Botulism in Horses and
Horse owners and veterinarians are commonly requesting information
regarding the use of haylage (hay-crop silage) and/or treated hay
as low-dust feed alternatives for horses. The dust in hay is formed
when the hay is insufficiently dried, resulting in heating and spoilage
and allowing the growth of molds. Haylage is one of the alternative
methods of preserving hay when weather conditions prevent the drying
of hay below 14% moisture content. Unfortunately, haylage is not
recommended when feeding horses due to the danger of botulism.
Haylage or grass silage is the process where young respiring plants are cut, partially wilted and placed in a silo or container such as a plastic bag where exposure to air is eliminated. The hay is baled at about 45-50% moisture and immediately wrapped with plastic, or placed in a bag, which reduces the presence of oxygen. The plants use the remaining oxygen in the bag, fermentation lowers the pH and the forage goes into a suspended state when the pH=5. Should the bag become punctured, then secondary fermentation will occur and the haylage will become spoiled in those areas where oxygen is present. Large round bales, e.g., 4 by 5 feet in size, present a greater risk of botulism. The big bale often has insufficient water-soluble carbohydrates for adequate lactic acid fermentation to achieve a stable pH (1). A higher dry matter content can also lead to a higher pH. Clostridial multiplication is inhibited below pH 4.5. The smaller commercially bagged bales (50 lbs.) are probably less prone to botulism due to better quality control over fermentation and a faster drop in pH.
Horses are the most sensitive of the domesticated animals to botulism. Botulism is a disease that occurs when toxins produced by the bacterium, Clostridium botulinum, enter the horse's body causing weakness which may progress to paralysis. The botulism bacterium is a spore-forming, anaerobic bacteria (grows in the absence of oxygen) which is found world wide. It is commonly present in soil and in decaying animal carcasses. It occurs less often in decaying plant material. Hay, and especially haylage, can be contaminated with the botulism bacterium during the raking and baling process. The higher moisture levels (in comparison to dry hay), the anaerobic conditions and a pH above 4.5 in some haylage are ideal conditions for the growth of this bacterium.
When the bacterium grows, it produces one or more toxins. These toxins block the connection between the nerves and muscles. As a result, affected horses often exhibit signs varying from muscle weakness to paralysis (1).
- usually have muscle tremors.
- may be so weak that they cannot stand up.
- lose control of their tongue so it may hang from their mouth.
- can't eat and they drool because they can't swallow.
- may walk stiffly with a short stride or they may be weak and stumble. Their tail may lose its tone.
Eventually they die because their respiratory muscles become paralysed or because they get other health problems from being down. These clinical signs can occur within several hours or up to 7-10 days post ingestion of the contaminated feed.
Horses can get botulism in any of three ways. In foals up to 8 months of age, botulism can occur if the bacterium grows in the foal's intestines (1). Foals that are growing well and are being fed grain are most likely to get into trouble. These foals are called "shaker foals" because the muscle weakness from the toxin makes them tremble.
Occasionally a wound can become infected with the bacterium and cause botulism in adults. Fortunately, this is rare. Far more commonly, botulism occurs when horses eat feed or water which contains preformed toxin. Clostridia grow on substrates (food sources) which are above a pH of 4.5 and are in an anaerobic (non oxygen) environment. Here they produce toxins. Improperly preserved haylage can be an ideal environment for clostridial growth. Water and feed can also be contaminated with the carcass of a dead animal. When several horses develop botulism, toxin in feed or water is usually the reason.
Several incidents of botulism occur each year after horses eat
wrapped or bagged round bale haylage. In some of these outbreaks,
the haylage looked and smelled spoiled. In others, the bales didn't
look as if they were spoiled but horses eating them developed botulism.
Seven distinct serotypes of botulinum toxin have been isolated (1). They are designated types A through G. There appears to be a geographical distribution of the various serotypes as well as association with different feed sources. The following indicate the serotype and the typical species involved in a poisoning:
Types A, B, and C have been seen in cattle.
Type A botulinum toxin has been incriminated in several outbreaks in horses in the northwestern United States (Washington, Idaho, Montana, Oregon).
Type B predominates and is referred to as forage botulism because of its association with contaminated forage.
Type C is referred to as carrion botulism because of the association with the ingestion of feed containing a decomposing carcass (e.g., rodent, cat, dog, bird) or from eating the bones of dead animals.
Types C and D are found in poultry and poultry manures, mink and wild ducks.
Type E occurs in fish or in association with the consumption of fish products.
The clinical signs of botulism are similar to other causes of central nervous signs, including rabies, the equine viral encephalitis diseases such as Eastern, Western or West Nile encephalitis and the nervous form of equine viral rhinopheumonitis. Botulism is diagnosed by eliminating other causes of central nervous disease and associating a point source such as the feeding of haylage. Rarely is it possible to detect botulinum toxin in the serum of affected animals or in suspect feed. The Mouse Toxin Assay is the gold standard for toxin detection and typing. However, it may take up to four days to complete the test. Although a positive test confirms the presence of the toxin, a negative test does not mean that an animal is not affected by the disease.
Botulism is difficult to treat. There is a polyvalent (A-E) anti-toxin which is available from Dr. Bob Whitlock at New Bolton Center, University of Pennsylvania. However, it costs about $3,000 US per horse. Other plasma products (Veterinary Dynamics) contain type B antitoxin. The University of Guelph and some other teaching hospitals maintain a supply of antitoxin. The antitoxin is most beneficial if used when animals are first seen to be sick. With supportive care, horses can recover but, if they are exposed to a large amount of toxin, most will die despite treatment.
An inactivated toxoid is used to vaccinate against botulism. A toxoid is a toxin which has been treated to destroy its toxicity but retains its ability to generate an immune response when injected into an animal. Neogen Biologics, Michigan, USA, manufactures Bot Tox-B (1). It is available in Canada from some suppliers. It protects against Type B only. A three-initial-dose vaccination program is recommended followed by a single annual vaccination.
Risk Factors which may increase the risk of Cl. botulinum in silage include:
- the raking of hay and thus incorporating earth in the hay,
- ensiling of drier haylage (probably less than 30% moisture),
- the use of chicken/turkey manure on the land and
- delays in wrapping or bagging of the plant material.
Recommendations to Horse Owners:
- Hay silage is a great feed when preserved properly but carries the danger of botulism.
- Don't feed silage to horses unless the horses have been vaccinated.
- When raking hay, lift the tines of the rake up so they don't pull earth into the hay.
- Don't apply poultry manure to hay fields intended for hay production.
- Watch out for the accidental incorporation of animal carcasses into the bales. (This is difficult when it comes to mice.)
- Ensure that the hay is baled in the 35-50% moisture level or use acid preservatives on the hay when baling. The acid and higher moisture levels are used to ensure that the pH drops below 4.5 rapidly (within 2 - 3 days of bagging).
11. Radostits OM, Gay CC, Blood DC, Hinchcliff KW. Veterinary Medicine, 9th ed. London: WB Saunders, 2000: 757-760.
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