Botulism in Horses
Image courtesy Fox Run Equine Center
By Brian S. Burks, DVM
Diplomate, ABVP
Board Certified in Equine Practice
Every horse owner’s nightmare is to find their horse ill in some way. Horses that are down (recumbent) are even more worrisome. Botulism is a progressive disease causing muscular weakness, dysphagia (difficulty eating/swallowing) and recumbency.
Botulism is caused by the toxins released from a bacterium known as Clostridium botulinum. This bacterium can be found in the soil and gastrointestinal tract of many animals. Rodents, rabbits, and the like that get baled into hay will leave spores and toxins in the hay, even as the body decays. Rotting vegetation and soil are more likely to have spores. This includes lawn clippings that get piled into a pasture or paddock.
There are 7 types of C. botulinum, A to G, differentiated on the antigenic specificity of the toxins. Types A, B and E are most important in people. C and D are most important in animal species. Toxins D-G have never been reported in horses. Clostridium botulinum is a gram positive, spore forming bacterium, and its toxin is one of the most lethal substances on earth; only 1.0 micrograms is a lethal dose in humans. Thus, the disease is zoonotic and a public health issue.
The neurotoxin impairs electrical impulse transmission at the neuromuscular junction, (from the nerve to the muscle) irreversibly inhibiting acetylcholine (Ach) release, leading to flaccid paralysis. The toxin is often ingested, but wounds may become infected with the spore form, which may allow proliferation of the bacteria in an oxygen poor tissue with subsequent formation of the neurotoxin. Spores are ubiquitous in the environment. These spores are sensitive to acid-base changes and do not proliferate or form toxins in a very acidic environment, but resist boiling for many hours. Hay that has adequate fermentation will more likely allow bacterial growth and neurotoxin elaboration.
There are three forms:
Ingestion of preformed toxin- often in round bales or silage/haylage
Toxicoinfectious botulism in foals, where spores are ingested with subsequent proliferation of toxin in the GIT. (‘shaker foal syndrome’)
Wound botulism, where spores get into a deep wound and form neurotoxin. This includes castration sites and clamped umbilical hernias.
Any animal of any age, sex, or breed can contract botulism. It is most common in cattle and horses, due to the source of botulism, but it also occurs in people from illicit drugs and spoiled foods. Type C C. botulinum causes a very high incidence of disease in wild waterfowl, with thousands of birds dying each year in outbreaks in the USA and Canada.
Botulism can begin with signs of colic- abdominal pain. This is because the toxin stops nerve function in the gastrointestinal tract, so that it no longer moves ingesta down the intestinal tract. Distention of the gut with fluid, gas and too much ingesta is painful.
The characteristic clinical sign is generalized flaccid paralysis. Horses show generalized, progressive weakness, with muscular trembling. Tongue tone is very weak, where a tongue pulled out of the mouth will not be retracted. They will be sluggish, lethargic, and exhibit exercise intolerance. Walking can worsen the clinical signs as acetylcholine is used up at the neuromuscular junction and is not reformed due to the neurotoxin. Eventually, horses can be weak enough to become recumbent, although they may try to stand. In some cases the only clinical sign may be sudden death.
Other clinical signs include decreased tail tone. The pupils may be dilated, exhibiting sluggish or absent pupillary light responses; vision is retained. Affected horses will be slow to eat grain and may have hay stuck in the mouth. There may also be difficulty with urination or defecation, requiring evacuation of each respected cavity. Dysphagia may be exhibited by the inability to chew and food protruding from the mouth or coming back through the nostrils. They lose the ability to swallow even saliva. Respiratory distress can eventually ensue from aspirated feed material and neuromuscular blockade of the phrenic nerve, which innervates the diaphragm. The latter is a terminal sign.
The degree of clinical signs is dependent upon the number of spores ingested and the amount of toxin formed. Type B toxin is found in the eastern United States, including Pennsylvania, and all along the eastern seaboard. This is most often associated with feeding round bales or “ag- bags” of 750-lb hay bales. Types A and C are less common and occur in the western states. Botulism can be contracted from square bales as well, though less commonly.
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. Diagnosis is dependent upon finding spores and toxins in the gastric or colonic content. Hay and grain may also be tested. Unfortunately, the tests take two-four weeks. The toxin is quite labile and difficult to identify; it may be best to take gastric content from a deceased animal. Clinical signs support the diagnosis.
Polymerase chain reaction (PCR) techniques to detect the neurotoxin gene of C. botulinum in samples from equine cases of botulism have been developed. The PCR assays identify the three clinically relevant types (types A, B, and C) and the results are available more quickly and the false negative rate is lower.
Treatment is largely supportive, though there is an antiserum to the type A, B & C toxins. The serum will only work on unbound toxin in the bloodstream. Once bound to the neuromuscular junction, the antiserum is ineffective; the antiserum should be administered as early in the course of disease as possible. Therapy includes oral or intravenous fluid therapy to maintain hydration, evacuation of the bladder and rectum, and keeping the horse in sternal recumbency. Horses may require parenteral or enteral nutrition provided by nasogastric intubation. Decubital ulcers are common, and horses need to have them cleaned daily. Changing the horse from side to side will help prevent such ulcers, but movement can also exacerbate the condition; slings are seldom, if ever, used to treat patients with botulism. Antibiotics may be required in some cases, but will not treat the disease, as it is the toxin, not the bacterium, that causes disease. Recovery can take several days to several weeks. The prognosis is guarded for recumbent horses.
Prevention of Type B botulism is by avoiding round bales or other bales associated with botulism. There is also a vaccine available, which is highly recommended along the eastern seaboard and Kentucky. Fortunately, 85% of botulism cases are type B, so the vaccine is effective. Vaccination requires three doses one month apart the first year, then annually thereafter.
Botulism is an extremely deadly disease of herbivores and other species. The most characteristic sign of disease is generalized flaccid paralysis, which can lead to death due to respiratory muscle paralysis. Treatment is largely supportive and prevention is via vaccination and avoiding hay most likely to be involved- round bales and haylage. Fatality is 80-100%. The antiserum reduces the mortality rate to 25% when used early in the course of disease.
