The most common signs of the disease are weakness and incoordination (ataxia), primarily in the hind limbs. Often, the effects are asymmetrical--one hind leg will be affected more than the other. As the disease progresses, the horse may develop muscle atrophy. In rarer cases, if the disease affects the brain, signs may include facial paralysis, seizures, difficulty swallowing, head tilt and behavioral changes.
Determining whether a horse has EPM can be difficult. Because most who are exposed to the protozoa never develop the disease, the presence of antibodies alone is not enough for a diagnosis. A horse who is positive for antibodies to one of the protozoa could still have neurological signs due to some other cause.
That said, however, some of the newer testing methods---an indirect immunofluorescence antibody test (IFAT) and enzyme-linked immunosorbent assays (ELISAs)---can be used to determine the titer (the concentration of antibodies) in a blood sample. Although these types of test results are not a definitive diagnosis, many veterinarians consider a higher titer, along with neurological impairment, to be evidence of probable EPM.
The most definitive type of testing looks for antibodies to the protozoa in the cerebrospinal fluid (CSF), which surrounds the brain and spinal cord. Evidence that the organisms have penetrated the central nervous system is an even clearer indication that the horse’s neurological signs are attributable to EPM. Finding high titers of antibodies in both the blood and the CSF is the best indication of EPM that is currently available. However, even this
evidence is not considered definitive proof that the EPM is the cause of any neurological signs. And because obtaining a sample of CSF is a more technically challenging and more invasive procedure, many veterinarians proceed on the assumption of EPM based on the blood tests and observation of signs alone.