Other Names
EPM, equine protozoal myeloencephalitis, equine protozoan myeloencephalitis.
What is Equine Protozoal Myeloencephalitis?
Equine protozoal myeloencephalitis (EPM) is a serious neurological disease of horses caused by protozoan parasites that invade and damage the central nervous system — specifically the brain, brainstem, and spinal cord. It is one of the most commonly diagnosed neurological diseases in horses in North America, where the primary causative organism, Sarcocystis neurona, is endemic. In the UK and Europe, EPM is uncommon but not unknown, and awareness of the condition is important for horse owners and veterinarians.
The disease causes a wide range of neurological signs depending on which areas of the CNS are affected. Because S. neurona can localise to virtually any region of the brain or spinal cord, EPM is often called “the great imitator” — it can mimic many other neurological and musculoskeletal conditions, making diagnosis challenging.
What Causes EPM?
Sarcocystis neurona is the primary causative organism, responsible for the vast majority of EPM cases. The Virginia opossum (Didelphis virginiana) is the definitive host in North America — it sheds S. neurona sporocysts in its faeces. Horses become infected by ingesting feed or water contaminated with opossum faeces. Sea otters, armadillos, skunks, and raccoons can carry the parasite as intermediate hosts.
Neospora hughesi is a less common but emerging cause of EPM-like disease in horses in North America.
Because the Virginia opossum is not native to the UK or Europe, S. neurona-related EPM is not endemic here. However, imported horses from affected regions and horses that have been in North America may carry infection. Neospora species circulate in European wildlife, and occasional European cases have been documented.
Risk factors for developing clinical EPM once exposed include immune suppression (illness, stress, heavy parasite burden, nutritional deficiency), concurrent disease, and heavy exposure to contaminated feed or water.
Symptoms and Signs
EPM produces a remarkably variable clinical picture because lesions can develop anywhere in the CNS. The classic teaching point is that signs are often asymmetric — more pronounced on one side — which is an important distinguishing feature from some other causes of equine ataxia.
Common signs include:
- Ataxia (incoordination) — particularly in the hindlimbs; the horse may stumble, cross its hind legs, or weave when walking
- Muscle atrophy — asymmetric wasting of hindquarter, topline, or facial muscles is characteristic
- Weakness — difficulty rising, leaning against walls, or collapsing
- Spasticity and stiffness in the limbs
- Cranial nerve deficits — facial nerve paralysis (drooping ear or lip), difficulty swallowing, abnormal eye position or movement
- Behavioural changes — apparent depression, altered personality
- Bladder dysfunction — loss of bladder control
- Skin hypersensitivity or loss of sensation in a band-like distribution (sweating in patches)
- Gait abnormalities — toe dragging, circumduction (swinging leg outward), stumbling
Grading of EPM neurological signs follows the same 0–5 scale used for other neurological conditions (Mayhew scale), where grade 1 is barely detectable and grade 5 is recumbent. Most horses present at grade 2–3.
Diagnosis
EPM diagnosis is challenging because no single test is perfectly sensitive and specific. Diagnosis is typically based on a combination of:
- Characteristic clinical signs (asymmetric neurological deficits)
- Rule-out of other neurological conditions
- Serological evidence of exposure and CNS invasion
Serology: Western blot testing of serum and cerebrospinal fluid (CSF) for antibodies to S. neurona surface antigens (SnSAG1, SnSAG2, SnSAG4/5) is widely used. The CSF:serum antibody ratio (intrathecal antibody production) is a more specific test for CNS infection, as seropositivity alone only indicates exposure. In North America, the IDEXX EPM test and IFAT are also used.
CSF analysis: CSF may show mild inflammatory changes. Elevated total protein in the absence of significant pleocytosis is sometimes seen.
Response to treatment: Improvement following initiation of antiprotozoal treatment supports an EPM diagnosis, though this is not diagnostic on its own.
See also our entry on equine encephalomyelitis for other neurological diseases requiring differentiation from EPM.
Treatment
Several antiprotozoal drugs are used to treat EPM:
Ponazuril (Marquis): An FDA-approved treatment in the USA; 28-day course. Effective with fewer side effects than older protocols.
Diclazuril (Protazil): Also FDA-approved; daily administration in feed over 28 days.
Sulfadiazine/pyrimethamine (ReBalance): An older combination treatment; requires careful monitoring for bone marrow suppression and folate deficiency. Daily administration; minimum 90 days recommended.
Anti-inflammatory treatment (NSAIDs or short-course corticosteroids) may be used alongside antiprotozoal therapy to reduce inflammatory damage in the CNS during the early phase of treatment. Vitamin E supplementation is widely used as an antioxidant to support neurological recovery.
Availability of licensed EPM-specific drugs in the UK is limited — consult your vet about accessing appropriate treatment if EPM is confirmed. Physical rehabilitation and physiotherapy support recovery alongside medical treatment.
Prevention
- Store feed in secure, opossum-proof containers when in North America or importing horses through affected regions
- Clean water troughs regularly and prevent wildlife access
- Maintain horses in good health and minimise stress — immune suppression increases susceptibility
- Ensure adequate nutrition and vitamin E levels — horses in work have higher vitamin E requirements
When to Call the Vet
- Any horse showing neurological signs — ataxia, weakness, facial asymmetry, muscle wasting, stumbling, or behavioural changes
- A horse that has recently returned from North America or been imported from a region where EPM is endemic
- Unexplained asymmetric muscle wasting over the hindquarters or topline
- Progressive neurological deterioration in a horse already under investigation for another condition
Prognosis
Prognosis depends heavily on disease severity at diagnosis and how promptly treatment is initiated. Horses with mild to moderate signs (grades 1–2) treated early have good prospects for full recovery — studies report 60–70% return to normal function with appropriate treatment. Horses with severe signs (grade 3–4) at presentation have a more guarded prognosis and may have residual deficits. Horses that are recumbent have a poor prognosis. Relapses can occur, particularly if treatment is stopped prematurely or underlying immunosuppression is not addressed.
Frequently Asked Questions
Is EPM common in the UK?
EPM caused by Sarcocystis neurona is uncommon in the UK because the Virginia opossum — the definitive host — is not native here. Most UK cases involve horses that have been imported or have spent time in North America. European cases linked to Neospora species have been documented occasionally. Any horse presenting with progressive asymmetric neurological signs should still have EPM included in the differential diagnosis list regardless of travel history.
How is EPM different from Wobblers (cervical vertebral stenotic myelopathy)?
Both conditions cause ataxia in horses, but EPM typically produces asymmetric deficits and can affect any region of the CNS including the brain and cranial nerves. Wobblers typically produces more symmetric hindlimb ataxia due to spinal cord compression at the cervical level. Muscle wasting is more characteristic of EPM. Cervical radiography and myelography or MRI can confirm Wobblers; serology and CSF analysis are needed for EPM. Both conditions may require specialist referral for accurate diagnosis.
Can EPM recur after treatment?
Yes. A proportion of horses treated for EPM relapse, particularly if antiprotozoal treatment is stopped prematurely or if the underlying cause of immune suppression is not addressed. Maintenance vitamin E supplementation and minimising stress may help reduce relapse risk. Some practitioners recommend a longer treatment course or a maintenance phase of treatment for horses with severe disease or multiple relapses.