical botulinum toxin injection, such as for treatment of spasticity, has been described in case reports (56). Increasingly, the use of botulinum toxin as an agent for bioterrorism is also a concern.

Before effective food processing, food-borne botulism was a major cause of acute paralysis and death. In 1897, Van Ermengen isolated the spore-forming, gram-positive anaerobe, Bacillus botulinum (later named Clostridium botulinum; botulism is derived from the Latin, botulus, for "sausage") from the spleen of an outbreak victim and from contaminated ham. Van Ermengen recognized that food-borne botulism originates from ingestion of preformed toxin rather than from direct infection with an enteric pathogen.

Wound and food-borne botulism remained the only disorders attributed to C botulinum until the early 1970s, when acute weakness in infants was linked to enteric colonization with the organism. This disorder, named infant botulism, caused acute bulbar and systemic weakness and respiratory failure (34; 52; 57; 09; 71). As food-borne outbreaks of botulism have declined, infant botulism is now the most common form of human botulism in the developed world (04; 51; 67). Infant botulism accounts for approximately 63% of botulism cases reported to local and state health departments in the United States (19).

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