Few horse owners are aware of this disease which is a progressive, paralyzing disease that is 80-100% fatal in affected horses.  Botulism is sometimes referred to as “forage poisoning” in adult horses or “shaker foal syndrome” in foals. The disease is caused by a potent toxin that is produced by the bacterium Clostridium botulinum. This bacterium lives in the soil as well as the intestinal tract of many normal birds and mammals, including the horse. It produces dormant spores that can be found in 18.5% 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 U.S. 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. Types B, C, and D toxins are usually involved in cases of equine botulism, with Type B responsible for 85% of horse cases in the U.S.

Horses of any age are susceptible to botulism which may be initiated by one of three ways. In the case of “forage poisoning” the horse ingests toxins that are contaminating feedstuffs such as grain or hay. Feed contamination is 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 caused by the bacteria entering the newborn foal’s body through the foal’s moist navel. Something that can be minimized by dipping the foal’s navel in mild iodine solution soon after birth. The third method in 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. Regardless of the route, once the bacteria have entered the horse’s body they produce toxins that block transmission of nerve impulses to the horse’s muscles. This results in a progressive paralysis of all the major muscle groups and is concluded with paralysis of the diaphragm, which results in death. Once symptoms develop, death may ensue in several hours or take up to a week.

The disease is difficult to diagnose because it resembles several other medical conditions and diseases such as choke, colic, rabies, EPM, and sleeping sickness. Blood samples very rarely contain toxin and necropsy following the death of the horse usually does not provide a conclusive diagnosis. 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 in adult horses suffering from “forage poisoning” initially include loss of facial expression, a sleepy 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 their 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 and the horse may take stiff, short steps as if walking on eggs. Eventually, the horse goes down and death results due to paralysis of the respiratory muscles. “Shaker foal syndrome” is usually seen in foals one to two months of age but can develop as early as two weeks or as late as 8 months of age. Early signs in foals are similar to those seen in adults in that the foal shows generalized weakness, poor tail tone, and loss of tongue control. The foal will often dribble milk from the mouth and nostrils because of an inability to swallow. Because of muscle weakness, the foal will lie down frequently. When it does rise, it soon develops muscle tremors and collapses. Affected foals may die within 12 hours of exhibiting symptoms or may linger for as long as a week.

Botulism is usually fatal if left untreated. Prior to the advent of antitoxin, the death rate among affected foals was greater than 90%. With the use of antitoxins in conjunction with antibiotics and supportive therapy, the mortality rate can be reduced to less than 25%. Animals unable to swallow should be fed through a nasogastric tube and placed on IV fluids. Once the toxin produced by the bacteria is attached to the nerve ending it cannot be neutralized by the antitoxin. Therefore, early treatment is critical. Even with aggressive therapy, recovery is slow and may require up to two weeks before the affected horse recovers.