Equine Protozoal Myeloencephalitis (EPM) is one of the most important neurological diseases of horses in North America. It’s caused by infection of the central nervous system by protozoal pathogen Sarcocystis neurona, and to a lesser extent, Neospora hughesi.
Horses with EPM can present with a variety of clinical signs, which can make identifying cases difficult. Some of the most common clinical signs include incoordination, weakness, and asymmetrical muscle atrophy (uneven muscle loss).
While many horses are exposed to one or both of the EPM pathogens, only a fraction of horses will progress to clinical disease. It is theorized that factors like stress, concurrent illness, or age at the time of exposure influence whether or not horses will develop EPM.
Join Dr. Fran Rowe, one of Mad Barn’s Veterinary Nutritionists, in learning more about EPM in horses! Dr. Rowe will take a deeper dive into the lifecycle of these pathogens, why diagnosis is challenging, and prevention strategies to reduce the incidence of exposure.
Interested in learning more about EPM in horses? We have a blog article online:
👉 https://madbarn.com/equine-protozoal-myeloencephalitis/
Want to evaluate your horse’s diet? Follow this link to get connected with an equine nutritionist or explore our horse nutrition calculator:
👉 https://madbarn.com/analyze-diet/?modal=show
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Transcript:
[0:00]
Hi everyone, welcome back to Mad Barn Academy. If you’re new here, then welcome — we hope to earn your subscription today. I’m Dr. Fran Row, one of the veterinary nutritionists here at Mad Barn. Our topic for today’s video is EPM, or equine protozoal myeloencephalitis.
[0:18]
EPM is an important disease unique to the Americas. Many of us have either owned or known a horse affected by it, or we’ve heard it discussed through social media, friends, farriers, or other sources. It’s a common topic among horse owners, so today we’ll dive into why it’s so significant.
[0:51]
EPM is a neurological disease in horses caused by infection with protozoal organisms — tiny parasites that damage the brain and/or spinal cord. The two protozoa identified as causes are Sarcocystis neurona and Neospora hughesi. Most cases are caused by S. neurona. Interestingly, many horses are exposed to one or both of these pathogens, but only a small number develop clinical EPM. It’s generally treatable, though not all horses make a full recovery.
[1:49]
So how do horses get exposed? The life cycle of S. neurona is well understood. It has a two-host life cycle, requiring an intermediate host before transferring to its definitive host. The opossum is the definitive host. Opossums pass immature stages of the parasite in their feces — think of them as tiny eggs — which are eaten by intermediate hosts while foraging on contaminated feed or water. In the intermediate host, the parasite matures in muscle tissue but can’t complete its cycle until it returns to an opossum. If the intermediate host dies, an opossum may scavenge it, ingest the infected muscle, and complete the parasite’s life cycle.
[3:06]
Intermediate hosts include domestic cats, raccoons, armadillos, and skunks. Horses become infected in the same way as intermediate hosts — by consuming feed or water contaminated with infected opossum feces. However, horses are considered “dead-end” hosts. The parasite can’t complete its life cycle in them, and infected horses do not pose a transmission risk to others.
[3:56]
We know much less about N. hughesi. Its transmission route and definitive host remain unknown, though related Neospora species live in canids like dogs and coyotes.
[4:32]
The geographic range of EPM closely follows the range of its host species. Since the opossum is the definitive host for S. neurona, EPM is most common where opossums live — across the entire eastern U.S. into Central America. Opossums have also been introduced west of the Rockies. Historically, they didn’t live farther north than the U.S.–Canada border, but milder winters and human activity have allowed them to expand into southern Ontario, Quebec, and British Columbia. EPM is rare in Canada, with only occasional case reports.
[6:00]
The clinical signs of EPM depend on which part of the central nervous system is affected — the brain, brainstem, spinal cord, or multiple areas. Onset varies: some horses show sudden, severe neurological signs, while others have a slow, progressive decline.
[6:46]
Horses with brain or brainstem involvement may have cranial nerve deficits such as head tilt, drooping of the eyes, ears, or muzzle, difficulty swallowing, or upper airway dysfunction. Central brain signs can include seizures, blindness, and diminished responsiveness to stimuli.
[7:25]
Horses with spinal cord involvement may show incoordination, stumbling, tripping, limb interference, weakness, lethargy, leaning on objects, lying down more, abnormal gaits, dragging feet, or signs that mimic mild lameness. A classic sign is asymmetrical muscle atrophy, especially along the topline or in the gluteal muscles.
[8:24]
EPM is challenging to diagnose. A definitive diagnosis is made postmortem by examining brain and spinal cord tissue under a microscope — not practical for living horses. In live horses, we test for antibodies to S. neurona or N. hughesi, called an antibody titer. The gold standard is to test both blood and cerebrospinal fluid.
[9:01]
According to the American Association of Equine Practitioners (AAEP) consensus statement, diagnosis should begin with a neurological exam showing signs consistent with EPM. This helps differentiate it from other neurological diseases.
[9:50]
Second, additional diagnostics should be performed to rule out other neurological conditions. This might mean taking radiographs of the cervical spine to check for Wobbler’s syndrome or submitting a nasal swab for EHV-1, for example.
[10:09]
Lastly, submitting both blood (serum) and cerebrospinal fluid (CSF) for antibody testing remains the gold standard for diagnosis. Collecting blood is straightforward — the challenge is determining whether the antibody titer reflects past exposure or active disease. This is where CSF comes in: it helps determine if infection is actively occurring in the brain or spinal cord, versus antibodies simply circulating in the bloodstream from previous exposure.
[10:54]
Collecting a blood sample is much easier than obtaining CSF, so in the field it’s common to submit only serum. However, interpreting serum alone can be tricky. As mentioned earlier, many horses are exposed to S. neurona or N. hughesi. A 2017 study measured the seroprevalence — the percentage of horses testing positive for antibodies — in healthy U.S. horses. For example, 84% of healthy horses in the South (defined in the study as Texas through West Virginia) tested positive for S. neurona antibodies.
[12:08]
The key takeaway: exposure is common across all U.S. regions, especially to S. neurona. Most horses testing positive on bloodwork are healthy — they are not neurological and not being evaluated for EPM. A positive result indicates exposure, not necessarily active disease. This is why diagnosing EPM is challenging, and why submitting both serum and CSF samples is the gold standard.
[13:06]
A horse with active EPM produces intrathecal antibodies — antibodies present in the fluid around the brain and spinal cord. Because the intrathecal space is protected by the blood-brain barrier, these antibodies only appear if there’s active infection.
[13:30]
All horses are susceptible to these pathogens, but less than 1% of exposed horses develop active EPM — thankfully. It’s unclear why some progress to disease while others do not. The leading theory is that immune suppression or an inadequate immune response plays a role, but the exact triggers remain unknown. Identified risk factors include stress (e.g., trailering, heavy exercise), concurrent illness, and age at the time of exposure.
[14:45]
For diagnosed horses, treatment options have improved greatly. Three FDA-approved products for horses include ponazuril (Marquis), diclazuril (Protazil), and sulfadiazine/pyrimethamine combination (ReBalance). Treatment can take several months, and most horses improve — many return to their original level of work. However, 30–40% will either stabilize (no improvement but no decline) or worsen, and some relapse within two years.
[16:05]
Prevention focuses on limiting exposure to S. neurona by reducing contact with opossums, the definitive host. While wildlife will inevitably come near barns seeking food and shelter, you can discourage them by securing feed bins, removing spilled feed and treats, maintaining sanitation, eliminating potential den sites (e.g., woodpiles, open hay storage), sealing barn entry points, and avoiding leaving pet food out. Feed barn cats and dogs away from horse areas and avoid leaving food out 24/7. Clean water buckets and troughs regularly to reduce contamination.
[18:04]
Barn cats, while intermediate hosts for S. neurona, cannot transmit the parasite to horses and can help control pests. If you have wildlife taking up residence, contact pest control or a wildlife specialist to relocate the animal humanely. Opossums play a valuable ecological role, so we don’t want to eliminate them — just keep them out of the barn.
[19:10]
Here are today’s references, and thank you for listening. Don’t forget to like and subscribe, and check out the other videos on our channel covering a variety of equine topics. Additional links are in the video description for those wanting to dive deeper into EPM in horses.









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