Horses get botulism by ingesting a powerful toxin produced by the bacterium Clostridium botulinum, which thrives in soil and decaying organic matter. The most common route is eating contaminated feed, particularly spoiled hay, wet round bales, or improperly fermented silage. Foals can also develop botulism when bacterial spores colonize their immature digestive tracts, and in rare cases, deep wounds provide the right conditions for the bacteria to grow.
Three Ways Horses Develop Botulism
Botulism in horses takes one of three forms, each with a different entry point.
Forage poisoning (the most common form): Horses eat feed that already contains preformed toxin. The toxin is produced when Clostridium botulinum bacteria multiply in decaying plant material or animal carcasses that have contaminated the feed. Wet round bales, moldy alfalfa, improperly ensiled haylage, and hay that has been in direct contact with soil (around feeders, for example) are all high-risk sources. A dead bird or rodent baled into hay is a classic scenario: the decomposing carcass acts as an anaerobic incubator, and the toxin it produces leaches into the surrounding feed.
Toxicoinfectious botulism (“shaker foal syndrome”): Foals with immature gastrointestinal tracts swallow bacterial spores that then germinate and produce toxin inside the gut. Foals with gastric ulcers or other GI problems may be especially vulnerable because damaged tissue creates low-oxygen pockets where the bacteria thrive.
Wound botulism: Clostridium spores from soil enter a deep puncture wound or surgical site. The oxygen-poor environment inside the wound allows the bacteria to multiply and release toxin directly into the bloodstream. This form is the least common in horses.
What Makes Feed Dangerous
Clostridium botulinum is everywhere in soil. It forms tough spores that can survive for years. The bacteria only become dangerous when conditions allow them to “wake up,” multiply, and pump out toxin. Those conditions are straightforward: moisture, lack of oxygen, and a pH above 4.5.
This is why large round bales and haylage carry outsized risk. Silage that is raked and ensiled too dry (under 30% moisture content), fermented at a pH below 4.5, wrapped late, or stored in damaged packaging is particularly likely to harbor the toxin. Properly fermented silage is acidic enough to suppress bacterial growth, but if the process goes wrong, the dense, oxygen-poor interior of the bale becomes an ideal breeding ground. Hay that sits on wet ground near feeders poses a similar problem: soil contact introduces spores, and trapped moisture does the rest.
Animal carcasses are the other major contamination source. The bacteria naturally live in the intestinal tracts of many animals. When a bird, mouse, or snake dies in a hay field and gets baled up, the carcass decomposes anaerobically inside the bale. Toxin forms in the carcass and spreads into the surrounding forage.
How the Toxin Causes Paralysis
Once absorbed into the bloodstream, botulinum toxin travels to the junctions where nerves connect to muscles. It binds to the nerve ending, gets pulled inside the cell, and then destroys a set of proteins that nerve cells need to release their chemical signal, acetylcholine. Without that signal crossing the gap to the muscle, the muscle cannot contract. The result is flaccid paralysis: muscles that are limp rather than rigid.
This paralysis is progressive. It typically starts with subtle signs like difficulty swallowing, a weak tongue, and a shuffling gait. As more nerve-muscle junctions are blocked, the horse becomes increasingly weak, may tremble (which is why the foal form is called “shaker foal syndrome”), and eventually loses the ability to stand. If the muscles responsible for breathing are affected, the disease becomes life-threatening.
Geographic Risk Across the U.S.
Botulism can strike anywhere, but geography shapes which toxin type a horse is most likely to encounter. Over 85% of U.S. equine cases occur in the mid-Atlantic states, where toxin type B dominates. Type B spores concentrate in soils east of the Mississippi, particularly in the Northeast, Appalachian region, and Kentucky. Type A is more prevalent in western U.S. soils. Type C, associated with decaying animal carcasses, appears sporadically throughout the country.
If you keep horses in mid-Atlantic states or Kentucky, botulism should be on your radar as a realistic threat rather than a rare curiosity.
Survival Rates and Why Speed Matters
Untreated botulism in horses is often fatal. In outbreak situations with limited treatment, survival rates have ranged from just 10% to 30% depending on the toxin type. A large veterinary hospital study covering 92 adult horses over 24 years found an overall survival rate of 48%, but the numbers tell a more nuanced story.
Treatment with antitoxin dramatically improved the odds of survival. Horses that were still standing when they arrived at the hospital survived 67% of the time. Those that arrived unable to rise survived only 13% of the time. Among treated horses that never lost the ability to stand, the survival rate was 95%. Once a horse went down and couldn’t get up, that figure dropped to 18%. The takeaway is clear: early recognition and rapid antitoxin treatment are the biggest factors in whether a horse lives or dies.
Recognizing Early Signs
The earliest signs of botulism are easy to miss. Difficulty swallowing is often the first clue. You might notice feed dropping from the mouth, excessive drooling, or the horse dunking its hay in water to make it easier to eat. A weak tongue is another hallmark. Some horses develop a stilted, short-strided walk and general muscle weakness before progressing to trembling and an inability to stand.
Because the toxin blocks nerve signals progressively, symptoms tend to worsen over hours to days. A horse that seems mildly uncoordinated in the morning can be recumbent by evening. If you notice swallowing difficulty or unexplained weakness, especially in a region or feeding situation that puts the horse at risk, time is critical.
Vaccination and Feed Management
A vaccine is available against type B toxin, which is the type responsible for the vast majority of U.S. cases. The American Association of Equine Practitioners recommends that horses that have never been vaccinated receive three doses at four-week intervals, followed by annual boosters. In endemic areas like Kentucky and the mid-Atlantic, vaccination is considered a core part of preventive care. Pregnant mares are typically vaccinated to pass protective antibodies to foals through colostrum.
Feed management is the other half of prevention. Inspect hay bales for signs of mold, unusual moisture, or embedded animal remains. Avoid feeding from round bales that have been sitting on wet ground. If you use haylage or silage, ensure it has been properly fermented to a pH below 4.5 and stored in intact wrapping. Keep feeding areas clean so hay doesn’t accumulate in contact with soil. These steps won’t eliminate every risk, but they address the conditions that allow toxin to form in the first place.