With foaling season upon us, vaccination for botulism is one of many management considerations facing North American horse breeders. This disease can be deadly in foals, and in adult horses which are unprotected, and it can be tremendously expensive to treat and save affected horses.

Botulism is caused by a neurotoxin produced by the anaerobic bacterium Clostridium botulinum, which was first identified in 1897 in Belgium during an outbreak of food poisoning traced to imperfectly smoked ham. Clostridium tetani, the organism which causes tetanus, is a close relative. The toxin produced by C. botulinum is one of the most potent known to man--in fact, it has at various times been considered a weapon of biological warfare. Horses are particularly sensitive to botulinum toxin, and untreated foals can suffer up to 90% mortality, with adult horses approaching 70%.

Eight toxin types, each produced by a different strain of the bacterium, have so far been identified: Types A, B, C1, C2, D, E, F, and G. Each type is unique in its geographic distribution and species susceptibility. Type B accounts for more than 80% of equine cases, with Types A and C making up the rest. Many other avian and mammalian species (including humans) are also vulnerable to botulism.

As noted in the March issue (page 12), symptoms of botulism can easily be confused with other conditions, such as rabies, equine protozoal myeloenchphalitis (EPM), tetanus, azoturia, or any disease associated with muscle weakness and dysphagia (inability to swallow). Unlike most of these, however, botulism can strike extremely swiftly. Once in the horse's system, botulism toxin works by inhibiting the release of the neurotransmitter acetylcholine at the neuromuscular junction (NMJ), the point at which nerve endings meet muscle fibers. Without acetylcholine, muscles are not stimulated to contract, become weaker, and finally are paralyzed. Affected horses lose the ability to swallow food or water, dribbling grain and saliva from their lips; move in a shuffling (but not ataxic) fashion, sometimes dragging their toes; and might exhibit other symptoms such as depression, muscle tremors, decreased tongue tone (in advanced cases, the horse might be unable to retract his tongue when it is gently pulled from his mouth), pupil dilation (mydriasis), constipation, colic, and shortness of breath. The muscle tremors might cause horses to thrash violently in some cases. Particularly with Type C botulism, there is a pronounced abdominal lift that is associated with extra expiratory effort. (The symptoms are always symmetric, which can help veterinarians distinguish this disease from EPM.)

In as little as 48 hours, horses affected with botulism toxin might be recumbent and unable to rise, typically with their chins resting on the ground. Respiratory paralysis usually forces euthanasia. The severity of symptoms, however, is largely dependent on the amount of toxin the horse has ingested. A horse with less toxin which is less severely affected might decline slowly--a characteristic which can confuse diagnosis.

How Horses Get Botulism

Horses can contract botulism in three ways. The most common scenario is ingestion of the toxin (not the bacterial spores themselves) through contaminated feed or water. The bacterium tends to inhabit muddy and aquatic environments and the surrounding soil. Decomposing carcasses of rodents or birds are often blamed for con-taminating feed; however, Robert Whitlock, DVM, PhD, of the New Bolton Center at the University of Pennsylvania, notes that it is far more common for hay or silage products to be contaminated through improper storage or poor fermentation. Hay cubes contaminated with carrion were implicated in a 1989 outbreak in California, where more than 40 horses were affected and 23 died. A recent outbreak in northern Ontario, which killed 11 broodmares, was traced back to excessively moist haylage.

Horses also can contract botulism through the entrance of C. botulinum into a wound from the soil. If the wound provides an anaerobic environment (such as is common in puncture wounds, which scab over quickly), the bacterial spores become active and start producing toxin.

In foals, botulism is most often contracted through the entrance of the organism through the necrotic (dead) tissue of the umbilical stump--a situation called toxico-infectious botulism. (Stressed foals also can develop gastric ulcers, which might allow spores ingested in food to enter the tissues at the site of the ulceration.) The resulting severe symptoms are commonly known as "Shaker Foal Syndrome," because the foal develops violent muscle tremors, a stilted walk, and dysphagia. The scene of a foal with milk dribbling from its mouth and nose is a classic sign of botulism. Death often occurs within 72 hours. Foals of two to eight weeks of age are at highest risk.

Diagnosis and Prevention

Diagnosis of botulism can be difficult, as serum analysis rarely turns up any sign of the toxin or its causative organism. Fecal analysis is somewhat more successful, turning up indications of C. botulinum about 30% of the time. The best way to determine that botulism is the culprit of an illness is to pinpoint the toxin in the feed. Spores from a contaminated source can sometimes be cultured (grown in media in the lab), a procedure that takes three to five days, but often no active spores can be found. Mouse bioassays are currently the most sensitive testing method to test for the toxin (present more frequently); this involves injecting the suspected toxin into pairs of mice, then administering monovalent (specific to one type of toxin) antitoxins into one of each pair. This can reliably identify the type of botulism with which horses are afflicted (the mice treated with the right antitoxin survive). This testing procedure takes three to four days to complete, quite at odds with the swiftness of the disease's progress.

Since the clinical signs of different types of botulism toxin can vary subtly, knowledgeable practitioners often choose to go ahead and treat the affected horses as quickly as possible, rather than wait for the results of the testing.

A vaccine for Type B botulism (the most common type in horses) is given routinely to horses in high-risk areas throughout the mid-Atlantic states and in countries such as Australia. (A new vaccine, which will immunize for both Types B and C, should be available within the next 1 1/2 years, according to Whitlock.) Vaccination in adult horses consists of three doses one month apart, followed by a yearly booster. Vaccinations for broodmares should be timed so they receive their final injection within 30 days of foaling to create a higher antibody content in their colostrum. Immunity gained by foals through the colostrum lasts 8-12 weeks. Foals can begin their vaccination series as young as two to four weeks of age, with a series of three inoculations given at two-week intervals.

Mares and foals can be protected by an even tighter vaccination schedule, according to research by Whitlock. A foal can have its initial vaccination series as close as one week apart, although a fourth dose might be necessary to ensure adequate immunity. If a mare has too little time left in her pregnancy to receive the standard series at 30-day intervals, her inoculations can come as close as one week apart and should produce similar antibody concentrations for her foal.

Whitlock remarked that when administered properly, the vaccine for botulism is one of the most efficacious on the market, with a prevention rate approaching 100%.


Treatment for horses which contract botulism consists of a plasma antitoxin, laboriously produced by vaccinating horses against botulism, then administering a specific type of botulism toxin to them repeatedly for a period of six months to a year. Horses eventually build up sufficient immunity in their systems that the "titre" or antibody level is high enough to harvest, whereupon serum is drawn and the antitoxin isolated for use in afflicted horses. The process is not only time-consuming, it's dangerous. The technicians handling the astonishingly virulent toxin must be trained and licensed by the Centers for Disease Control, and they also must receive an experimental human vaccine before they are deemed safe to administer the injections. Since the demand is low, the shelf-life short, and the production so complex, the antitoxin is understandably quite expensive--costing up to $500 per horse.

Furthermore, the antitoxin (which must be specific to the type of toxin causing the disease) has no impact once the toxin is bound at the neuromuscular junction. The antitoxin works to bind any free toxins that have not been taken up by the horse's body. To be effective, the antitoxin must be administered early in the progress of the disease while the toxin is still "free" in the bloodstream. Response to it, therefore, is quite variable, but those horses which recover usually do so over a period of a month or less, during which time they can be helped by tube feeding and stall rest.

More Botulism?

The incidence of botulism in horses might be on the rise. The recent outbreak in Northern Ontario, for example, took many researchers by surprise, as the disease is extremely rare in Canada. Practitioners are now beginning to suspect that many cases of botulism have been mis-diagnosed in the past. The increasing practice of feeding fermented silage products to horses is also having an impact.

Whitlock said, "What we're finding is that haylage and silage products are notorious for botulism. As more farms use these products, I think we'll be seeing more and more cases.

"Many people," he continued, "don't really consider botulism as a disease of horses--and owners may also not be calling their vets early enough. It's important to understand how quickly this disease progresses."

Vaccination is obviously the first line of defense against botulism. Any farm considering using haylage or silage products as horse feed should also consider doing regular pH testing. Whitlock notes that C. botulinum is very pH sensitive, and it thrives at a pH level over 4.5. Feedstuffs that test at a pH level below 4.5 are probably acid enough not to be contaminated with the toxin.

About the Author

Karen Briggs

Karen Briggs is the author of six books, including the recently updated Understanding Equine Nutrition as well as Understanding The Pony, both published by Eclipse Press. She's written a few thousand articles on subjects ranging from guttural pouch infections to how to compost your manure. She is also a Canadian certified riding coach, an equine nutritionist, and works in media relations for the harness racing industry. She lives with her band of off-the-track Thoroughbreds on a farm near Guelph, Ontario, and dabbles in eventing.

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