This serious disease can be difficult to diagnose because its signs often mimic other health problems in the horse and signs can range from mild to severe. The disease is not transmitted from horse to horse. Rather, the organism Sarcocystis neurona is spread by the definitive host, the opossum, which acquires the organism from cats, raccoons, skunks and armadillos and sea otters.
Prickett, Rooney, and others described 44 cases of the disease in 2 and 52 cases of the disease in 1 at the annual meeting of the American Association of Equine Practitioners AAEP. Protozoa were first observed in association with characteristic lesions in34 and the disease was given its current name, equine protozoal myeloencephalitis by Mayhew et al.
The opossum Didelphis virginiana is the definitive host for S.
The sporozoites are infectious for the intermediate hosts, which include skunks, 14 raccoons, 15 armadillos, 16 and cats. Opossums are commonly infected with S.
Horses are infected with S. Thus, opossums are the major source of S. The exact mechanisms by which S. Canids are a definitive host for the related species Neospora caninum, 26 but it has not been established that dogs or wild canids are a definitive host for N.
Vertical transmission of N. Studies in both mice and horses experimentally infected with S. It is unclear what influences the progression to severe neurologic disease.
A smaller retrospective study of 82 horses with histologic lesions compatible with EPM suggested that EPM risk was highest among male Standardbreds. In general, the seroprevalence of N.
Serum antibodies against N. EPM usually occurs sporadically and seldom involves more than 1 horse on a farm, 564 although clusters of cases can occur. EPM occurred the least in the winter, with the risk 3 times higher in spring and summer and 6 times higher in the fall.
On a given premise, the presence of opossums 2. Immune suppression because of stress or advanced age might predispose a horse to development of EPM. Not surprisingly, horses with EPM that were treated with an anticoccidial drug were 10 times more likely to improve than untreated horses.
Occasionally, the clinical signs stabilize, only to relapse days or weeks later.
The variability of clinical signs is because of infection of both white and gray matter at multiple sites in the CNS. Signs of gray matter involvement include focal muscle atrophy and severe muscle weakness, whereas damage to white matter frequently results in ataxia and weakness in limbs caudal to the site of infection.
Early signs of EPM such as stumbling and frequent interference between limbs can be confused with lameness. Horses affected with EPM commonly exhibit a gradual progression in severity and range of clinical signs.
In some cases, however, a gradual onset can give way to a sudden exacerbation in the severity of clinical illness, resulting in recumbency.
The vital signs in affected horses are usually normal and animals appear bright and alert. Some horses with EPM appear thin and mildly obtunded.
Neurologic examination often reveals asymmetric ataxia, weakness, and spasticity involving all 4 limbs. Areas of hyporeflexia, hypalgesia, or complete sensory loss are occasionally present.
For highest accuracy in antemortem diagnosis, the following steps are recommended. CSF titer ratio are the only tests currently offered commercially that provide information regarding intrathecal antibody production based on serum and CSF titers.The American Association of Equine Practitioners’ summer education event, Focus on the Foot and the 17th Annual Practice Management Seminar, will provide a comprehensive continuing education package for equine practitioners July in Columbus, Oh.
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equine protozoal myeloencephalitis (EPM), West Nile virus, or certain poisons. . Stay up-to-date on the latest news about your horse's health with FREE newsletters from ashio-midori.com Topics include Nutrition, Soundness & Lameness, Equine Behavior, Farm & Barn, Older Horse Care.
EQUINE PROTOZOAL MYELOENCEPHALITIS Equine protozoal myeloencephalitis (EPM) is neurological damage caused by lesions on the brain and spinal cord left by protozoa. In the United States, it is estimated that about fifty percent of all horses have been exposed to the organism that causes EPM.