Lives In The Balance–Botulism

Botulism, an often-deadly disease in foals, can be prevented easily and inexpensively with proper management. Botulism is a familiar term to most of us as a disease that humans get from eating improperly preserved food. In horses, botulism cause


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Botulism, an often-deadly disease in foals, can be prevented easily and inexpensively with proper management. Botulism is a familiar term to most of us as a disease that humans get from eating improperly preserved food. In horses, botulism causes extreme muscle weakness, and foals affected with the disease often are called “shaker foals” because their muscles tremble when they attempt to stand. The name botulism was derived from the word “botulus” (meaning sausage) to describe a fatal food poisoning outbreak in the year 1870. The organism was discovered in 1897 during an outbreak of food poisoning linked to imperfectly smoked ham in Belgium.

Botulism is found most commonly in the mid-Atlantic states and in Kentucky, but also has been found in Florida and on the West Coast, as well as Australia and several countries in Europe.

How can you protect your foal from this horrible disease? How do you know if your otherwise healthy foal is at risk? What is the treatment for these “shaker foals,” and what are their chances for survival? We’ll answer these questions and more in this article.

What Causes Botulism?

Botulism is caused by the proliferation of bacteria called Clostridium botulinum. These bacteria can gain entrance into adult horses and foals through three different methods. The organism is often found in the soil, so it can be introduced into the adult horse and foal through deep wounds, or through the umbilicus in the foal. This is called wound botulism. In adult horses, the botulism toxin can be ingested with spoiled foodstuffs, which often is called forage poisoning. In that situation, the organism grows and produces its toxin in decaying foodstuffs or in a rotting animal carcass. The horse can be inadvertently fed the toxin if the carcass is accidentally baled into hay, if a dead rodent contaminates a grain bin, or if contaminated/spoiled silage or haylage is fed.

In foals, the bacteria often are ingested as spores from the environment, and the bacteria begin to proliferate inside the intestinal tract of the foal. This is called toxicoinfectious botulism. Many veterinarians believe that after the Clostridium botulinum spores gain access to the foal’s gastrointestinal tract, the spores can harbor and proliferate inside gastric ulcers or any other small gastric wounds of foals, as these deep ulcers provide an ideal environment for the bacteria. The Clostridium bacteria are anaerobic organisms, so they need an environment without oxygen to thrive. However, the bacteria can survive in aerobic (with oxygen) environments in spore (inactive) form.

When a spore is ingested or introduced into a deep wound, the anaerobic environment of the wound or within the intestinal tract activates the spore. It then germinates and begins to grow and multiply. Once the bacteria set up shop in either location, they begin to proliferate and produce a very potent neurotoxin (chemical that affects the neurologic system) that is released into the animal’s body. You might be more familiar with this type of scenario as it pertains to a related bacterium Clostridium tetani, which produces a toxin that causes the fatal disease tetanus. These toxins are among the most potent poisons in the world. The botulism toxin, once released into the body, leads to clinical signs of profound muscle weakness in foals and adults.

The Botulism Toxin

The different strains of the botulism organism produce eight different types of the botulism toxin (A, B, Ca, Cb, D, E, F, and G). Each species of animal has a different sensitivity to each toxin, with horses being much more sensitive than other species in general. For example,the amount of toxin it takes to cause disease in the horse might not even affect another species. Horses are most susceptible to the types B and C toxins, where-as cattle are most sensitive to types B, C, and D. Type B is responsible for most of the equine botulism cases in the United States.

In order to understand how Clostridium botulinum toxin produces the disease, first it is necessary to know how the nervous system interacts with the muscular system.

Nerves leave the spinal cord and brain stem, then travel to the various muscles they supply (innervate). When a muscle group needs to contract, an electrical signal is propagated down the nerve toward its target muscle, thus stimulating the muscle to contract. The area where the nerve connects to the muscle is called the neuromuscular junction (NMJ). When the “contract” signal reaches the nerve end at the NMJ, it causes the release of a chemical called acetylcholine, which diffuses across the very small space between the nerve and muscle. That induces a change in the muscle membrane, triggering another signal that spreads through-out the muscle and causes it to contract.

With botulism, after the toxin enters the animal’s system, it makes its way to the NMJ, presumably via the bloodstream. Upon reaching the NMJ, the toxin affects the nerve ends so that the release of acetylcholine is inhibited. With progressive loss of acetylcholine to trigger muscle contraction, the horse gradually loses the ability to use its muscles and eventually becomes paralyzed.

Clinical Signs

Horses and foals have slightly different clinical presentations with this disease. Typically only one animal on the farm will be affected; however, outbreaks of multiple cases have been seen with spoiled feed. Affected foals usually are two to eight weeks of age, but can be younger. The foals usually are strong and healthy, then rapidly develop signs over several hours to a few days. Once the organism is ingested, the incubation period ranges from one to seven days until the first clinical signs appear.

The foal’s skeletal muscles are not the only muscles affected. Some of the first signs of botulism are dribbling milk or saliva from the mouth. This is caused by the muscles of the pharynx becoming so weak that the foal has trouble swallowing. As the disease progresses, then the foal begins to show generalized muscle weakness characterized by muscle trembling—thus, the term “shaker foal.” If able to walk, the foal will have a stiff gait. A foal with botulism might have a fever, but not all cases will have one.

If left untreated, the foal eventually will become recumbent (unable to rise) and eventually will succumb as the respiratory muscles become paralyzed. Nearly 100% of foals will die within two to three days without intensive care and treatment.

Adult horses with the disease can develop signs very quickly (within hours) or slowly over several days. The severity of the disease often depends on how much pre-formed toxin was ingested or how many bacteria are producing toxin within the horse. A horse with the rapid onset of signs has a poorer prognosis for recovery. An adult horse with botulism is weak like the “shaker foal,” but might seem to improve after rest. The muscular weakness might cause the adult horse to be unable to keep its tongue in its mouth, and it frequently will drool.

As the disease progresses, the horse will be unable to swallow food or water, and his gait becomes short and stiff. While the death rate is not 100% for adults (some mildly affected hor-ses will survive without treatment),almostall horses succumb without treatment.

The diagnosis of botulism in a horse usually is based on the history and clinical signs. There is no blood test that will help pinpoint the disease. The toxin can be found in the gastrointestinal contents of dead animals and in contaminated feed, but this might take days. Fecal culturesfromaffected horses can be performed, but again, this can take a long time. Treatment must start immediately if the animal is to survive.


Horses affected by the botulism toxin are very weak and have difficulty eating or drinking, so supportive care is imperative. Most foals will need to be treated in a neonatal intensive care facility, as their care usually requires someone present 24 hours a day. Intravenous fluids are very important to keep the foal hydrated, as is a feeding tube for foals which have lost the ability to swallow. Those foals will have to be fed milk every two to three hours, 24 hours a day, to ensure adequate nutrition. Some foals in an attempt to nurse will aspirate milk (get liquid into their lungs). Aspiration pneumonia is a common complication of botulism. If the foal is severely affected, then a ventilator might be necessary to breathe for him. Urinary catheters also could be necessary as these foals lose the ability to empty their bladders.

The treatment of choice to destroy the botulism organism present in the body is intravenous penicillin. However, penicillin has no effect on the neurotoxin that is causing the clinical signs. An antitoxin is available for administration to horses and foals. Although it is expensive, it is extremely important for a successful outcome.

Horses which are recumbent or have rapidly progressing signs might die despite the use of the antitoxin, which will bind any toxin that has not yet reached the NMJ. However, it will not affect the toxin that already has damaged the NMJ (meaning it won’t reverse the clinical signs already present). Foals and adult horses, even with appropriate treatment, can take weeks or months to recover fully from a case of botulism. However, use of the antitoxin and good intensive care improves the recovery rate to around 80%.

Risk Factors

Several risk factors have been identified for contracting botulism. Obviously for forage poisoning, the risk factors are feed or pastures contaminated with dead or decaying animals. The botulism organism will proliferate in the carcasses, and even after the carcass is gone, the organism or toxin can be left on the ground for your horse to eat.

Foals which seem to be at greatest risk are those in the mid-Atlantic states and Kentucky. Often the affected foals are the more robust foals whose dams are producing large quantities of milk. Many cases in foals happen soon after a stressful event, especially after severe weather changes. In those cases, silent (asymptomatic) gastric ulcers might form, and the botulism spores take up residence and multiply as discussed previously. If you have had cases of botulism on your farm or in the area, your animals might be at risk, and preventive measures are in order.


The best way to prevent botulism (forage poisoning) in adult horses is to maintain a clean farm and prevent the spoiling of the feed and water supply with rodents or other carcasses. There is a vaccine available for protection against the bacterial strain that produces type B toxin, which is the most common. This vaccine should be used on all pregnant mares and other adults in endemic areas (where botulism is known to occur).

The botulism toxoid has an initial series of three doses given one month apart. An annual booster should be given to all pregnant mares and other adults. Mares should only be vaccinated in the last four to six weeks of pregnancy so that antibody levels will be high in the colostrum. If vaccinating a pregnant mare for the first time, the last dose should be two to four weeks before foaling. A high level of circulating antibodies in the mare will ensure that the mare’s colostrum will be rich in botulism antibodies, which will protect the foal.

Mares should not be vaccinated early in a pregnancy, as that could cause resorption of the fetus. A foal can be vaccinated very early if its dam was not vaccinated or if it did not absorb adequate immunoglobulins from the mare (failure of passive transfer). In those cases, the three-dose series can start as early as one week of age.

Although botulism is a very serious disease, if the clinical signs are noticed early, then recovery is very likely with appropriate treatment. Best of all, prevention of type B botulism with the botulism toxoid is available for areas with a known history of the disease.


Bernard, W.V. Botulism. Current Therapy in Equine Medicine, 4th ed. Ed. N.E. Robinson. Philadelphia: W.B. Saunders, 1997

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Written by:

Christina S. Cable, DVM, Dipl. ACVS, owns Early Winter Equine in Lansing, New York. The practice focuses on primary care of mares and foals and performance horse problems.

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