Botulism in Horses

Horses are extremely sensitive to botulinum toxin. Amounts of toxin which are sublethal in mice may rapidly cause the death of adult horses if administered i.v.

(Kinde et al., 1991). Exposure of the horse to botulism may occur from ingesting preformed toxin in contaminated feed (forage poisoning) or rarely may result from enteric (adult horses or very young horses [shaker foal syndrome]) or wound infection with C. botulinum and subsequently production of toxins in vivo (Galey, 2001). Clinical paralysis and death may result within hours from exposure to a high toxin level or, as in many cases, may develop and progress over a period of two to three weeks or more.

Forage poisoning was confirmed to be caused by C. botulinum by Graham and Brueckner in 1919 (Kriek and Odendaal, 1994). Forage is often the source, especially poorly ensiled silage or haylage and that contaminated with carrion.

Forage poisoning most often is caused by consumption of feed contaminated with type B toxin (Galey, 2001). In North America, horses are affected most frequently by type B botulism (> 85% of cases), occasionally by type C, and only rarely by type A

botulism (Galey, 2001). Type B and D have been reported in cases of equine botulism in England (Ricketts and Greet, 1984). Type C2 is also reported together with C1 causing botulism in horses (Kinde et al., 1991). In general forage contaminated with carrion tends to have type C or D toxin (Galey, 2001).

Toxico-infection occurs mainly in very young horses (skaker foal syndrome) in the intestine, which is predisposed by ulcer or necrosis, and appears to be potentiated by excessive amounts of corticosteroids contained in the fat of the milk of mares (Swerzek, 1980). TI botulism in foals (similarly in human infants) thought to be due to lack of an established normal gut flora that permits germination of spores and growth of C. botulinum in the GI tract (Bartlett, 1986). Shaker foal syndrome usually is attributed to type B toxin. However, a case of type C in a two-month old foal was reported (Semrad and Peek, 2002). It is sporadically occurs in foals between two weeks and eight months of age; mainly in the fast growing period at 2-4 weeks of age (Swerczek, 1980). Signs of shaker foal syndrome are stiff gait, muscular weakness and tremors (shaking prior to recumbency) without ataxia, dysphagia, decreased tail tone may also be noted, dyspnoea with extension of head and neck is seen as the disease progressed, recumbency and death that occurs more often 24-72 h after the onset of clinical signs (Swerczek, 1980). TI botulism in adult horses sporadically occurs (Swerczek, 1980; Hartigan, 1985) and is always associated with an altered GI environment; for example following GI disease, abdominal surgery, or recent antibiotic therapy (Chia et al., 1986). On one particular thoroughbred horse farm, 91 cases of TI botulism occurred among foals, yearlings, and adult horses and only two animals survived, which showed typical clinical signs of botulism (Szabo et al., 1994).

The equine grass sickness disease now is strongly considered as a TI form of botulism (Hunter et al., 1999; Böhnel et al., 2003).

Wound botulism in horses is mainly reported due to type B (Whitlock and Buckley, 1997). It has been associated with castration, inguinal or injection abscesses, trauma and surgery in adult horses and in foals with omphalophlebitis, umbilical hernias and with infected leg wounds (Whitlock and Buckley, 1997; Semrad and Peek, 2002).

The clinical signs of equine botulism are the same regardless of the pathogenesis;

however, subtle differences may be produced by the various toxin types (C versus A

and B). The time of onset of clinical signs of botulism of horses depends on the dose of toxin ingested or absorbed from GI tract or a wound. The first clinical signs are observed from 12 h to ten days following ingestion of the toxin. Generalized muscle weakness, dysphagia or both are first appear, decreased excercise tolerance and colic follow in some cases. Anorexia, labored breathing and increased salivation, mydriasis and ptosis may happen, decreased tail tone is often, decreased tongue tone, stiff stilled gait, but not ataxic, muscle tremor mainly in type C, increased heart and respiratory rate, urinary retention, constipation and ileus are common signs in recumbent horses with agonal signs and some peddling (Galey, 2001). Aspiration pneumonia may be a complication. Death is caused by respiratory paralysis.

Recovery may occur in mildly affected horses.

Definitive diagnosis of botulism in the laboratory is elusive. No pathognomonic gross or histological lesions and circulating toxin levels are often low (Galey, 2001).

Analytical methods, such as the mouse bioassay, are of insufficient sensitivity relative to the extreme sensitivity of the horse (Galey et al., 2000). Horses are suggested to be 1-10,000 times more sensitive than the mouse bioassay (Kinde et al., 1991). Source material may have higher and more easily detectable toxin levels, but it is often unavailable for testing. So, diagnosis often depends on clinical signs, lack of post-mortem lesions and elimination of other potential neurological diseases.

The major definitive test used to identify botulism toxin uses the mouse protection bioassay. Samples of source material (faeces, gut contents, liver) can be assayed.

Recently, sensitive immunoassays such as ELISA test were developed for BoNT detection (e.g. Doellgast et al., 1993; Ferreira et al., 2003). However, immunoassays are most often less sensitive than the mouse bioassay. Culture of faecal material or intestinal contents and PCR assays may help to identify the bacterium (Szabo et al., 1994; Fach et al., 1996). However, presence of C. botulinum naturally among gut flora makes this detection questionable if no toxin is detected in the sample.

Treatment largely depends on supportive care and injection of antiserum (polyvalent or monovalent antitoxin), if done early before recumbency occurs it may be of benefit (Rocke, 1993). Horses with mild disease may recover without antitoxin therapy.

Antibiotic therapy to prevent bacterial growth e.g. in wound botulism or to treat complications of paralysis like aspiration pneumonia may be used. But drugs that

potentiate neuromuscular weakness (aminoglycosides, tetracyclines and procaine penicillin) should be avoided. Mineral oil may be used to combat ileus and constipation. In addition histamine blockers may be used to prevent gastric ulcers.

Severely affected and recumbent animals may require ancillary therapy, including mechanical ventilation, bladder catheterization and oral alimentation (Whitlock and Buckley, 1997). Xylazine and diazepam can be used to sedate horses and foals that struggle excessively in recumbency. However, as with many diseases, the best way to deal with botulism is prevention. Good husbandry, check forage for carrion or toxic plants or other foreign matter, not to feed poor-quality hay to horses and prevention of wounds to occur and if be cleaned and treated, are important measures.

Vaccination of valuable animals is done especially in endemic areas, however, the vaccines (toxoids) are not easy to obtain and are expensive. In southern Africa botulism is currently well controlled by vaccination, although sporadic outbreaks of the disease still occur (Kriek and Odendaal, 1994). The use of antisera in horses has been shown to reduce mortality rates from 80-30 % (Swerczek, 1980).