Botulism in Horses
C. botulinum is a Gram-positive, spore-forming, anaerobic bacterium. Spores are found in soil and aquatic sediments throughout most of the world, but the distribution of types varies based on environmental factors. Eight types of C. botulinum neurotoxin exist- A, B, C1, C2, D, E, F, and G. While all cause similar disease, there is variation in geographic distribution, potency, and antigenicity. In North America, botulism in horses is most often caused by type B toxin and less often by toxin types A and C1.
Three forms of equine botulism are recognized:
- Intraintestinal toxicoinfectious botulism (shaker foal syndrome) develops in rapidly growing foals 1-2 months of age. This form develops following ingestion and overgrowth of botulinum in the gastrointestinal tract, typically caused by type B. Young foals have a less developed gastrointestinal microflora, which can permit spore activation, vegetative growth, and subsequent neurotoxin production. Proliferation of C. botulinum type B in gastric ulcers, foci of hepatic necrosis (diseased livers), navel or lung abscesses, and skin and muscle wounds have also been reported.
- Forage poisoning, the most common form of intoxication in adult horses, follows ingestion of preformed neurotoxin in poorly preserved hay, haylage, silage, or other feedstuffs. Silage and large, round hay bales are most frequently implicated in botulism caused by neurotoxins type A and B. In horses, intoxication is most commonly associated with forage and almost never with commercial grain. Forage with a pH >4.5 is most associated with the growth of botulinum and toxin production. Type C botulism is associated with ingestion of feed or water contaminated with an infected rodent or small animal carcass.
- Wound botulism, a less common form, results following infection of the umbilicus or a wound, such as a castration site. Regardless of type, botulinum neurotoxin acts primarily at the neuromuscular junction. The toxins are internalized at the nerve ending and through a series of steps inhibit the release of neurotransmitters needed for muscle contraction, which results in flaccid paralysis.
Once bound, toxin neutralization is not possible, and normal neurotransmitter release from the affected neurons will only return once new motor end plates have been generated, which might take 10-14 days. Clinically, symmetrical flaccid paralysis is a consistent finding with the onset and rate of progression dependent on the amount of toxin that is absorbed.
Initial clinical signs include difficulty eating with apparent excess salivation, weak eyelid tone, weak tail tone, and exercise intolerance. Affected animals also spend increased amounts of time resting due to generalized muscle weakness, which is associated with tremors, carpal (knee) buckling, and ataxia (incoordination).
Pharyngeal and tongue paralysis predisposes the horse to aspiration pneumonia and quidding (dropping) food. Paralysis of the diaphragm and intercostal muscles can also result in an increased respiratory rate and decreased chest wall expansion. Severely affected animals ultimately die from respiratory paralysis and cardiac failure.
Botulism should be suspected in animals with flaccid paralysis displaying the aforementioned clinical signs. Botulinum toxin does not affect the spinal cord or brain but does affect the cranial nerves; thus, symmetrical cranial nerve deficits in an animal with normal mentation can help differentiate botulism from other disorders.
A mouse bioassay can be used to obtain a definitive diagnosis by inoculating serum or gastrointestinal contents from an affected horse into a mouse. However, horses are extremely sensitive to the toxin, and false negative test results are common; the mouse bioassay identifies botulism from fecal samples in only about 30% of adult horses with clinical disease.
Detection of antibodies to botulinum toxin in a recovering unvaccinated horse also supports a diagnosis of botulism. However, antibody detection has limited treatment impact due to the time required for antibodies to develop. Demonstration of spores in the intestine is not diagnostic, as they can be ingested and detected as contaminants.
A quantitative real-time PCR (qPCR) for detection of the neurotoxin genes of C. botulinum types A, B, and C exists but is not currently available for commercial use. The combination of false negative tests and lack of PCR testing means a diagnosis of equine botulism is typically based on clinical signs, known exposure to a feed or wound source, and/or response to treatment.
Immediate treatment with a polyvalent antitoxin prevents further binding of the toxin to presynaptic membranes. However, antitoxin cannot reactivate neuromuscular junctions that have already been affected. Thus, antitoxin administration might have little effect in severely affected animals. Generally, only one dose of antitoxin is needed and provides passive protection for up to two months.
Antibiotics should be administered if toxicoinfectious botulism is suspected or if there are secondary lesions such as aspiration pneumonia or decubital ulcers. Antibiotics that can cause neuromuscular blockade and possibly exacerbate clinical signs, such as aminoglycosides, should be avoided, and neurostimulants, such as neostigmine, should not be used.
Supportive care, including the provision of a deep bed and a quiet environment, is essential. Frequent turning of recumbent animals, nasogastric feeding, and fluid support for animals with pharyngeal and lingual paralysis, frequent catheterization of the urinary bladder, the application of ophthalmic ointments, and ventilatory support might be required.
A survival rate of 88% has been reported in foals with toxicoinfectious botulism that received intensive nursing care (including mechanical ventilation and botulism antitoxin). However, this type of treatment is not available in all areas and is quite expensive. Without aggressive supportive care, the mortality rate is high, with death usually occurring one to three days after the onset of clinical signs.
The prognosis is variable in adult horses that have ingested preformed toxin (forage poisoning), depending on the amount of toxin absorbed and the severity of clinical signs. Mildly affected animals might recover with minimal treatment, while severely affected animals that become recumbent have a poor prognosis.
The mortality rate has been reported to be as high as 90% in recumbent adult horses, with death occurring within hours of the appearance of signs. In animals that survive, complete recovery is most common, although development of full muscular strength can take weeks to months. Persistent tongue weakness, not affecting the ability to eat, has been reported following recovery.
A type B toxoid vaccine is available and should be used in areas in which type B botulism is common; vaccination is particularly important in areas where neonatal botulism occurs. Importantly, the type B vaccine only provides protection against type B toxin. There is no cross protection against type C toxin, and there is not a type C toxoid vaccine licensed for use in North America.
If botulism is suspected to have been caused by ingestion of preformed toxin in feed, an alternate feed source should be provided while the origin of intoxication is investigated. Potentially contaminated feeds should be either safely disposed of or sent for confirmatory testing. Silage, haylage, and other fermented feeds should be fed with caution to horses because of the risk of botulism.
Regulations requiring the reporting of botulism vary by state and country (i.e., botulism is required to be reported to the Kentucky State Veterinarian). If you suspect an animal has ingested botulism from a contaminated food source, the U.S. Food and Drug Administration’s Center for Veterinary Medicine or other regulatory body should be contacted.
Editor’s note: This is an excerpt from Equine Disease Quarterly, Vol. 32, Issue1, funded by underwriters at Lloyd’s, London, brokers, and their Kentucky agents. It was written by Nathan M. Slovis, DVM, Dipl. ACVIM, of Hagyard Equine Medical Institute.
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