Equine Botulism
Written by Dr. Tom Lenz on behalf of AQHA
Botulism is sometimes referred to as “Forage poisoning” in adult horses or “shaker foal
syndrome” in foals. Fe horse owners are aware of the disease, a progressive, paralyzing disease
that is 80-100 percent fatal in affected horses.
The disease, caused by a potent toxin produced by the bacterium Clostridium botulinum, lives in
the soil as well as the intestinal tract of many birds and mammals, including the horse. It
produces dormant spores that can be found in 18.5 percent of soil samples tested in the United
States. The disease is most prevalent in Kentucky, Ohio, Maryland, Pennsylvania, California and
Tennessee, although it can occur in any state in the continental United States.
Clostridium botulinum produces several different toxins. Type A toxins are often implicated in
human infant botulism and are most often found west of the Rocky Mountains. Type B, C, and D
toxins are usually involved in cases of equine botulism, with Type B responsible for 85 percent
of horse cases in the United States.
Botulism can be initiated in one of three ways. In the case of “forage poisoning,” the horse
ingests toxins that are contaminated grain or hay, most often due to putrefied carcasses of birds
or rodents.
A Type C botulism outbreak that killed a number of horses in California several years ago was
traced back to hay that contained the infected carcass of a rabbit. The bacteria can also enter a
horse’s body via contamination of a wound, especially a deep puncture wound. A good example
is “shaker foal syndrome,” which is most frequently cased by the bacteria entering the newborn
foal’s body through the foal’s moist navel. The risk for that infection source can be minimized
by dipping the foal’s navel in mild iodine solution soon after birth.
The third method by which the disease can be initiated is by ingestion of the spores in the soil.
The ingested spores activate in the horse’s intestinal tract where they produce potent toxins that
are then absorbed.
Once in the horse’s body, the bacteria block nerve impulses to the horse’s muscles, resulting in a
progressive paralysis of all the major muscle groups, paralysis of the diaphragm and death.
The disease is difficult to diagnose because it resembles several other medical conditions and
diseases. Blood samples rarely contain toxin. Because the bacteria often occur naturally in the
horse’s intestinal tract, isolation of the organism from the sick horse’s intestine is not diagnostic.
Clinical signs of the disease include the loss of facial expression, a sleep appearance, saliva
drooling from the corner of the mouth, loss of tongue control and loss of tail tone. The horse’s
appetite is good, but it has a great deal of difficulty in chewing food and appears to be “playing”
in its feed and water buckets.
As muscular weakness becomes more profound, the horse will experience muscle trembling,
generalized sweating and labored breathing. A weakened, shuffling gait may develop.
Eventually, the horse goes down and death results due to paralysis of the respiratory muscles.
“Shaker foal syndrome” is usually seen in foals 1 to 2 months of age but can develop as early as
2 weeks or as late as 6 months of age. Early signs in foals are similar to those seen in adults.
Botulism is usually fatal if left untreated. Once the toxin produced by the bacteria is attached to
the nerve ending, it cannot be neutralized by the antitoxin. Early treatment is critical. Even with
aggressive therapy, recovery is slow.
Prevention through vaccination is critical. A Type-B toxoid vaccine is available and is quite
effective in preventing the disease. In areas where the disease is prevalent, pregnant mares
should be initially vaccinated at the eighth, ninth and 10th month of gestation and thereafter at the
10th month of each pregnancy. Yearly vaccination of adults in areas where the disease frequently
occurs is also recommended.
ABOUT THE AUTHOR: Thomas R. Lenz, DVM, M.S., Diplomate of the American College of
Theriogenologists, is a trustee of the American Horse Council, past chairman of AQHA’s
research committee and past president of the American Association of Equine Practitioners. This
article is provided courtesy of AAEP Alliance Partner, AQHA.