Equine protozoal myeloencephalitis (EPM) is a neurological disease caused by a parasite that invades a horse’s brain and spinal cord. It’s one of the most common infectious neurological conditions in horses across the Americas, and while roughly 45% to 55% of horses in the United States test positive for exposure to the parasite, only a small fraction ever develop clinical disease.
How Horses Get EPM
The primary culprit is a single-celled parasite called Sarcocystis neurona. Opossums are the definitive host, meaning the parasite completes its reproductive cycle inside them. An infected opossum can shed millions of microscopic egg-like structures called sporocysts in its feces for months. When those droppings contaminate a horse’s hay, grain, water, or pasture, the horse inadvertently swallows the sporocysts.
Once ingested, the parasites break free in the small intestine and enter the bloodstream within one to eight days. From there, they can cross into the central nervous system and begin damaging tissue in the brain or spinal cord. A less common parasite, Neospora hughesi, can also cause EPM, though it accounts for a much smaller share of cases.
Horses are considered dead-end hosts. They don’t shed the parasite and can’t pass it to other horses, so EPM is not contagious between animals in a barn.
Signs and Symptoms
The specific symptoms depend entirely on where the parasite settles in the central nervous system. Spinal cord damage tends to produce gait abnormalities, incoordination, weakness, and muscle wasting. Brainstem involvement can look very different: lethargy, behavioral changes, facial paralysis, tongue weakness, or difficulty swallowing.
The hallmark feature that sets EPM apart from many other neurological conditions is asymmetry. Signs are often noticeably worse on one side of the horse than the other. You might see muscle loss over one hip but not the other, or stumbling that’s more pronounced on the left hind than the right. Some affected horses stand with their feet splayed in unusual positions or lean against walls and fences for support, reflecting a loss of body awareness (proprioception).
Symptoms can appear suddenly or develop gradually over weeks to months. In some horses the onset is so slow that early signs get dismissed as a training issue or mild lameness before the neurological nature becomes apparent.
How EPM Is Diagnosed
Diagnosing EPM is tricky precisely because so many healthy horses carry antibodies from prior exposure. A positive blood test alone means very little. The most reliable approach combines a thorough neurological exam with analysis of cerebrospinal fluid (CSF), the liquid surrounding the brain and spinal cord.
Your veterinarian will typically collect both a blood sample and a CSF sample, then compare antibody levels between the two using a specialized test. The comparison produces a ratio that helps distinguish true active infection in the nervous system from simple environmental exposure. A low ratio (below 50) carries an extremely high specificity of about 98.8%, meaning it’s very unlikely to flag a horse that doesn’t actually have active disease. A high ratio (200 or above) is strong evidence against EPM as the diagnosis.
The true gold standard for confirming EPM is postmortem examination of nervous system tissue, which obviously isn’t helpful for living horses. That’s why the CSF-to-serum ratio, combined with clinical signs and ruling out other conditions, forms the practical diagnostic foundation.
Conditions That Look Similar
Several other neurological problems can mimic EPM, and telling them apart matters because treatments differ completely.
- Cervical stenotic myelopathy (Wobblers): This condition results from compression of the spinal cord in the neck. It causes incoordination much like EPM, but the signs are typically symmetric or only mildly asymmetric, affecting both sides of the horse roughly equally. EPM’s unevenly distributed weakness and muscle loss is the key distinguishing clue.
- Equine herpesvirus-1 (EHV-1): This viral infection can cause sudden-onset hind limb weakness and loss of bladder control. It’s distinguished from EPM through specific infectious disease testing of blood and spinal fluid rather than any single clinical sign.
- Vitamin E deficiency: Low vitamin E levels can cause neurological symptoms that overlap with EPM. A simple blood test can rule this in or out.
Because EPM can mimic so many conditions, veterinarians often run a panel of tests including spinal fluid analysis, vitamin E levels, infectious disease screens, and sometimes advanced imaging to narrow the diagnosis.
Treatment Options
Two FDA-approved antiprotozoal medications are available for treating EPM, and both are given orally.
The first, ponazuril (sold as Marquis), follows a 28-day protocol. It starts with a loading dose on day one at three times the normal rate, then continues at the standard daily dose for the remaining 27 days. It comes as an oral paste in a syringe, similar to a dewormer.
The second approved option, diclazuril (sold as Protazil), is given as a daily top-dressed pellet mixed into feed.
A third treatment option, a combination of sulfadiazine and pyrimethamine (sold as ReBalance), requires a much longer commitment: a minimum of 90 days of daily dosing, and some horses are treated for up to 270 days. Because these drugs work by blocking the parasite’s ability to use folic acid, they can also affect the horse’s own blood cell production. Some horses on this regimen develop bone marrow suppression and need supplementation with a form of folic acid to recover.
Recovery and Relapse
Recovery from EPM varies widely. Horses caught early with mild symptoms have the best chance of returning to full athletic work. Those with severe, longstanding damage to the nervous system may improve but retain some degree of permanent deficit.
Relapse is a real concern. In one controlled investigation, about 20% of treated horses relapsed after treatment ended. Other reports have placed that number between 10% and 30%. Relapse doesn’t necessarily mean the treatment failed; the horse may be reinfected from the environment, or residual parasites may reactivate when the immune system dips. This is why ongoing monitoring after treatment matters.
Improvement is not always immediate. Nerve tissue heals slowly, and it can take weeks to months after completing treatment to see the full extent of neurological recovery.
Reducing the Risk
Because opossums are the source of infection, prevention centers on keeping their feces out of your horse’s food and water. Store grain and hay in sealed containers or enclosed feed rooms that opossums can’t access. Use feeders that keep hay off the ground rather than feeding directly on pasture. Keep water troughs clean and covered when possible. Remove fallen fruit, pet food, and garbage that attract opossums to the barn area.
There is no vaccine for EPM. Some veterinarians use low-dose antiprotozoal medications on a preventive schedule in high-risk areas, though this is an off-label approach. The most practical line of defense remains limiting opossum access to anything your horse eats or drinks.