ISSN 2398-2977      




  • Flaccid neuromuscular paralysis caused by a clostridial neurotoxin.
  • Incidence: uncommon; sporadic.
  • Cause: Clostridium botulinum Clostridium botulinum - 3 routes of infection:
    • Ingestion of pre-formed toxin in contaminated feed (classic botulism most common - especially in big bale silage).
    • Ingestion of spores with local toxin production and absorption in the gastrointestinal tract (toxicoinfectious botulism - foals).
    • Wound contamination by spores.
  • Signs: foals - paralysis and inability to stand, severe muscle tremors ('Shaker foal'), sudden death; adults - acute onset flaccid quadriplegia, pharyngeal paralysis, sudden death, tongue paresis. More gradual progression possible with generalized, symmetric weakness and dysphagia.
  • Diagnosis: clinical signs and history.
  • Treatment: specific botulism antitoxin.
  • Prognosis: guarded - dependent upon 'dose' of toxin, rapidity of onset of symptoms, speed of treatment. Fair/good with small toxin 'dose' and rapid administration of antitoxin.
Print off the Owner factsheet on Botulism to give to your clients.



  • Toxin produced by Clostridium botulinum Clostridium botulinum.
  • Toxin type varies in different areas/countries:
    • Type B - Kentucky, mid-Atlantic seaboard.
    • Type C - Europe, Florida.
    • Type D.
  • Grows in preferably neutral or alkaline soils.
  • Rapidly forms spores.
  • Will produce toxin in anerobic environments, eg decaying vegetable matter, animal carcasses, damaged tissues.

Predisposing factors


  • Geographical environment especially neutral to alkaline soil type.
  • Moist or spoiled feeds.
  • Feed source contaminated by anaerobic decaying vegetable or animal matter.
  • Stagnant water sources contaminated by carcasses.


  • Feeding spoiled or contaminated forage especially round bale hay or silage - toxin Types A and B (if organism present before fermentation reduces pH to 4.5 or less).
  • Decomposing carcasses - Type C toxin.
  • Presence of gastric ulcers especially in foals Stomach: gastric ulceration.
  • Wounds especially abscesses; damaged tissue →  anaerobic conditions, eg infected umbilical remnants (foals), castration wounds (adults).
  • Stress - onset of clinical signs has been associated with stress, eg racing, foaling, weaning.


  • Toxin → interference with acetylcholine release at a variety of nerve endings/junctions → neuromuscular paralysis.
  • CNS and sensory nerves are not affected.
  • There are three recognized routes of botulism exposure.

Ingestion of pre-formed toxin

  • Most common in adults (forage poisoning).
  • In US, involves either processed feed contaminated by animal carcass or big bales.
  • In UK usually involves big bale silage or similar products.
  • Cases occur sporadically or as outbreaks.

Toxicoinfectious botulism

  • Ingestion of spores that germinate → toxin within digestive tract.
  • Especially seen when local GI environment is favorable for overgrowth, eg gastric ulceration Stomach: gastric ulceration, especially in foals (normal intestinal flora of adults inhibits spore growth).

Wound infection

  • Contamination of wound → toxin production (rare).
  • Neurotoxin spreads throughout body → blocks acetylcholine release at:
    • Neuromuscular junctions.
    • Peripheral cholinergic nerve terminals in preganglionic nerve endings.
    • Postganglionic parasympathetic nerve endings.
  • CNS and sensory nerves are not affected.
  • Proposed mechanisms of toxin action include:
    • Interference with calcium function at nerve terminal.
    • Inhibition of acetylcholine release.
    • Blockage of exocytosis of synaptic vesicles.


  • Incubation periods from 2 h to 2 weeks; symptoms usually develop within 12-24 h of exposure.
  • Related to toxin dose, ie patients with gradual presentation and slow progression of signs have probably been exposed to small doses of toxin; rapid onset and severe signs are more common with large toxin doses.


This article is available in full to registered subscribers

Sign up now to obtain ten tokens to view any ten Vetlexicon articles, images, sounds or videos, or Login


This article is available in full to registered subscribers

Sign up now to obtain ten tokens to view any ten Vetlexicon articles, images, sounds or videos, or Login


This article is available in full to registered subscribers

Sign up now to obtain ten tokens to view any ten Vetlexicon articles, images, sounds or videos, or Login


This article is available in full to registered subscribers

Sign up now to obtain ten tokens to view any ten Vetlexicon articles, images, sounds or videos, or Login

Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Stratford C H, Mayhew I G & Hudson N P H (2014) Equine botulism: A clinical approach to diagnosis and management. Equine Vet Educ 26 (8), 441-448 WileyBlackwell.
  • Johnson A L et al (2012) Quantitive real-time PCR for detection of the neurotoxin gene ofClostridium botulinumtype B in equine and bovine samples. The Vet J 194 (1), 118-120 PubMed.
  • Aleman M et al (2011) Repetitive stimulation of the common peroneal nerve as a diagnostic aid for botulism in foals. J Vet Intern Med 25 (2), 365-372 PubMed.
  • Frey J et al (2007) Alternative vaccination against equine botulism (BoNT/C). Equine Vet J 39 (6), 516-520 PubMed.
  • Wilkins P A & Palmer J E (2003) Mechanised ventilation in foals with botulism: 9 cases (1989-2002). J Vet Intern Med 17 (5), 708-712 PubMed.
  • Wilkins P A & Palmer J E (2003) Botulism in foals less than 6 months of age: 30 cases (1989-2002). J Vet Intern Med 17 (5), 702-707 PubMed.
  • McCann J L (2000) A suspected case of botulism in a horse. Equine Vet Educ 12 (3), 114-119 VetMedResource.
  • Dyson S, Marr C M & Barr T J (1997) Equine botulism. Vet Rec 141 (2), 56 PubMed.
  • Whitlock R H & Buckley C (1997) Botulism. Vet Clin North Am Equine Pract 13 (1), 107-128 PubMed.
  • Szabo E A, Pemberton J M, Gibson A M et al (1994) Application of PCR to a clinical and environmental investigation of a case of equine botulism. J Clin Microbiol 32 (8), 1086-1991 PubMed.
  • Roblot P, Roblot F, Fauchere J L et al (1994) Retrospective study of 108 cases of botulism in Poitiers, France. J Med Microbiol 40 (6), 379-384 PubMed.
  • Wichtel J J & Whitlock R H (1991) Botulism associated with feeding alfalfa hay to horses. JAVMA 199 (4), 471-472 PubMed.

Other sources of information

  • Hurcombe S (2010) Botulism in foals and adult horses. In: Proc NAVC. pp 150-152.
  • Bernard W V (2003) Botulism in the foal. In: Proc NAVC. pp 128.


  • British Equine Veterinary Association, UK - Polyvalent equine-origin botulism antitoxin Botulinus antiserum available here.
  • University of Pennsylvannia, School of Veterinary Medicine, New Bolton Center, Kennet Square, PA, USA. Polyvalent equine-origin botulism antitoxin Botulinus antiserum available here.

Related Images

Want more related items, why not
contact us

Can’t find what you’re looking for?

We have an ever growing content library on Vetlexicon so if you ever find we haven't covered something that you need please fill in the form below and let us know!


To show you are not a Bot please can you enter the number showing adjacent to this field

 Security code