02/25/2025
Yes they're cute, but they can take a hike! Opossums have no place around the horses or anything that they eat. It took a lot of $ and a lot of time to bring our Rosie back to health when she was surrendered with EPM. We loved her through it all and she is now 2nd in command among the mare herd.
Equine Protozoal Myeloencephalitis (EPM)
By Brian S. Burks DVM, Dipl. ABVP- equine specialty
Equine Protozoal Myeloecephalitis is a neurologic disease caused by Sarcocystis neurona or occasionally Neospora hughesi. A protozoa is a single celled, motile organism. It is ingested in the f***s of opossums in contaminated water, hay or grain. Many animals can serve as vectors, spreading the sporocyts over some distance. The horse is an aberrant, or dead end, host for S. neurona, meaning that it cannot spread the infection to other horses. Infection with S. neurona or similar organisms has been observed in many other species, including the zebra, domestic cat, Canadian lynx, domestic canines, sea otter, seal, mink, fisher, ferret, raccoon, and skunk.
Once ingested, the sporocyts excyst in the small intestine and the resulting sporozoites enter the blood stream. They then pe*****te the central nervous system, where they multiply in the neurons, resulting in cell death. Clinical signs of EPM are due to cell death and inflammation and swelling, which disrupts the structure of the spinal cord and compromises blood flow and oxygen delivery. The incubation period is 10 days to several months- the time from ingestion to clinical signs. Stress, which causes the release of endogenous cortisol, can precipitate disease; trailering, pregnancy, other disease, and corticosteroid administration can all trigger disease by allowing the parasite to replicate in the spinal cord.
There can be a variety of clinical signs due to the multifocal nature of EPM. Occurring as an insidious disease, EPM occurs in adult horses most commonly. Horses may initially appear lame; this lameness does not resolve with nerve blocks. Muscle atrophy, usually most pronounced in the gluteal musculature, is common. Affected horses have mild to severe ataxia, and are often weak due to both muscle and CNS lesions. Other signs may include a head tilt, facial paralysis, dysphagia, head shaking, spasticity, and seizures. I have seen horses present with their head down, unable to raise the head and neck.
The CNS has limited ways to express disease, and thus can appear similar to many other nervous system diseases. These include Cervical Stenotic Myelopathy (wobblers) EHV-1, Equine Degenerative Myelopathy, West Nile Virus, polyneuritis equi, and others. Clinical signs emanating from trauma can also be similar. Aberrant parasite migration can also mimic EPM, but is uncommon in horses that have been on a deworming program.
Diagnosis is via testing CNS fluid (cerebrospinal fluid- CSF). This fluid can be obtained from several places along the spinal column: the atlanto-occipital space, between cervical vertebrae 1-2, and the lumbo-sacral space. The first requires general anesthesia, while the latter two approaches are done in the sedated, but standing, horse.
As there are many vectors and opossums are widespread, subclinical infestation is common. Many horses are seropositive (have antibodies) without any sign of illness, thus blood testing is considered to be of limited value, only determining the absence of exposure to the organism. In fact, in the Ohio Valley, and much of the northeast, 80% of horses have been exposed to S. neurona. Seroprevalence is much less in the western United States. Routine blood work (CBC, Chemistry panel) is usually unremarkable, but is important to rule out other disease, such as hepatoecephalopathy. Thus CSF testing is the most useful test, and can also help to rule out other diseases (EHV-1, WNV, meningitis). Imaging studies such as MRI and CT may show lesions of the spinal cord or brain. The gold standard is sectioning of the spinal cord for histopathology.
Treatment of EPM is aimed at stopping disease progression, improving the neurologic status, and preventing self-trauma. As such, supportive care is very important. This may include deep bedding and slinging when necessary.
Medications used in the treatment of EPM include anti-inflammatory medications such as phenylbutazone, Banamine, and DMSO, Vitamin E and selenium, and an anti-protozoal medication. The latter includes pyrimethamine/sulfamethoxazole (Re-Balance) ponazurila (Marquis) and diclazuril (Protazil). No matter which medication is used, the expected success rate is 70%; that is the percentage of horses expected to improve at least one grade. Approximately 20% of horses may not improve. An additional percentage of horses may improve two or more grades of ataxia.
The former medication is used for six months or more. The latter two pharmaceuticals are generally used for 28 days, though in refractory cases may need to be used longer. Corticosteroids such as dexamethasone may be used sparingly- a few days at most- because the immune system may be further suppressed, allowing exacerbation of clinical signs. No herbal medications or immunostimulants have been scientifically shown to improve EPM; their reported anecdotal success may be due to spontaneous improvement of this or some other disease.
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