Causative agent

  • Clostridium botulinum (anaerobic gram positive)
  • AB toxin producing organism
    – Other AB toxin producing organisms (ABCDE: P.Aeruginosa, B.anthracis, B.pertussis, Cholera, C.dificile/perferingens, Diphteria, Enteroinvasive E.coli)

Types of toxins

  • A: more associated with neurological symptoms
  • B and E: more associated with autonomic symptoms

Classification of botulism according to age and causes:

  • Infant botulism: normally via inhalation route, because the gut is permissive for germination therefore toxin is released after the organism is inhaled into the body (contrast to other forms in which preformed toxin is the cause).
  • Food botulism: most commonly improperly canned food, shellfish, honey, milk
  • Wound botulism


  • Botulism toxin blocks the rleease of Ach by blocking peptide formation between synatic membrane protein and the vesicles (= no fusion).
  • Once damaged, need the formation of a new synapse since the blocked one will be useless. This will take weeks.
  • Because Ach release is blocked, anticholinergic symptoms will present (dry mouth, constipation, urinary retention, orthostatic hypotension).
  • Importantly, the toxin does not go into CNS, so no AMS happen in patients.

Signs and symptoms

  • Prodromal GI symptoms (resembling food poisoning)
  • Bilateral descending weakness (starting with IOM weakness i.e. dilated pupils and EOM weakness i.e diplopia –> dysphagia, dropped neck –> weakness in upper trunk –> respiratory failure)
  • No sensory deficits
  • No fever (fever suggests other diagnosis or co-infection)
  • No change in consciousness (unless progressing to type II respiratory failure)
  • Autonomic symptoms: dry mouth, constipation, urinary retention, alteration in HR and BP


  • Mainly on clinical symptoms.
  • ELISA: toxin detection in food samples
  • Culture rarely yield anything


  • Respiratory failure: intubation with mechanical ventilation. Consider when VC < 12 mL/kg.
  • Antitoxin/ BIG (botulism immunoglobulin G)
    Note with using antitoxin, skin test will be needed since hypersensitivity reaction rates vary between 10-20 percent
  • Wound botulism: antitoxin/BIG + wound debridement + penicillin G/metronidazole
    – Use of antibiotics is appropriate but not evidence based (to kill the bacteria in the wound)
    – AVOID using aminoglycoside and tetracycline –> cause more NM blockade

Differential diagnosis

  • Myasthenia gravis
    – Normally is asymmetrical and fluctuating.
    – Absent autonomic symptoms
  • LEMS
    – Can mimic botulism but normally starts with proximal muscles of extremities.
    – Weakness diminishes as patient moves around.

Some quick points:

  • C.botulism is AB toxin producing organism.
  • Bilateral symmetrical weakness in botulism. Autonomic symptoms can present.
  • Mechanism of the toxin is to block fusion of vesicles and synapse protein and therefore no Ach release.
  • No fever and no AMS usually.
  • Infant form is normally via inhalational route.
  • Before using antitoxin, need to do skin reaction test as rate of hypersensitivity rxn ranges from 10-20 percent.
  • If antibiotics are used in botulism, avoid aminoglycoside and tetracycline. PCN G/metronidazole is preferred.

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