Equine Protozoal Myeloencephalitis
Equine protozoal myeloencephalitis (EPM) is a debilitating protozoal disease of the central nervous system that is typically caused by infection with Sarcocystis neurona, although recent reports have suggested that it may less commonly be caused by infection with Neospora sp. EPM is a difficult disorder to study because the life cycle of the organisms and mode of transmission are not always known. The assessment of exposure to S. neurona and N. hughesi has become possible with the introduction of an indirect fluorescent antibody test, developed and validated by members of our team. This assay has become a valuable tool in performing seroepidemiologic studies and has allowed many of us to reliably diagnose neurologic neosporosis and S. neurona infection in affected horses. Although the ecology of Neospora sp. in horses is still unresolved, many comparisons have been drawn with N. caninum, the causative agent of ascending neuromuscular disease in dogs and abortion in cattle worldwide. The domestic dog excretes oocysts of N. caninum in its feces and, after sporulation, these oocysts are infectious to cattle. Potential sources of horizontal infection amongst cattle also include colostrum or milk from infected cows, infected placentae and fetal fluids. It appears, however, that vertical transmission is of major importance in the spread of N. caninum in cattle and accounts for as much as 95% of seropositive animals in endemically affected herds. A similar transmission route was recently reported for horses, where endogenous transplacental infection was documented from persistently infected broodmares to their offspring. Only one out of 9 foals born from two persistently infected mares over a six year period developed neurological signs compatible with EPM during the first year of life. The true clinical impact of horses infected with N. hughesi remains to be determined beyond the sporadic development of central nervous infection. It is likely that latently infected horses may be at higher risk of developing clinical disease following an immunosuppressive event.
A recent study using laboratory blood submissions from horses with suspected EPM determined that N. hughesi seropositive horses originated from 25 states. The wide geographic origin of N. hughesi seropositive horses highlights the need to test for both S. neurona and N. hughesi in neurologically affected horses.
We are in the process of further investigating the life cycle of N. hughesi by screening potential domestic and wild reservoir hosts from farms with documented high seroprevalence to this apicomplexan protozoal organism. And we are working at establishing preventive measure by studying the daily use of anti-protozoal drugs.