|
Equine protozoal myeloencephalitis (EPM) is a protozoal disease affecting the central and peripheral nervous system in horses. The protozoan most commonly associated with EPM is Sarcocystis neurona. However, Neospora hughesi has been associated with some cases of EPM. The parasites cause inflammation and necrosis of the spinal cord, brainstem and brain. Depending on the location of the lesion, the clinical signs vary greatly. The horse is a dead end host for the parasite (there is no further transmission from a horse to any other horse). The Virginia opossum (Didelphis virginiana) is the definitive host, with a number of intermediate hosts identified (9-banded armadillo, raccoon, skunk). The disease is naturally occurring in North and South America. There is widespread exposure of horses to the parasite in these naturally occurring countries. All ages of horses may be affected, with the majority of cases seen in horses 4-5 years of age or younger. It is not seen as commonly in ponies. Multiple cases per farm are rare but can occur. The epidemiology of EPM has been studied over the past few days. The seroprevalence (positive serum titer) in horses differs between states. In the United States, a seroprevalence rate of approximately 50% has been suggested. It is important to realize that seroprevalence does not indicate that the horse is going to be clinically affected by EPM. Many seropositive horses do not show clinical signs of EPM. This status only indicates exposure of the horse to the protozoa. The pathogenesis of EPM is still unclear. It is assumed that affected horses ingest S. neurona sporocysts that are passed in opossum feces. Once ingested, the sporocysts excyst and release sporozoites, which penetrate the gut and enter the arterial endothelial cells of various organs. At this time, meronts develop and rupture the host cell, releasing merozoites into the bloodstream. This is most likely followed by a second round of merogony throughout the body. At this stage, it is likely that the formation of sarcocysts in the muscle occurs. The mechanism by which the merozoites enter the central nervous system is unknown, but is most likely via infected red blood cells or through the cytoplasm of endothelial cells (cells that line the blood vessels). 
Figure: Life cycle of Sarcocystis neurona The reasons for development and severity of EPM are unknown. Postulated reasons include the size of the infective dose, the immune competency of the horse and environmental stressors. Diagnosis of EPM has been difficult in part due to a lack of understanding between the pathogenesis of the disease and the variety of clinical signs. Due to the ability of the protozoan to affect all parts of the nervous system, the clinical signs are varied and may resemble other neurologic diseases. Common signs include asymmetric ataxia, associated muscle atrophy, gait abnormalities (knuckling over, stumbling), cranial nerve deficits and cranial nerve deficits. The onset of signs may be acute or chronic, over several weeks to months. Diagnosis is usually made by a combination of clinical signs and Western Blot testing on CSF. Blood work is typically normal. Performing Western Blot testing on serum does not confirm a lesion in the central nervous system, it only determines that the horse has been exposed to the protozoan. Other tests that can be included are the albumin quotient (AQ) and IgG index on CSF and serum. The AW is a measure of blood-brain barrier integrity and the IgG index is a measure of intrathecal antibody production (antibody production within the CNS). False positive results are frequently due to contamination of CSF with red blood cells. Due to this, we recommend that a spinal tap be done at the antlanto-occipital site under general anesthesia. A spinal tap performed at the lumbosacral site is often contaminated with blood and may not give us an accurate diagnosis. Other tests are available to rule out N. hughesi as a cause of these clinical signs. Treatment involves using anti-protozoal drugs that kill the offending parasite. Other treatments include reducing the inflammation present in the spinal cord, and often include the use of anti-inflammatories such as flunixin meglumine and phenylbutazone. If the onset of clinical signs is acute and the signs are severe, a more potent anti-inflammatory such as corticosteroids (typically dexamethasone) may be included in the treatment regimen. Other anti-inflammatories that may be of use are DMSO. The intial treatment protocol consisted of pyrimethamine and sulfonamides. This protocol is still available in a commercially available form. The dosage for pyrimethamine is 1 mg/kg by mouth and for sulfadiazine is 20 mg/kg by mouth once daily. The treatment is generally pursued for a mimimum of 5 months. The side effects for this treatment are bone marrow suppression, anemia, colitis (diarrhea) and teratogenesis (fetal abnormalities). We recommend that horses treated with this protocol have routine blood work performed in order to assess their red and white blood cell counts. Recently, ponazuril (Marquis) and nitazoxanide (Navigator) have been used to treat EPM. Our drug of choice is Marquis, at a dose of 5 mg/kg by mouth once daily for 28 days. No adverse signs effects have been noted with Marquis in my experience. The prognosis for horses with EPM is individual and variable. Approximately 60-70% of horses will improve at least one neurologic grade. Fewer than 25% of affected horses return to their original function. Horses that have been showing clinical signs for a short duration of time may be more likely to respond to treatment. Relapse of the clinical signs is a possibility even post-treatment, and this may be due to the parasite being in a latent stage, due to the presence of a small and persistent focus of infection, or may be due to re-exposure of the horse to the parasite. The only vaccination available at this time is a conditional license vaccine. Due to the lack of conclusive evidence for vaccination efficacy, we are not recommending that horses be vaccinated at this time. In addition, the vaccination can interfere with accurate testing for EPM.
|
