The Basics of Botulism in Horses

A rare but often deadly form of poisoning, botulism must be identified quickly if a horse is to survive. By Joanne Meszoly for EQUUS magazine.

Botulism in horses is a nightmare no one wants to face: Last night your horse was his usual cheerful self. This morning, you find him standing alone with muscle tremors, his head low and his lips slack, drooling heavily, too weak to manage more than a shuffling walk.

Botulism in horses is a devastating illness that occurs when they ingest toxins produced by the Clostridium botulinum bacteria. The resulting disruption of communication between nerves and muscles leads to debilitating and potentially deadly neuromuscular impairment. Without prompt treatment, botulism in horses is almost always fatal.

No hard figures are available, but Robert Whitlock, DVM, PhD, of the University of Pennsylvania School of Veterinary Medicine, estimates that roughly 150 to 250 horses succumb to botulism poisoning each year. Most cases occur in states east of the Mississippi, but it can happen virtually anywhere. Complicating matters is the fact that botulism can be difficult to recognize. “It’s a rare disease and unfortunately, practitioners without experience dealing with botulism have difficulty properly diagnosing it,” says Whitlock. A horse’s chances of survival depend on how quickly treatment begins and how rapidly the disease signs progress.

Which makes it important to understand how botulism poisoning occurs, what it looks like, what can be done to treat it and–perhaps, most critical–what you can do to reduce your horse’s risk of exposure to the causative organism. Here’s what you need to know.

It’s impossible to completely avoid C. botulinum bacteria.C. botulinum spores are found in the soil, on vegetables and foods–they are literally everywhere,” explains Whitlock. “Inert spores can live in the environment for decades without causing any harm. It is when they are given a favorable environment for toxin formation that they pose a danger.” Botulism spores are most likely to form toxins in moist, anaerobic (with little or no oxygen) conditions where protein is rich and acidity is low (pH greater than 4.5). A prime location is decaying vegetable matter. More rarely, toxins may form in decaying animal tissues.

Various strains of C. botulinum are capable of producing seven different neurotoxins (A through G), not all of which can sicken horses. Most cases of equine botulism are caused by type B toxin, which can be found anywhere but is most prevalent in the Northeast and the Appalachian states.

Equine illness linked to type C toxin has been reported in Florida, California, New Mexico, Utah, Arizona, the New England states and Canada. Type C toxin is usually associated with decomposing animals but is also in bird droppings. A third form of the botulism toxin, type A, is found in soil in the northwestern states of Washington, Idaho, Montana and Oregon as well as Utah and Ohio. Type A toxicity is uncommon in horses.

Horses are especially sensitive to C. botulinum. “A dose of botulism toxin capable of killing a horse probably would not make a cow or a dog sick,” explains Whitlock. “Horses are much more susceptible as a species. Even humans are more resistant than horses.” Evidence in literature suggests that vultures, due to their subsistence on carrion, have developed a natural resistance to botulism.

C. botulinum can affect horses in three ways:

  • The term “botulism” most often describes poisoning that occurs when horses ingest the preformed toxins present in hays or feeds contaminated with the active bacteria.
  • Intestinal toxicoinfection, also called “foal botulism” or “Shaker foal syndrome,” develops when a foal ingests C. botulinum spores, which vegetate, colonize and release toxins in the immature gastrointestinal tract. “[This] risk declines about the time the foal is weaned and the mature microflora of the gut prevent the overcluster of C. botulinum,” says Nathan Slovis, DVM, DACVIM, of Hagyard Equine Medical Institute in Lexington, Ky.
  • Wound botulism, the rarest form, results when C. botulinum enter a wound that closes over quickly–such as an injection site or puncture wound–providing an anaerobic environment that enables them to become activated and multiply. Castration wound infections and umbilical hernia repair with clamps have both been associated with wound botulism in horses.

Botulism toxins are among the most potent in the world. Botulism toxins can permanently damage the nervous system. They travel through the horse’s bloodstream, eventually reaching the myoneural junction, where signals pass from motor neuron to muscle fiber. After penetrating neuron cells, the toxins bind to the synaptic vesicles, sacs that contain the molecules (acetylcholine) that signal the muscle to contract. This prevents the chemical’s release, and the result is paralysis.

“Essentially, the toxin disrupts the communication from nerve to muscle,” says Pamela Wilkins, DVM, PhD, professor of medicine at University of Illinois College of Veterinary Medicine. “It’s like cutting a telephone line. The signal is still coming in, but when you pick up the line, there’s nobody there.”

The toxin’s effects are seen first on the horse’s most frequently used muscle groups: those used for chewing, swallowing, standing, blinking and swishing the tail. “Typically you see tongue tone weakness, eyelid and tail weakness, an inability to eat normally, a stiff, short gait, trembling and increased recumbency,” says Wilkins. “But clinical appearance depends on the dose of the toxin. Some horses won’t eat and are a little weak and that’s as bad as they get; others are down and paralyzed.”

Signs may appear anywhere from a few hours to several days after exposure to the toxins. Death, says Wilkins, is usually due to suffocation when pulmonary muscles are compromised.

Feeding round bales increases a horse’s risk of developing botulism–but not for the reasons you might think. Most of us have heard that the rotting bodies of rodents, birds or other wildlife swept up during the hay baling process are a major source of botulism poisoning. But this simply isn’t true.

“That is an all too common misconception,” says Whitlock. “The truth is that 90 percent of botulism cases are in no way associated with dead animals. Most horses have type B botulism and that comes from soil, not from deceased animals [which are linked to type C].”

In fact, “the spores are [in the hay] all the time, whether they are picked up during harvest or baled along with the flecks of dirt with the grass. If the hay remains dry, then it’s fine. But if you have enough botulism spores with an anaerobic environment and spoilage in this tightly packed bale, the spores grow and make toxins,” says Whitlock. “That’s especially true when the bale is thrown out in a field or even stored in a shed but on the ground where dirt and moisture can get in.”

A less common and often overlooked source of botulism poisoning is loose hay thrown out onto muddy or damp ground in paddocks or other enclosures: “The horses will stomp on it and the hay gets packed down,” says Whitlock. “By the time the horses come back and dig it out of the mud, the environment is conducive for spores in the soil to form toxins.”

The swiftness of onset and severity of botulism signs are good predictors of a horse’s prognosis. The greater the amount of botulinum toxin a horse ingests the worse his illness is likely to be. And the sooner a horse is given botulism antitoxin, the better. The polyvalent antitoxin (which works against both type B and C) and a monovalent antitoxin (against type B) contain antibodies that bind to the free-floating toxins in the blood that would otherwise attach themselves to neurons. But the antitoxin cannot repair the damage already done to neurons.

“The antitoxin does not reverse clinical signs, it abates the progression of them from that point on,” says Whitlock. “If the horse is already down, or very weak and approaching that point, it’s too late.” Once the antitoxin is administered, the body can begin the process of growing new nerve cells.

In addition to the administration of antitoxin, horses with botulism often require intense supportive care, which usually consists of antibiotics, intravenous fluids, catheterization and rectal evacuation. Bedsores from long periods of lying down, corneal ulcers due to poor eyelid tone, and pneumonia from insufficient respiratory activity are among the most common complications.

The total cost of care and treatment for a horse with botulism typically ranges from $10,000 to $15,000, depending on the length of hospital stay. Affected horses may not recover their full muscle strength for six months or longer.

A small percentage of affected horses survive without treatment, says Whitlock, “but only when they’ve had a low dose of toxin and the clinical signs are very slow and gradual over a period of days.”

Laboratory tests can confirm botulism, but results may be available too late to matter. Botulism is confirmed using a mouse inoculation test–also called mouse bioassay–which can detect toxins in serum, manure or gut contents. A diluted sample is injected into mice and they are observed for signs of botulism. If they are affected, more samples and specific botulism antitoxins are injected into other mice, which are observed for clinical signs to determine the type of botulism poisoning.

The test can take five to 10 days and may be inconclusive if the amount of toxin from the sample is insufficient. That’s why, says Wilkins, most cases of botulism are diagnosed based on clinical signs alone: “We’ll use lab tests as confirmation, but by the time the results are in, [a horse with botulism] is either better or isn’t alive anymore.”

Nonetheless, she adds, signs can be subtle and easily confused with other illnesses. “Botulism can present like colic,” says Wilkins, “and it has been confused with severe renal failure.” In addition, botulism poisoning in horses can also look like rabies, Eastern equine encephalomyelitis, West Nile encephalitis, equine herpesvirus and plant toxicity.

The most effective way to prevent botulism is through vaccination. Available since the mid-1980s, the equine botulism vaccine is effective against toxin type B, the most common form in horses. Statistics show that the inactivated toxoid vaccine is effective in about 95 percent of cases, and even when protection is incomplete it can increase a horse’s chances of survival.

The American Association of Equine Practitioners recommends botulism vaccination of pregnant mares and of foals, primarily to prevent Shaker foal syndrome.

Whitlock, who describes the vaccine as “one of the safest and most efficacious in the industry,” strongly advises administering it to horses who are fed round bales as well as those in areas where previous cases of botulism have occurred. “I can’t tell you how many times I hear, ‘My vet never told me about this [vaccine],'” he says. “This is a situation where an ounce of prevention is worth a pound of cure.”

This article appeared in the October 2008 issue of EQUUS magazine.




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