Editor's Note: This is an excerpt from Understanding Equine Preventive Medicine by Bradford G. Bentz, VMD. This book is available from www.ExclusivelyEquine.com.

Botulism is a disease caused by a toxin produced by the bacterium Clostridium botulinum.  As in the case of tetanus, toxin is produced by a clostridial organism. However, instead of the spastic paralysis produced by tetanus, botulism produces flaccid paralysis and weakness when nerve transmission to the muscle is inhibited by the binding of toxin and blockage of nerve-to-muscle transmission.  Botulism is the most potent biologic toxin known, and horses are highly sensitive to its presence and effects.  The clinical effect on the horse may become severe enough to cause the horse to become recumbent and eventually to die from paralysis of respiratory muscles. 

There are three major forms of botulism, which are categorized by the mode of entry of the toxin. Ingestion of pre-formed endotoxin (forage poisoning) from contaminated feedstuffs may be the most common means of entry. Ingestion of the Clostridium botulinum spores may lead to production of toxin within the gastrointestinal tract, as is most commonly the mechanism in foals (shaker foal syndrome).  These types of botulism may be associated with contaminated feed or hay and may be a particular concern for horses being fed round bales or grazing in pastures with animal carcasses or decaying plant material. Finally, infection of a wound with Clostridium botulinum may lead to the production of the toxin after the spores vegetate. 

There are eight recognized types of botulism toxin. Horses appear to be most susceptible to types B and C.  Almost all cases of shaker foal syndrome appear to be caused by type B toxin, and foals between two weeks and seven months of age in Kentucky and Mid-Atlantic seaboard states appear to be at greatest risk. However, shaker foal syndrome is reported sporadically in other areas of the country.

There appears to be a geographic distribution of the subtypes.  Type A appears to be concentrated in areas west of the Rocky Mountains, type B in Kentucky and in the Mid-Atlantic seaboard, and type C found more commonly in Florida.  To date, the available toxoid vaccine (BotTox-B) is directed only against type B toxin, and there is no cross-protection provided to other types of botulism toxin.  Therefore, in addition to vaccination, methods for the control of botulism should involve good husbandry: vermin removal, disposal of animal carcasses, and avoidance of spoiled feedstuffs.

Vaccination of pregnant mares produces protection in the foal against type B botulism (shaker foal syndrome) but should be restricted to the final trimester of pregnancy.  Pregnant mares that have not been previously vaccinated should receive a primary series of three doses administered four weeks apart and scheduled so that the final dose is administered four to six weeks before foaling.  Mares that have already received the initial series can be boosted at four to six weeks prior to foaling in order to maximize protection conferred by colostral antibody to the foal. 

Maternal antibody in the foal does not appear to inhibit the development of an immune response and production of antibody by the foal itself; thus, vaccination of the foal can begin at two to three months of age or older in endemic areas.  The primary series in the foal should consist of three doses administered at four-week intervals.  All other horses should also receive a three-dose primary series at four-week intervals and a yearly booster vaccination thereafter. For broodmares, yearly boosters are best timed at four to six weeks before foaling.

Horses that develop clinical disease associated with botulism toxin may be treated with intravenously administered botulism antitoxin. However, the administration of the antitoxin carries no effect for toxin that is already bound to receptors in the junction between the nerve and muscle.  The utility of the antitoxin is in its ability to bind toxin that is still circulating.  Clinical signs of the horse may continue to deteriorate for 24 hours beyond the administration of the toxin. Recovery of the horse is optimal when the animal has received antitoxin, the progression of clinical signs is slow, and the horse does not become recumbent.  The recommended dose of the type B antitoxin is 30,000 IU for the foal and 70,000 IU for an adult horse.

About the Author

Bradford G. Bentz, VMD, MS, Dipl. ACVIM, ABVP (equine)

Brad Bentz, VMD, Dipl. ACVIM, ABVP, ACVECC, owns Bluegrass Equine Performance and Internal Medicine in Lexington, Ky., where he specializes in advanced internal medicine and critical care focused on helping equine patients recuperate at home. He’s authored numerous books, articles, and papers about horse health and currently serves as commission veterinarian for the Kentucky State Racing Commission.

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