Botulism

Basics

Description

  • A paralytic illness caused by a neurotoxin produced by the anaerobic bacterium Clostridium botulinum
  • Characterized by acute onset of cranial nerve dysfunction (diplopia, difficulty swallowing or speaking), symmetric descending weakness, and flaccid paralysis
  • Eight antigenic types of C. botulinum (A to H). Types A, B, E, and, in rare cases, F, cause disease in humans.
  • Forms include (1):
    • Foodborne: ingestion of preformed toxin
    • Infant botulism: caused by ingestion of C. botulinum that produces toxin in the GI tract
    • Wound: caused by wound infection with C. botulinum and subsequent toxin secretion
    • Aerosolized/inhalational botulism: bioterrorist weapon with high toxicity; <1 μg is lethal human dose; not known to occur naturally
    • Adult intestinal toxemia: similar to infant botulism; rare in adults
    • Iatrogenic: injection of toxin for cosmetic or therapeutic (spastic neuromuscular disorders, glandular hypersecretion, pain) effect
  • System(s) affected: neuromuscular, respiratory, GI
  • Synonym(s): sausage poisoning; Kerner disease

Epidemiology

Incidence

  • 205 confirmed cases in the United States in 2016, with three deaths: two foodborne, one unknown (2)
  • 73% of cases were infant botulism, 14% were foodborne, 12% were wound related, and 1% were due to unknown etiologies (2).
  • No person-to-person transmission documented (2)

Prevalence

  • Predominant age (2)
    • Foodborne: median 39 years; range 23 to 89 years
    • Infantile: median 4 months, range 0 to 10 months
    • Wound: median 45 years, range 25 to 68 years, 93% injection drug users
  • Predominant gender (2)
    • Infantile: male = female
    • Foodborne: male > female
    • Wound: male > female

Etiology and Pathophysiology

  • C. botulinum is an anaerobic gram-positive, spore-forming, rod-shaped bacillus.
  • Eight distinct toxin types: A, B, C, D, E, F, G, and H
  • A, B, E, and F cause disease in humans.
  • Disease results from ingestion of Clostridium, followed by local toxin production in GI tract (e.g., from home-canned vegetables).
  • Infantile botulism due to ingestion of spores in environment or foods (e.g., honey)
  • Wound contamination with toxin-producing C. botulinum can produce clinical disease with hematogenous spread of toxin.
  • The toxin inhibits acetylcholine release at presynaptic membranes, blocking neuromuscular transmission and causing paralysis.

Risk Factors

  • Foodborne: ingestion of home-canned or prepared foods that are contaminated
  • Infantile: ingestion of environmental spores; ingestion of honey (minor but preventable source)
  • Immunocompromised state
  • Wound: IV drug use (black tar heroin), “skin popping,” snorting cocaine

General Prevention

  • Foodborne: proper handling, processing, preparation (heating), and storage of food; avoid eating from bulging cans or unprepared/underprepared food (1).
  • Infant: caretaker hand washing. Avoid honey in infants <1 year of age (1).
  • Wound: proper wound care; abstain from injection drug use or snorting cocaine (1).
  • Health care providers: universal precautions (1)
  • If meningitis is suspected in patients with flaccid paralysis, use droplet precautions (1).
  • Raking soil and algae to introduce oxygen prevents spore development.
  • Heat food or drink to internal temperature of 85°C for at least 5 minutes (1).
  • After exposure to C. botulinum toxin, clean clothing and skin with soap and water (1).
  • Clean contaminated objects or surfaces with 0.1% bleach solution. Promptly discard all potentially contaminated food (1).
  • Vaccination has been discontinued (1).

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