Equine Protozoal Myeloencephalitis (EPM)

TL;DR. Equine Protozoal Myeloencephalitis (EPM) is a serious, potentially debilitating neurological infection in horses caused by a protozoan parasite that attacks the brain and spinal cord, requiring prompt veterinary diagnosis and targeted antiprotozoal therapy.

Ataxia and hind-limb weakness are among the most common early signs of EPM.

What is it?

Equine Protozoal Myeloencephalitis (EPM) is a complex, infectious neurological disease that primarily affects horses. It is caused by the microscopic protozoan parasite Sarcocystis neurona. When this parasite gains access to a horse's body, it migrates to the central nervous system, which includes both the brain and the spinal cord. Once inside these delicate tissues, the parasite multiplies, causing localized inflammation, tissue destruction, and swelling.

Because the central nervous system acts as the primary communication highway for the body, any damage to these tissues disrupts the electrical signals traveling between the brain and the muscles. This disruption leads to a wide array of neurological symptoms, most notably incoordination, weakness, and muscle wasting. EPM is a major concern for horse owners because it can affect any horse, regardless of age or discipline, and can lead to permanent performance-limiting damage or even death if left untreated.

Understanding EPM is vital for horse owners because the disease is highly unpredictable. The symptoms can develop slowly over several months or appear suddenly overnight. Because the parasite can attack any part of the brain or spinal cord, no two cases of EPM look exactly alike. A horse might show mild hind-limb weakness that resembles a lameness issue, while another might suffer from severe, life-threatening incoordination.

Causes & risk factors

The primary culprit behind EPM is the protozoan parasite Sarcocystis neurona. To understand how a horse contracts this disease, it is helpful to look at the parasite's life cycle. The definitive host for Sarcocystis neurona is the opossum. Opossums ingest the parasite from intermediate hosts (such as raccoons, sea otters, cats, or skunks) and then shed the infective stage of the parasite, called sporocysts, in their feces.

Horses become accidental, "dead-end" hosts when they ingest food or water that has been contaminated with opossum feces containing these sporocysts. Once inside the horse, the sporocysts hatch, penetrate the intestinal wall, and undergo asexual reproduction in the horse's blood vessels before migrating across the blood-brain barrier into the central nervous system. Because horses are dead-end hosts, they cannot transmit the disease to other horses; an infected horse poses no risk to its pasture mates.

Several risk factors increase a horse's likelihood of developing clinical EPM:

• Geographic Location: EPM is primarily a disease of the Americas, where opossums are native.
• Feed Storage: Unsecured grain bins or hay lofts that are accessible to opossums significantly increase the risk of feed contamination.
• Stress: High stress levels from transport, heavy training, weaning, or concurrent illness can suppress the horse's immune system, making it easier for the parasite to cross the blood-brain barrier.
• Age: While EPM can affect horses of any age, it is most frequently diagnosed in young performance horses (under five years old) and older horses, both of whom may have more vulnerable immune systems.

There are currently no documented breed predispositions for EPM; any horse exposed to the parasite under the right conditions can develop the disease.

Signs to watch for

The clinical signs of EPM are highly variable and depend entirely on where the parasite settles within the brain or spinal cord. The disease is classic for causing asymmetric neurological deficits, meaning the symptoms are often worse on one side of the horse's body than the other.

Common Signs

• Ataxia: This is the most common sign of EPM. It manifests as incoordination, stumbling, toe-dragging, a swaying gait, or a general lack of awareness of where the limbs are positioned (proprioceptive deficits).
• Asymmetric Muscle Atrophy: Rapid wasting of muscles, particularly in the hindquarters (gluteal muscles) or the muzzle and jaw, is a frequent indicator of localized nerve damage.

Occasional Signs

• Depression: The horse may appear dull, lethargic, or uninterested in its surroundings.
• Seizures: If the parasite causes significant inflammation in the cerebrum of the brain, the horse may experience seizures.
• Cranial Nerve Deficits: This can include a drooping ear, a tilted head, difficulty swallowing, or a paralyzed lip.

Asymmetric muscle wasting, particularly in the hindquarters, is a classic sign of EPM.

How vets diagnose it

Diagnosing EPM can be highly challenging because its symptoms mimic many other neurological conditions, such as Wobbler syndrome (cervical vertebral stenotic myelopathy), West Nile Virus, Equine Herpesvirus-1 (EHV-1), or rabies. Your vet will begin with a thorough physical and neurological examination.

During the neurological exam, the vet will observe the horse walking and trotting in straight lines and tight circles, backing up, and walking up and down hills. They may perform a "tail pull" test, where they pull the horse's tail to one side while it is walking to assess its pelvic limb strength and coordination.

Because many healthy horses have been exposed to Sarcocystis neurona and carry antibodies in their blood without ever developing the disease, a simple blood test is rarely sufficient for a definitive diagnosis. The gold standard for confirming EPM is a CSF Western Blot test.

To perform this test, your vet must collect cerebrospinal fluid (CSF) via a spinal tap. This procedure is typically performed under sedation and local anesthesia, either at the lumbosacral space (over the pelvis) or, less commonly, at the atlantooccipital space (at the base of the skull). By comparing the ratio of antibodies in the blood to the ratio of antibodies in the spinal fluid, the laboratory can determine if the parasite has actively invaded the central nervous system, providing a highly accurate diagnosis.

Treatment options

Once EPM is diagnosed, treatment must begin immediately to halt the replication of the parasite and minimize permanent damage to the nervous system. Veterinary medicine utilizes several classes of antiprotozoal medications to target the parasite.

Triazine Antiprotozoals

These medications work by targeting specific cellular structures within the protozoa, effectively halting their reproduction.

• Ponazuril: This is a widely used oral paste designed specifically for horses. It is highly effective at crossing the blood-brain barrier to reach the site of infection.
• Diclazuril: Administered as an oral top-dress pellet, this medication is another highly effective triazine antiprotozoal that is easy to administer with the horse's daily grain.

Folate Antagonists

This class of medication works by blocking the parasite's ability to synthesize folic acid, which is essential for its survival and replication.

• Pyrimethamine and Sulfadiazine: This combination therapy is a historical and highly reliable treatment option. A leading veterinary internal medicine reference notes:

"ReBalance ® (pyrimethamine/sulfadiazine suspension in a 1:20 concentration) is labeled for the treatment of horses with equine protozoal myeloencephalitis (EPM) caused by Sarcocystis neur"

This drug combination is well-absorbed by the horse's digestive tract and successfully reaches the central nervous system to combat the infection:

"Sulfadiazine is apparently well absorbed after oral administration to horses and enters the CSF."

However, owners must be aware of potential side effects associated with long-term folate antagonist therapy. The reference notes that signs can include:

"loose stools, slight increases in ALP in some horses, declines in RBC, HCT, Hgb, and PCV, and depressed appetite."

Because of these potential side effects, your vet may recommend monitoring your horse's complete blood count (CBC) during therapy. Additionally, this drug combination is contraindicated in horses with known hypersensitivities to either active ingredient and must never be used in horses intended for human consumption.

Antiparasitic Agents

• Nitazoxanide: This is another antiparasitic agent that may be utilized by your veterinarian in specific cases to target the protozoan organisms.

Managing the "Treatment Crisis"

When antiprotozoal treatment begins, a large number of parasites die off rapidly. This mass die-off can trigger a significant inflammatory response within the brain and spinal cord, leading to a temporary worsening of the horse's neurological signs. This is known as a "treatment crisis." To manage this, your vet may concurrently prescribe anti-inflammatory medications, such as flunixin meglumine, dexamethasone, or dimethyl sulfoxide (DMSO), to protect the nervous tissue during the initial phase of therapy.

Prognosis

The prognosis for horses with EPM is guarded to favorable, depending heavily on how quickly the disease is diagnosed and treated. Horses that receive prompt treatment generally have a much better outlook than those that have suffered from chronic, undiagnosed neurological damage.

It is important to understand that while treatment can successfully eliminate the parasite, it may not completely reverse all clinical signs. Nerve tissue heals very slowly, and severe inflammation can leave behind permanent scar tissue in the spinal cord or brain. Approximately 60% to 70% of treated horses show significant improvement in their neurological status, but only a smaller percentage return to their original level of athletic performance. A temporary worsening of signs during the first week of treatment is common, and some horses may experience relapses months or years after successful therapy.

Prevention

Because there is currently no highly effective, long-lasting vaccine for EPM, prevention relies almost entirely on management practices designed to minimize your horse's exposure to opossums and their feces.

• Secure Feed Storage: Keep all grain and supplements in tightly sealed, wildlife-proof metal or heavy plastic bins.
• Feed Off the Ground: Avoid feeding hay or grain directly on the ground where it can easily be contaminated by passing wildlife. Use feeders and clean up spilled grain promptly.
• Water Hygiene: Clean water troughs regularly and cover them if they are located near trees or structures where opossums might travel.
• Deter Wildlife: Keep opossums out of your pastures and barns by clearing away brush piles, fallen logs, and trash that could serve as nesting sites. Do not leave cat or dog food outside, as this attracts opossums.
• Minimize Stress: Provide proper nutrition, routine veterinary care, and gradual conditioning to keep your horse's immune system strong.

When to call your vet

Neurological symptoms in horses should always be treated as a medical emergency. If you notice any of the following red flags, contact your veterinarian immediately:

• Sudden onset of stumbling, swaying, or weakness in the hindquarters
• Inability to stand or difficulty rising from a lying position
• Asymmetrical muscle wasting on the hindquarters or face
• Seizures or sudden, unexplained changes in behavior
• Difficulty swallowing or drooling

Early intervention is the single most important factor in preventing permanent spinal cord damage and giving your horse the best chance at a full recovery.

Sources

• Plumb's Veterinary Drug Handbook, pages 3107, 3108, 3109, 1116, 2941.