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