Neurologic disease in horses has multiple causes. Of these, the most common and likely the most important is cervical vertebral stenotic myelopathy (CVSM), commonly referred to as “wobbler” or “wobbler syndrome.” A less common cause is equine degenerative myeloencephalopathy (EDM), an inherited neurodegenerative disease affecting many breeds and often presenting as horses with behavior changes. Finally, there are two major infectious causes, equine herpesvirus myeloencephalopathy (EHM) caused by central nervous system (CNS) disease by equine herpesvirus-1, and equine protozoal myeloencephalitis (EPM) caused by CNS invasion by protozoan (single cell) parasites.

Collectively, equine neurologic diseases have a significant economic impact. According to DVM 360, veterinary epidemiologists estimate that the annual neurological disease incidence rate is about 0.3% across the approximately six million U.S. horses, totaling at least 180,000 cases each year. Assuming a conservative 50% mortality rate, the industry loses roughly 90,000 horses per year to these diseases. Considering the livestock value and the loss of the horse’s yearly direct/indirect economic contributions (approximately $14,000 per horse), the total annual U.S. economic impact from mortality alone could amount to $1.2 billion.

Of the two diseases with infectious etiologies (EHM and EPM), EPM is more common. The vast majority of EPM cases are caused by the protozoan parasite Sarcocystis neurona, which is transmitted to horses when they ingest material contaminated by feces of infected opossums. Interestingly, it is apparent that horses are commonly exposed to S. neurona (approximately 75% seroprevalence across the U.S. in one comprehensive study) but few infections result in EPM (less than 1% incidence) based on serologic and epidemiologic studies. Thus, the mere presence of antibodies against S. neurona in the blood of a horse is of minimal concern since the risk of disease is relatively low.

The related parasite Neospora hughesi has been found to be a second, albeit minor, cause of EPM. Although not confirmed definitively, this parasite species is likely transmitted to horses in the feces of infected canids (dogs, foxes, coyotes, etc.), with vertical transmission from infected mare to developing fetus being a second possible route of infection. The risk that a N. hughesi infection will lead to neurologic disease remains unclear since studies looking at the seroprevalence of this parasite in horses have yielded discrepant results.

Recently, experts have proposed that a third related parasite, Toxoplasma gondii, is involved in causing EPM as the primary etiologic agent and/or as a comorbidity. This parasite is transmitted in the feces of infected cats as well as in raw and undercooked meats such as pork, lamb, or venison. Toxoplasma gondii is a cosmopolitan parasite that is found worldwide and can infect most warm-blooded animal species. Horses are probably exposed to T. gondii somewhat routinely through ingestion of food and water that has been contaminated with feline feces. Thus far, however, only serologic evidence has been presented to suggest that T. gondii might play a role in neurologic disease in horses; the parasite has yet to be shown as the cause of an EPM case. Horses appear to be quite resistant to T. gondii, with only a single documented case of systemic toxoplasmosis in a horse that had no apparent neurologic involvement. More salient perhaps is that T. gondii has been shown to infect animals on all continents of the world, including Antarctica. If T. gondii had the capacity to cause neurologic disease in horses, EPM would be a global problem and not restricted to North and South America.

Based on the collective evidence currently available regarding T. gondii and horses, altering the existing recommendations for EPM diagnosis and treatment does not seem warranted. As always, EPM diagnosis begins with a thorough neurologic exam, looking for clinical signs consistent with EPM; that is, having the 3-A’s, which stand for ataxia, asymmetry, and atrophy. To rule out other possibilities, veterinarians should perform additional diagnostic testing, such as radiographs of the neck and back, collecting cerebrospinal fluid (CSF) for cytology, measuring vitamin E levels, and sometimes muscle biopsies. When testing for antibodies against S. neurona or N. hughesi, it is important to measure antibodies in serum and CSF to assess production in this space as an indicator of active CNS infection since the presence of antibodies in blood alone is not very informative.

When veterinarians diagnosis a horse with EPM, there are several antiprotozoal drugs available that have been proven effective for treatment. These include the triazinone drugs, diclazuril and ponazuril, as well as the antifolate drug combination pyrimethamine and a sulfonamide. Notably, these drugs will be effective against any of the parasites that have been implicated to play a role in causing EPM, whether as the primary etiologic agent or as an opportunistic comorbidity.

Editor’s note: This is an excerpt from Equine Disease Quarterly, Vol. 35, Issue 3, funded by Equus/Standardbred Station Inc. and M&J Insurance. It was written by Stephen Reed, DVM, MS, Dipl. ACVIM, of Rood & Riddle Equine Hospital in Lexington, Kentucky, and Daniel Howe, PhD, of the University of Kentucky’s Gluck Equine Research Center in Lexington.