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Equine botulism is a severe neuroparalytic disease caused by exposure to botulinum neurotoxins (BoNTs), which are produced by an anerobic, spore-forming, ubiquitous microorganism called Clostridium botulinum. There are several different strains of C. botulinum, each with their own unique toxin---type A through E. These toxins are extremely potent and act on nerve endings blocking acetylcholine release. This causes interference with nerve function which results in respiratory and musculoskeletal paralysis.

Horses are one of the most susceptible animal species to infection with C. botulinum. Equine botulism can be caused by type A, B, C, and D toxins. The main initial signs in adult horses include:
  • Generalized muscle weakness
  • Dysphagia
  • Decreased tail, eyelid, and tongue tone
  • Mydriasis
  • Prolonged pupillary light reflex
  • Loss of appetite
  • Weight loss
  • Hypersalivation
  • Tachycardia
These signs are frequently followed by recumbency, respiratory failure, and death. Horses with type C botulism may have more prominent mydriasis, more labored breathing, or less dysphagia than horses with type A or B botulism. In foals, clinical signs of botulism closely resemble those seen in foals with shaker foal syndrome. Usually the initial presenting sign is onset of muscle tremors leading to recumbency. Other signs include:
  • Frequent urination
  • Reduced eyelid, tongue, and tail tone.
  • Constipation
  • Dysphagia
  • Mydriasis
  • Sluggish pupillary light reflexes.

Where Clostridium botulinum is Found

C. botulinum is found worldwide and plays a vital role in the natural carbon recycling process, growing in decaying organic matter (eg. animal carcasses) and producing high levels of BoNTs. The organism requires a high protein substrate to grow, because it lacks the ability to synthesize certain amino acids. pH, salinity, and temperature also play a crucial role for growth and toxin production. The optimum growth temperature is between 25°C and 42°C (77°F to 107.6°F).

How Horses get Botulism

Horses may ingest C. botulinum by grazing near animal carcasses, drinking from contaminated water sources (with dead rodents or other rotting vegetation), pastures which have been dragged with poultry litter, hay, and commercial horse feed.


Generalized weakness
Decreased tail, anal, eyelid, and tongue tone
Frequently lying down
Difficulty swallowing
Standing with all four legs close together
Lack of appetite
Weight loss
Sluggish or prolonged pupillary light reflexes


  • History
  • Clinical signs
  • Physical exam
  • Laboratory tests



Botulism antitoxinIf administered early enough and available (as it is not available for use in certain countries)
Intravenous penicillin
Supportive care


  • Vaccination
  • Biosecurity
  • Frequently clean water sources
  • Don't allow horses access to ponds, bogs, or other slow moving water sources in pastures.


Most cases are fatal.

Scientific Research

General Overviews

Risk Factors

  • Feeding horses large round bales of hay in pastures
  • Feeding horses silage.
  • Large rodent populations and infrequently cleaning water sources
  • Exposure to dead animal carcasses or rotting vegetation
  • Access to ponds, bogs, or other slow moving water sources in pastures.
  • Spreading poultry litter over pastures.
  • Buying poor quality horse feed or hay

Horse Case Stories



Causative agent