Botulism in Horses

Botulism is caused by a toxin, or poison, that is produced by the bacterium, Clostridium botulinum. This toxin works by blocking synapses between nerves and muscles, and eventually, all of the muscles fail, including respiratory muscles.

C. botulinum is a spore-forming, anaerobic bacterium. This means that upon exposure to air, the bacterium goes into a dormant stage, forming a spore. This spore can survive indefinitely in the soil. Under the right conditions, the bacterium can leap into activity and produce large amounts of toxin.

There are three major ways that the bacterium can enter the horse's body and cause the disease that we know as botulism.

What to Watch For


Horses are exquisitely sensitive to the effects of botulinum toxin, so it can be very difficult to make a definitive diagnosis. Diagnosis is usually based on clinical signs and by ruling out other causes.


It can be very difficult to treat botulism. It is possible to use an antitoxin, but it must be used very early in the disease to be effective. In some cases, antibiotics may be helpful.

The most important treatment is good supportive and nursing care.


Many of the guidelines for good husbandry are useful in preventing botulism. Throw away any feed that appears spoiled and don't expose your horse to any rotting vegetation. Make sure to keep mice and rats out of your barn and dispose of any dead animals carefully.

If you are in an area that is endemic for the toxicoinfectious form of botulism (Shaker foals), your veterinarian will probably advise you to vaccinate with Bot Tox-B®.

Clostridium botulinum is a bacteria that is able to survive indefinitely in the soil in spore form. As a spore, it is inactive and protected. When the clostridium bacterium finds the right conditions, such as rotting vegetation or a puncture wound, it starts to proliferate and produce an extremely potent toxin. Horses, for reasons we do not understand, are more sensitive to this toxin than most other species. This means that it takes a very small amount of toxin to kill a full-grown horse.

The Toxin

All mammals use a chemical called acetylcholine to act as a signal from the nerves to the muscles. Signals pass from the brain, to the peripheral nerves, and then via the action of acetylcholine, to the muscles. The botulism toxin binds to the ends of the nerves, and prevents the acetylcholine from being released – and the end result is that the muscles gradually cease to work.

Since muscle action is important in many different organ systems, the effects of botulism can result in the gastrointestinal system slowing down, defecation becoming difficult and inability to urinate, in addition to many other signs of muscle weakness. Once the toxin has bound to the nerve ending, it cannot be moved.

There are many different subtypes of botulinum toxin – the ones that we worry about in horses are types B and C. We tend to see C.botulinum type B in Kentucky, Pennsylvania, and the mid-Atlantic area, whereas type C has been found primarily in Florida. This means that there tend to be more cases of botulism in these areas. In addition to different subtypes, there are different forms of botulism.

Forage Poisoning

This is the most common type of botulism in adult horses. The bacterium finds a good place to proliferate – often rotting vegetation or carrion. Typical signs include weakness and muscle trembling, difficulty swallowing (dysphagia), drooling, stiff or stilted gait, and recumbency. Oftentimes, these signs will improve temporarily with rest, and then become severe again. Horses may also present with signs of colic, because the gastrointestinal system is no longer working properly.

With forage poisoning, the bacteria have already formed the toxin, which the horse then eats. If the disease is detected early, then antitoxin may help. The antitoxin works by binding the toxin that is floating free in the serum. Once the toxin has bound to nerve terminals, then the antitoxin is ineffective. Because forage poisoning is due to pre-formed toxin, antibiotics are of little use.

The mainstay of treatment for the chronic stages of forage poisoning is good supportive care. This can be both very expensive and labor-intensive. For instance, the horse that cannot swallow will likely need both intravenous fluids and nutritional support. The down horse may need to be maintained in a special sling apparatus, and is likely to develop multiple pressure sores, despite the caregiver's best efforts. In the case of the horse whose respiratory muscles have failed, it will be necessary to begin mechanical ventilation. For a full-grown, adult horse, this is often impossible even in a referral hospital, due to the size of the horse.

Shaker foals are equally difficult to diagnose. Ancillary diagnosis should include gastroscopy in order to determine whether the foal does indeed have gastric ulcers.

Prior reports have indicated that the prognosis is very poor – less than a 10 percent chance for survival. However, if the facilities exist for mechanical ventilation, antitoxin is given early, appropriate antibiotics are delivered, and the owner is committed to the foal financially, there is a fair chance for recovery.


If the disease is detected, or suspected early in its course, an antitoxin can be used. Once the toxin is no longer free in the blood, the antitoxin is no longer effective. Other treatments may include:


In general, it seems as though horses with a slow onset of signs have a better prognosis than those in which the disease progresses very rapidly. Because it is easier to give good supportive care to smaller animals, foals and ponies seem to have a better prognosis.

Complete recovery may take several months. By the time horses have actually recovered from the disease itself, they are often thin, weak, and debilitated, and a slow return to normal life may take quite a few more months.