Food-borne Botulism

(The previous, incomplete entry was posted in error – here is the revised, complete version)

In the news this week, we have another food-borne outbreak, botulism in Ohio. Following up on our post about listeria, lets see what botulism has in store (no pun intended).


Foodborne botulism is caused by ingestion of foods contaminated with botulinum toxin, causing a distinct clinical syndrome of symmetrical cranial nerve palsies followed by descending, symmetric flaccid paralysis of voluntary muscles, which may progress to respiratory compromise and death. The mainstays of therapy are meticulous intensive care (including mechanical ventilation, when necessary) and timely treatment with antitoxin.

The Organism and its Toxins

  • Organism
    • Clostridium botulinum is ubiquitously found in soil and aquatic sediments.
    • C. botulinum grows and elaborates toxin only when the food presents conditions that include an anaerobic milieu, a pH of 4.5, low salt and sugar content, and a temperature of 4C–121C.
  • Toxin
    • Human cases are caused mostly by toxin types A, B, E, and (rarely) F.
    • The toxins exert their action on the cholinergic system at the presynaptic motor-neuron terminal by blocking acetylcholine transmission across the neuromuscular junction, causing neuromuscular blockade, resulting in flaccid paralysis. The toxins also affect the adrenergic system, but this apparently happens without significant consequences.
    • In contrast with the spore, botulinum toxins are temperature sensitive, and all toxins are inactivated by heating to 85C for 5 min.
  • Spores
    • Under stress, C. botulinum forms a spore that survives standard cooking and food-processing measures.
    • The technique of modern industrial canning (i.e., retort canning) was developed expressly for killing C. botulinum spores.
    • Spores do not germinate in the human intestine – ingestion of spores is not toxic

Clinical Manifestations

  • Cranial nerve palsies are invariably presenting symptoms of botulism. The absence cranial nerve palsies or their onset after other true neurological symptoms have made their appearance rules out the disease.
  • Gastrointestinal symptoms (nausea and vomiting) may precede neurological symptoms
  • Flaccid, descending, completely symmetric paralysis of voluntary muscles, affecting (in order) the muscles of the neck, shoulders, the proximal and then distal upper extremities, and the proximal followed by distal lower extremities.
    • Paralysis of the diaphragm and accessory breathing muscles may result in respiratory compromise or arrest
    • Constipation is a nearly universal symptom
    • Deep tendon reflexes progressively disappear
  • Rate of progression and severity are proportional to the dose of toxin
  • The sensory system is unaffected. Intellectual function is preserved throughout.
  • Death in patients with untreated botulism results from airway obstruction from pharyngeal muscle paralysis and inadequate tidal volume, resulting from paralysis of diaphragmatic and accessory respiratory muscles.

Differential Diagnosis

  • GBS, myasthenia gravis, stroke syndromes, Eaton-Lambert syndrome, and tick paralysis.
  • Less likely conditions include tetrodotoxin and shellfish poisoning, antimicrobial-associated paralysis, and a host of conditions due to even rarer poisons.


  • Routine laboratory tests and radiological studies are not useful for diagnosis of botulism.
    • Lumbar puncture reveals normal CSF values—in particular, the protein level is normal, in contrast to Guillain-Barre´ syndrome (GBS).
    • Brain imaging studies may help rule out rare stroke syndromes that produce nonlateralizing symptoms.
    • The Tensilon test helps for diagnosis of myasthenia gravis.
    • EMG: can be an exceedingly helpful adjunct to diagnosis. In affected muscles, findings consistent with neuromuscular junction blockage, normal axonal conduction, and potentiation with rapid repetitive stimulation are indicative of botulism
  • Specialized testing: only performed in a few labs around the country
    • Confirmation of botulism rests on demonstration of the toxin in specimens of patient serum, gastric secretions, or stool or in a food sample
    • Demonstration of C. botulinum in a patient’s stool sample or in cultures of wound material is generally satisfactory for diagnosis of adult botulism syndromes


  • Management with supportive intensive care and anti-toxin must begin before diagnosis is confirmed, as specialized testing can take up to 48 hours at reference labs (plus transit time for the specimen).
  • Call the state health department immediately to speak to an expert!
  • Supportive intensive care
    • Frequent monitoring of vital capacity and institution of mechanical ventilation if required.
    • Paralysis due to botulism is protracted, lasting weeks to months, and meticulous intensive care is required during this period of debilitation.
  • Anti-toxin
    • Can arrest the progression of paralysis and decrease the duration of paralysis and dependence on mechanical ventilation
    • Should be given early in the course of illness, ideally <24 h after onset of symptoms, because antitoxin neutralizes only toxin molecules that are yet unbound to nerve endings.
    • Adverse effects: anaphylaxis, other hypersensitivity reactions, and serum sickness
    • Before administration of antitoxin, skin testing should be performed to test for sensitivity to serum or antitoxin.

Modified from Clinical Infectious Diseases 2005; 41:1167–73