Equine Protozoal Myeloencephalitis (EPM) – NAVLE Study Guide

Overview and Clinical Importance

Equine Protozoal Myeloencephalitis (EPM) is the most common infectious neurological disease of horses in the Americas. It is caused by infection of the central nervous system (CNS) with the apicomplexan protozoan parasites Sarcocystis neurona (approximately 95% of cases) and, less commonly, Neospora hughesi. The disease can affect any region of the CNS, from the cerebrum to the caudal spinal cord, resulting in highly variable clinical presentations.

EPM is characterized by asymmetric neurological deficits, which is a key distinguishing feature from other equine neurological diseases. While approximately 50-90% of horses in endemic areas have been exposed to S. neurona (as evidenced by seropositive status), fewer than 1% of exposed horses develop clinical disease.

Etiology and Life Cycle

Causative Agents

EPM is caused by two apicomplexan protozoan parasites: Sarcocystis neurona (responsible for approximately 95% of cases) and Neospora hughesi (a minority of cases). Both organisms are obligate intracellular parasites that target neural tissue.

Sarcocystis neurona Life Cycle

Neospora hughesi

N. hughesi causes a minority of EPM cases but produces clinically indistinguishable disease from S. neurona. Key differences include:

• Natural hosts and life cycle are poorly understood
• Transplacental transmission has been documented (unlike S. neurona)
• Lower seroprevalence than S. neurona (positive serology has higher positive predictive value)
• May be associated with abortions and neuromuscular disease

Epidemiology and Risk Factors

Geographic Distribution

EPM is endemic throughout the Americas wherever opossums are present. The disease has been reported in most of the contiguous 48 US states, southern Canada, Mexico, and Central and South America. Cases outside the Americas occur only in horses imported from endemic regions.

Risk Factors

Clinical Signs and Presentation

EPM is often called the "great mimicker" because it can affect any part of the CNS and produce highly variable clinical signs. However, certain patterns are characteristic and should raise clinical suspicion.

Cardinal Features of EPM

Three hallmark features that are highly suggestive of EPM:

• Asymmetric neurological signs - clinical deficits that differ in severity between left and right sides
• Multifocal signs - neurological deficits that localize to more than one area of the CNS
• Focal muscle atrophy - neurogenic muscle wasting (evidence of lower motor neuron involvement)

Clinical Signs by Neuroanatomic Location

Modified Mayhew Ataxia Grading Scale

Diagnosis

Definitive diagnosis of EPM requires postmortem confirmation of protozoal organisms in CNS tissue. Antemortem diagnosis is presumptive and based on: (1) clinical signs consistent with EPM, (2) exclusion of other neurological diseases, and (3) demonstration of intrathecal antibody production against S. neurona or N. hughesi.

Diagnostic Approach

• Complete neurological examination - document deficits and assign ataxia grade
• Rule out differential diagnoses - cervical radiographs (for CVSM), infectious disease testing
• Immunodiagnostic testing - serum and CSF antibody testing with ratio calculation

Available Diagnostic Tests

CSF Analysis

CSF analysis in EPM horses is often within normal limits. When abnormal, findings may include mild mononuclear pleocytosis and elevated protein. CSF cytology is more useful for ruling out differentials than confirming EPM.

Differential Diagnosis

Treatment

FDA-Approved Antiprotozoal Drugs

Adjunctive Therapy

• NSAIDs (flunixin 1.1 mg/kg IV or phenylbutazone 2-4.4 mg/kg PO) - first few days to reduce inflammation from parasite die-off
• Vitamin E (20 IU/kg PO daily or 10,000 IU/day) - antioxidant support
• Corticosteroids (dexamethasone 0.1 mg/kg IM q24h for 4 days) - severe cases with brain involvement only
• Immunomodulators (levamisole, killed Parapoxvirus ovis) - limited evidence but sometimes used

Prognosis

• Approximately 60-70% of treated horses show improvement
• Only 15-25% recover completely
• Earlier treatment initiation correlates with better outcomes
• Horses with mild signs (Grade 1-2) have better prognosis than severely affected horses
• Relapse is possible and relatively common; cause is poorly understood
• Clinical signs may temporarily worsen during first week of treatment due to inflammation from parasite death

Prevention

• Prevent opossum access to feed and water - use covered feed bins, elevated feeders, clean up spilled grain
• Do not feed from ground in areas with opossum activity
• Remove dead wildlife and carcasses from pastures promptly
• Minimize stress in horses (transport, competition, illness)
• Control intermediate host populations (raccoons, skunks) when feasible
• Vaccination: A vaccine exists but efficacy is not well established; not routinely recommended

Memory Aids for the NAVLE

EPM = "Every Part May be affected"

Reminds you that EPM can affect any part of the CNS and produce variable signs.

"OPOSSUM = Only Protozoal Source for Sarcocystis, Spreading Under Most conditions"

The opossum is the definitive host - geographic range of EPM matches opossum range.

"ASS" = Asymmetric Signs in Sarcocystosis

The hallmark of EPM is asymmetric neurological deficits (vs. symmetric in CVSM/EDM).

Treatment: "PD-SP" = Ponazuril/Diclazuril (28 days), Sulfadiazine-Pyrimethamine (90+ days)

Triazines (P, D) are shorter; folate inhibitors (S-P) require longer treatment.