QUESTION: My horse has mild, intermittent hind-end lameness. What are the chances it's equine protozoal myeloencephalitis (EPM)?
DR. STEVE REED: Equine protozoal myeloencephalitis is a common cause of neurologic disease in horses that was initially described as segmental myelitis of unknown cause. In 1976, Dubey suggested that EPM was caused by a member of the genus Sarcocystis and an organism was eventually cultured from the spinal cord of an affected horse and named Sarcocystis neurona. A second protozoan parasite (Neospora hughesi) has been shown to be a cause of EPM in the horse.
EPM is one of the most commonly diagnosed neurologic diseases of the horse in the Western Hemisphere. Horses used primarily for racing had a greater risk compared with horses used primarily for pleasure. Young horses had a higher risk of developing EPM than older ones and recent transportation increased odds of disease.
Despite the often-high rate of exposure to the organism, only a small percentage of horses develop clinical illness. This suggests that immune clearance of the parasite is very effective but that factors such as parasite dose, physiologic stress associated with shipping, training, showing, and pregnancy appear to make animals more susceptible to EPM. Confirmation of disease is through demonstration of protozoa in central nervous system (CNS) lesions. However, the diagnosis is frequently made presumptively when organisms are not detected but characteristic inflammatory lesions are found.
The clinical signs associated with S. neurona infection vary from acute to chronic with insidious onset of focal or multifocal signs of neurologic disease involving the brain, brainstem, or spinal cord. The variable nature of the clinical signs reflects the random distribution of the lesions that may occur within the CNS and many times horses will present for lameness which is difficult to localize but often involves one thoracic or pelvic limb. Signs include focal muscle atrophy and weakness which with variable amount of ataxia, which is what makes separation of this problem from a lameness difficult.
In some horses the physical examination is within normal limits, and the horse appears bright and alert, although one may observe muscle atrophy in concentrated areas. Neurologic examination typically reveals asymmetric ataxia, weakness, and spasticity involving all four limbs. Some horses show signs of brain or brainstem involvement making those horses easier to diagnose.
Having said that, many race and show horses present for abnormal airway function or an unusual lameness. Horses with a slowly progressive ataxia may sometimes present because of stumbling or interference between limbs and may well have a musculoskeletal disorder and often require diagnostic nerve blocks along with the neuro exam to confirm the diagnosis.
As part of the separation for lameness versus ataxia caused by EPM, a lameness exam should accompany the neurologic exam. Depending on the results of those examinations radiographs, a spinal tap as well as diagnostic nerve blocks may be necessary. In my opinion the most important aid is immunodiagnostic testing of serum and CSF to confirm intrathecal antibody production against S. neurona or N. hughesi. A negative serum test usually indicates that the horse has not been infected, however, a recently infected horse may display clinical signs before seroconversion, and retesting in 10 to 14 days is recommended. A whole organism indirect fluorescent antibody test (IFAT) is currently available from the University of California Diagnostic Laboratory. Another useful test is the SnSAG ELISAs, quantitative tests based on S. neurona surface antigens, have been evaluated as a diagnostic tool.
Given the variety of clinical abnormalities that may be expressed in horses with EPM, the differential diagnosis includes virtually all diseases of the equine CNS as well as some causes of lameness. Results of a careful history, physical examination, and neuroanatomic localization help to limit the number of rule outs and guide further diagnostic efforts.
Treatment of horses for EPM begins with antiprotozoal medication. Food and Drug Administration (FDA) approved compounds for the treatment of EPM include sulfonamide drugs combined with pyrimethamine, marketed as an FDA approved product Re-Balance (PRN Pharmacal). Another FDA-approved drug for the treatment of EPM was ponazuril (Marquis, Boehringer-Ingelheim) administered as an oral paste. Diclazuril is a third FDA approved medication sold as Protazil.
Dr. Reed is currently an Internal Medicine Specialist and shareholder of the Practice at Rood & Riddle Equine Hospital, Emeritus Professor of The Ohio State University, an Adjunct Professor at the University of Kentucky and is currently the Chairman of the Grayson-Jockey Club Research Advisory Committee. He is world renowned for his expertise in internal medicine and neurological disorders.
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