Equine Botulism Reviewed

The most common way adult horses contract the disease is by eating feed, such as hay or grain, that contains animal remains.

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Equine botulism is most frequently observed in Kentucky and the Mid-Atlantic region of the eastern United States, although it has been reported worldwide. The disease is also known as shaker foal syndrome, forage poisoning, and grass sickness.

Botulism is a neuromuscular disorder of horses caused by neurotoxins of the bacteria Clostridium botulinum that results in flaccid paralysis by the action of the various botulinum neurotoxins. Of the three types, botulism Type B occurs throughout the United States but is more predominant in the Mid-Atlantic states and Kentucky. Type A botulism occurs primarily in the west while botulism type C occurs in Florida. Botulism neurotoxins type B and C are the most commonly reported types in foals.

Botulism results from exposure to the toxin by three main routes. Ingestion of preformed toxin is the most common form affecting adult horses when they eat feed, such as hay or grain, that contains animal remains. Swallowing the botulism organism with subsequent elaboration of toxin in the intestines is known as shaker foal syndrome, which is associated with 1- to 3-month-old foals, but can occur as early as one week of age. Rarely, wound infection with C. botulinum occurs and the subsequent release of the toxin in the body causes disease.

Clinical signs after exposure to toxin occur from 12 hours to several days and could be dependent on dose and type of botulinum neurotoxin involved. Sudden, unexplained death of one or more horses might be the initial signal of an outbreak. Decreased eyelid, tongue, and tail tone can be observed early in disease. Horses that can walk might have a stilted, short-strided gait without ataxia. Muscle trembling and weakness can be apparent, particularly in foals. Pupillary dilation with sluggish pupillary light reflexes and difficulty swallowing (dysphagia) is frequently observed. Clinical signs could rapidly progress to recumbency. Tachycardia can occur, particularly in foals. Death is generally attributed to respiratory failure secondary to respiratory muscle paralysis.

Diagnosis is made based on clinical signs. Definitive diagnosis requires detection of the toxin in serum, feces, gastrointestinal (GI) contents, or feed by enzyme-linked immunosorbent assay (ELISA), radioimmunoassay (RIA) or polymerase chain reaction (PCR). Specific toxin activity can be confirmed by a mouse inoculation test and is supported by isolation of C. botulinum from serum, feces, GI contents, or feed.

Treatment consists of blockade of any circulating toxin by intravenous administration of plasma containing specific antibotulism neurotoxin antibodies (generally against types B and/or C). Supportive care, including fluid, nutritional, antimicrobial, and respiratory supportive therapies, is critical. Adults and foals with mild respiratory signs can frequently be treated with intranasal oxygen insufflation and positioning in sternal recumbency. Mechanical ventilation can be life-saving in foals. Antimicrobial administration (avoiding procaine penicillin, aminoglycosides, and tetracyclines) is employed to prevent or reduce complications of the disease, such as aspiration pneumonia caused by dysphagia. Nutritional management can be provided to foals by feeding milk or milk replacer via indwelling nasogastric or nasoesophageal tubes while in adult horses, periodic nasogastric intubation of slurry meals or commercially available liquid diets can be provided.

For type B botulism, the survival rate in appropriately treated foals less than six months of age is greater than 90%. Affected adult horses that remain standing have a good prognosis (albeit a prolonged recovery ahead), while recumbent adults are less likely to survive. Vaccination with Clostridium botulinum type B toxoid is thought to be almost 100% protective against type B in adult horses and should be undertaken in endemic regions. Vaccination of pregnant mares will be at least partially protective to their foals assuming adequate passive transfer of immunity.

CONTACT: Pamela Wilkins, DVM, MS, PhD, Dipl. ACVIM, Dipl. ACVECC—217/333-2000—pawilkin@illinois.edu—University of Illinois College of Veterinary Medicine, Champaign-Urbana, Ill.

This is an excerpt from Equine Disease Quarterly, funded by underwriters at Lloyd's, London, brokers, and their Kentucky agents.

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Equine Disease Quarterly

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