Study: Polyparasitism An Unlikely EPM Player in the Eastern U.S.
Scientists don’t know why some horses develop the debilitating neurologic disease equine protozoal myeloencephalitis (EPM) and others don’t. But clues might lie in how the causative protozoan parasite Sarcocystis neurona affects other species—namely sea mammals, which suffer more severe disease when both S. neurona and Toxoplasma gondii, another protozoal parasite, are on board.

Sarah Schale, DVM, a clinical fellow in Large Animal Internal Medicine at Oregon State University’s College of Veterinary Medicine, in Corvallis, recently assessed whether horses with S. neurona-caused EPM had also been exposed to the protozoa Neospora hughesi and T. gondii. She presented her results at the Second EPM Society Workshop, held Oct. 25-27, 2017, in Tahoe City, California.

Schale explained that T. gondii’s definitive host is the cat (a reason doctors recommend pregnant women avoid cleaning litterboxes because of the risk for fetal toxoplasmosis infection). “Seroprevalence in horses is reportedly low in the United States, and horses are generally considered to be resistant to toxoplasmosis,” she said. “N. hughesi is the second causative agent of EPM, whose life cycle is largely unknown. Seroprevalence is also relatively low in horses in the U.S. and it has been rarely known to cause clinical disease.”

Her study included 101 neurologic cases seen at the University of Pennsylvania’s New Bolton Center, in Kennett Square; 49 horses had EPM (48 due to S. neurona, one caused by N. hughesi) and 52—the control group—had cervical vertebral stenotic myopathy (CVSM), a structural condition causing spinal cord compression.

“We found that a significantly increased proportion of the EPM cases were likely to be positive for S. neurona on serum, CSF (cerebrospinal fluid), and serum-CSF titer ratios compared to the CVSM cases,” she said, which isn’t unexpected. For N. hughesi, “about 14% of our cases total were positive for Neospora on serum, however, there was no statistically significant difference (in the N. hughesi serum titers, which are concentrations of antibodies) between EPM and CVSM cases.”

She went on to describe T. gondii seroprevalence among the horses, noting that 14.9% overall were positive, “and that was either a weak or very weak positive and, so, due to our lack of overall strong positive results, we didn’t pursue additional testing on CSF.” As with N. hughesi, there was no statistically significant difference between EPM and CVSM cases’ Toxoplasma titers.

“So, in conclusion, we did not identify cases with EPM that had immunologic evidence of co-infection with either Toxoplasma or Neospora,” she said. “There was one confirmed case that had evidence of Neospora infection, but this horse did not have concurrent S. neurona infection. We found high seroprevalence for S. neurona, as evidenced by 96% of our horses with EPM, and 77% of our horses with CVSM testing positive on serum.”

Citing the low seroprevalence of T. gondii and N. hughesi (both under 15% in all horses), with similar numbers in both EPM and CVSM horses—but also noting the small sample size and relatively small geographic area as limiting factors—Schale said that polyparasitism does appear to have a substantial role in the eastern U.S.

“Polyparasitism … is still a relatively new area of study in veterinary species, but has been studied extensively in humans,” she said. “So immune modulation, whether that be in response to parasitic infections or other types of infections may play a role in EPM, but further research is needed in this area.”

Schale’s co-investigators on the study included Dan Howe, PhD, and Michelle Yeargan of the University of Kentucky Gluck Equine Research Center, in Lexington; Jennifer Morrow, PhD, and Amy Graves, MT(ASCP), of Equine Diagnostic Solutions LLC, also in Lexington; and Amy Johnson, DVM, Dipl. ACVIM, of the University of Pennsylvania School of Veterinary Medicine’s New Bolton Center, in Kennett Square.