History
The pathologic lesions of equine protozoal myeloencephalitis were first described by Dr. Jim Rooney in the 1960's. Horses
that had died of severe neurologic disease were found to have regions of inflammation in the brain, brainstem or spinal
cord. The etiologic agent (causative organism) was not identified in the lesions.
Protozoa were first identified in EPM lesions in 1974 independently by several groups, including Drs. Beech and Dodd,
Cusick and associates and Dubey and associates. These organisms were originally considered to be Toxoplasma gondii,
primarily because this species had been identified as a cause of protozoal myeloencephalitis in humans and other animals.
However, detailed ultrastructural studies performed by Dr. Dubey showed that the parasite was not T. gondii, but rather a
Sarcocystis sp (Dubey et al., 1991a).
Further detailed ultrastructural study was permitted when the organism was isolated from an infected horse by culturing in
bovine monocytes in vitro. This parasite was shown to react with S. cruzi polyclonal antisera, but not T. gondii antisera,
supporting its placement into the genus Sarcocystis. This evidence permitted the designation Sarcocystis neurona for the
parasite (Dubey et al., 1991a. Comparisons of DNA sequences confirmed the placement of this protozoan into the genus
Sarcocystis (Fenger et al., 1994).
The in vitro culture of S. neurona permitted the development of diagnostic tests for EPM. Antigen analysis by indirect
immunofluorescent antibody (IFA) was compared with Western blot (immunoblot) by Dr. Dave Granstrom of the
University of Kentucky. Western blotting, or immunoblotting, was determined to have greater specificity for detection of
exposure to S. neurona than other test methods. This method was expanded to the detection of anti-S. neurona antibodies in
CSF, and found to be useful for the diagnosis of disease. Extensive analytical validation was performed at Neogen
Corporation, where the test is currently available.
In the mid-1990s, using DNA manipulating techiniques (molecular biology) Dr. C. Fenger found that the opossum is the
source of infection for the horse (Fenger et al., 1995; Fenger et al., 1997, a). The opossum is a critical part of the life cycle
for S. neurona, whereas the horse acts as an aberrant host. The parasite never encysts and never completes its natural life
cycle in the horse, and horses cannot transmit S. neurona to other horses, or other animals, including opossums.
In recent years, the number of researchers studying this disease has skyrocketed. Hopefully, this means that the critical
questions will be answered soon, including the identity of the intermediate host, the reason why some horses become
infected and others do not, and finally, some method of prevention of the disease.
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