Equine Protozoal Myeloencephalitis

CHAPTER 136 Equine Protozoal Myeloencephalitis



Debra C. Sellon


Equine protozoal myeloencephalitis (EPM) was first described as a focal myelitis-encephalitis of horses in the early 1970s. In 1991 a protozoan apicomplexan parasite was successfully cultured from the spinal cord of a horse with EPM and named Sarcocystis neurona. Subsequent development of a Western immunoblot assay to detect antibodies to S. neurona in the serum and cerebrospinal fluid (CSF) of horses greatly facilitated diagnosis of infection. Today EPM is recognized as one of the most common infectious neurologic diseases of horses in the Americas.



ETIOLOGY AND LIFE CYCLE


S. neurona is the most common etiologic agent identified in horses with EPM, but similar parasites, including Neospora hughesii, have been isolated from a few affected horses. Opossums (Didelphis virginiana and Didelphis albiventris) are the definitive hosts for this organism. Unlike most Sarcocystis species, which have a restricted intermediate host range, S. neurona can use any of a number of mammalian species, including raccoons, skunks, domestic cats, nine-banded armadillos, and sea otters, as intermediate hosts. The raccoon is probably the most important intermediate host for S. neurona in the United States. Domestic cats probably play little role in the natural life cycle of the parasite. Although S. neurona antibody is detectable in 5% of free-roaming cats (higher in cats that reside on horse farms), no sarcocysts were observed in muscle sections from 50 such cats.


Opossums become infected by ingesting mature sarcocysts in the tissues of intermediate hosts. In the gut lumen of the opossum, bradyzoites are released from the sarcocysts and immediately transform into male and female gamonts. Organisms undergo sexual reproduction to produce oocysts, which sporulate in the lamina propria of the gastrointestinal tract, producing two sporocysts, each with four sporozoites. Fully sporulated oocysts (sporocysts) are excreted in the feces of the opossum, contaminating pasture and soil. Intermediate hosts ingest sporocysts. Sporozoites are released, invade the intestinal epithelium, and undergo asexual multiplication, eventually forming sarcocysts, the encysted stage of the organism, in many tissues. When intermediate hosts die, their muscles, containing mature sarcocysts, are ingested by opossums, completing the life cycle. Intermediate hosts do not generally develop recognizable clinical signs as a result of S. neurona infection, but encephalomyelitis has rarely been described in the cat, raccoon, mink, skunk, sea otter, Pacific harbor seal, Canadian lynx, fischer, and dog. Horses are considered aberrant intermediate hosts for S. neurona in which sarcocysts do not form. However, there is one report of sarcocysts in the tongue and skeletal muscle tissue of a 4-month-old-foal with neurologic abnormalities consistent with EPM, suggesting that horses may, on rare occasions, act as competent intermediate hosts in the life cycle of S. neurona.



EPIDEMIOLOGY


The geographic range of the opossum, the definitive host for S. neurona, confines the geographic range of EPM in horses to the Americas. Affected horses in Europe, South Africa, and Asia have invariably been imported from the Western Hemisphere. The only reports of clinical disease in equids other than horses are single case reports in a pony and a Grant’s zebra. In areas where opossums are common, about 50% of horses are seropositive, indicating exposure to S. neurona. In areas where opossums do not reside (e.g., Montana, Wyoming), seropositive rates in native horses approach 0%. Serum antibodies against S. neurona can be detected for many years after horses have been removed from an endemic area. Persistent antibodies may be attributable to the long half-life of the antibodies, chronic infection or ongoing antibody production, or both. Despite the obvious high levels of exposure of horses in the United States to S. neurona, in 1998 the incidence of clinical disease in horses was estimated to be less than 1%. Factors associated with an increased likelihood of clinical disease include diagnosis in the fall season, hay storage not secure from wildlife, age 1 to 5 years, use of the horse for racing or showing, previous diagnosis of EPM on the premises, and a recent (less than 90 days) adverse health event for the horse (e.g., lameness, parturition, injury, colic). Apparent protective factors include age of less than 1 year, use for breeding, and observation of birds, but not opossums, on the premises.



PATHOGENESIS


Despite efforts by numerous investigators, Koch’s postulates have not been fulfilled to confirm unequivocally the role of S. neurona in the pathogenesis of EPM, largely because of difficulties with consistently reproducing disease in experimental models and subsequently isolating the organism from affected horses. These same experimental difficulties have also hindered progress toward elucidation of the pathogenesis of disease in horses. However, the information gleaned from pathologic and epidemiologic reports of natural infection, results of experimental equine infections, and extrapolation from murine models of disease suggest the likely pathogenesis of disease in horses. After ingestion of sporocysts from opossum feces, S. neurona replicates to a limited extent in equine gastrointestinal epithelial cells. Cell-associated parasitemia provides parasites with access to visceral and central nervous system (CNS) tissues, where subsequent rounds of asexual reproduction occur. After hematogenous spread to the CNS, S. neurona may localize in any area, from cerebrum to spinal cord, but is not found in peripheral nerves. Merozoites and schizonts of S. neurona may be observed in various cell types in the CNS of horses with EPM, including neurons, mononuclear cells and glial cells. Specific immune responses limit parasitemia and visceral organ infection but do not always prevent CNS invasion and disease. The site of parasite replication in the CNS of an infected horse determines the type and severity of clinical signs that are observed. Some types of immune suppression and stress may increase the likelihood of neurologic disease after infection with S. neurona.



CLINICAL SIGNS


Clinical findings in horses with EPM vary greatly, depending on the location of parasite replication and the extent of associated inflammatory response within the gray or white matter of the CNS. Lesions may be focal, diffuse, or multifocal. Most affected horses are bright and alert and have normal vital signs. About 80% to 90% of horses with EPM have progressive neurologic disease manifested as ataxia, weakness, and conscious proprioceptive deficits of one or more limbs, indicating spinal cord involvement. Asymmetric muscle atrophy is evident in about 15% of affected horses, most often in the gluteal or quadriceps muscles. Clinical signs may be mild, resulting in an asymmetric gait deficit that is mistaken for lameness, behavioral, or training issues or masked by real lameness caused by injuries resulting from the abnormal gait. Examples of performance problems that have been attributed indirectly to EPM include frequent bucking, head tossing, excessively high head carriage, difficulty maintaining a specific lead, back pain, upward fixation of the patella, and difficulty negotiating turns. Clinical signs in most affected horses will gradually progress over time. However, some horses may exhibit an acute onset or exacerbation of clinical signs with sudden recumbency and inability to rise as the initial clinical sign recognized by owners.

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May 28, 2016 | Posted by in EQUINE MEDICINE | Comments Off on Equine Protozoal Myeloencephalitis

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