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Botulism has been observed in horses as a result of the action of potent toxins produced by the soil-borne, spore-forming bacterium, Clostridium botulinum:

  1. Wound botulism results from vegetation of spores of Cl. botulinum and subsequent production of toxin in contaminated wounds.
  • Shaker Foal Syndrome (toxicoinfectious) results from toxin produced by vegetation of ingested spores in the intestinal tract.
  • Forage poisoning results from ingestion of preformed toxin produced in decaying plant material, including improperly preserved hay or haylage, or animal carcass remnants present in feed.

Botulinum toxin is the most potent biological toxin known and acts by blocking transmission of impulses from nerves to muscles, resulting in muscle weakness progressing to paralysis, inability to swallow, and frequently, death. Of the 8 distinct toxins produced by sub-types of Cl. botulinum, types A, B and C are associated with most outbreaks of botulism in horses, however, type A is rarely seen east of the Mississippi river in the U.S.


A killed vaccine (toxoid) directed against Cl. botulinum type B only is licensed for use in horses in the United States. Vaccination is warranted for all horses, as C. botulinum type B can be found in soil samples from many areas of the country and movement of horses or forage from non-endemic to endemic regions occurs frequently.  Vaccination is recommended for horses at increased risk of developing botulism due to residence in (or travel to) endemic regions, including Kentucky and the Mid-Atlantic states.  Particularly susceptible groups within those regions include adult horses fed high-risk forages and foals born to unvaccinated mares.  The feed sources most commonly linked to “forage poisoning” in adult horses include fermented feeds (haylage or silage) and improperly processed or stored large bales of hay.

Foals born in endemic regions are at risk for toxicoinfectious botulism (Shaker Foal Syndrome) unless protected by colostral transfer of antibodies produced by vaccination of the pregnant mare. Almost all cases of Shaker Foal Syndrome, a significant problem in Kentucky and in the mid-Atlantic seaboard states in foals between 2 weeks and 8 months of age, are caused by Cl. botulinum type B. Limited information suggests that foals vaccinated with the toxoid at 2 weeks, 4 weeks and at 8 weeks of age developed adequate serologic response, even in the presence of passive maternal antibodies.

Currently, no licensed vaccines are available for preventing botulism due to Cl. botulinum types A or C or other subtypes of toxins. Cross-protection between subtypes does not occur.


Vaccination Schedule:

  • Previously vaccinated pregnant mares:  Vaccinate annually with a single dose 4 to 6 weeks before foaling.
  • Previously unvaccinated pregnant mares:  Vaccinate during gestation with a primary series of 3 doses administered at 4-week intervals and scheduled so that the last dose will be administered 4 to 6 weeks before foaling to enhance concentrations of immunoglobulin in colostrum (i.e. months 8, 9, 10 of gestation).
  • Foals of vaccinated mares (in endemic areas):  Administer a primary series of 3 doses, at 4-week intervals, starting at 2 to 3 months of age. As maternal antibody does not interfere with vaccine response, foals at high risk may have the vaccination series initiated as early as 2 weeks of age.
  • Foals of unvaccinated mares (born in, or moving to, endemic areas):  Administer a primary series of 3 doses, at 4-week intervals, beginning at 1 to 3 months of age. Foals at high risk may have the vaccination series initiated as early as 2 weeks of age.  Foals of unvaccinated mares may benefit from transfusion of plasma from a vaccinated horse or from administration of Cl. botulinum type B antitoxin. The efficacy of these practices needs further study.
  • All other horses (where indicated):  Administer a primary series of 3 doses of vaccine given at 4-week intervals and followed by annual revaccination.
  • Horses that are naturally intoxicated or exposed: Duration of immunity following natural intoxication is highly variable; clinical experience suggests that in many cases natural intoxication does not stimulate a protective immune response.  A primary 3-dose series (given at 4-week intervals between doses) should be initiated as soon as clinical disease is recognized, as serum antibody does not interfere with response to vaccination.  In outbreak situations involving unvaccinated animals, an accelerated vaccination schedule is frequently recommended, with the 3-dose series administered at 2-week intervals.