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Prevention of Equine Protozoal Myeloencephalitis (EPM)

By William Saville, DVM, Dipl. ACVIM, Ph.D; Stephen Reed, DVM, Dipl. ACVIM; and J.P. Dubey, MVSc, Ph.D

Equine protozoal myeloenencephalitis (EPM) is one of the most important neurologic diseases in the horse and remains a problem for horses and their owners. Over the past several years work has been directed at better understanding this disease problem in horses along with how to treat the problem.  In addition several investigators have worked on ways to help owners prevent this disease in their horses.  Despite this concern and interest prevention has been more difficult than anyone imagined. As we learn more about the disease, we find that wildlife management, risk-factor manipulation and use of prophylactic medications remain the center of attention for ways to prevent the disease.  Efforts towards development of a vaccine has proven ineffective to this point in time.  

Although the disease has received much publicity, scientific knowledge has been sorely lacking regarding pathophysiology of the disease and the mechanisms by which the parasite has been maintained in nature. In the last several years, we have continued to make progress in better understanding of the life cycle of the causative organisms (S neurona and N. hughesi).  Better understanding the life cycle can help owners and veterinarians in the prevention of EPM.  Original research in the mid-1990s led to the discovery of the opossum as the definitive host for Sarcocystis neurona, the primary parasite that causes EPM in horses. Most Sarcocystis spp. have a predator-prey life cycle, which allows the parasite to cycle in nature and to perpetuate itself.  Interestingly the opossum is the host of at least threeSarcocystis spp. For the S neurona organism we know of several intermediate hosts including skunks, raccoons, armadillo and even domestic cats as well as sea otters and the harbor seals.


Completion of the life cycle for S. neurona was first accomplished in a laboratory setting by using the domestic cat as the intermediate host species. Subsequent work by the same research group examined exposure rates of barn and feral cats to S. neurona in the state ofOhio. Horse farms were targeted where there were horse cases of EPM, there were resident cats and the farms were in sylvatic areas, hence wildlife present. Exposure rates of cats to S. neurona were high (40 percent) on these premises. Another subset of cats that were presented to a mobile spay-and-neuter clinic were sampled, and those cats had a much lower (10 percent) exposure rate. These studies suggest that the domestic house cat does play a role in transmission of S. neurona in nature and therefore likely has an impact on EPM in the horse. The extent to which the cat is involved needs to be determined before we understand how big a role it may play in the life cycle of S. neurona


Following publication of the cat as the intermediate host, a natural intermediate host with high levels of exposure to S. neurona was reported: the nine-banded armadillo. All 19 wild-caught armadillos had detectable S. neurona antibodies in their serum. This fact coupled with the production of sporocysts after feeding sarcocyst-infected muscle from road-kill armadillos is strongly suggestive that the nine-banded armadillo is a natural intermediate host for S. neurona. Further work also needs to be done to determine the extent of their environment. 


Subsequent to the cat and armadillo discoveries, a third species was determined to be a laboratory intermediate host for S. neurona. There was a report that S. neurona antibodies were found in the striped skunk. Completion of the life cycle with the striped skunk along with the reports of S. neurona antibodies in wild skunks is also suggestive that the striped skunk may very well be a natural as well as a laboratory intermediate host. 


Another more recent natural intermediate host to complete the life cycle of S. neurona is the raccoon. This high seroprevalence rate in raccoons is similar to the exposure rate in horses. This finding of high exposure rates in combination with the feeding of wild-caught raccoon muscle to produce sporocysts makes for a compelling argument that the raccoon is an ideal intermediate host in the life cycle of S. neurona

Sea Otter

The latest intermediate host to complete the life cycle of S. neurona thus far is the sea otter. The role of the sea otter in the contamination of the environment with S. neurona sporocysts is likely limited. However, what it does demonstrate is that the number of natural intermediate hosts may be numerous and thus make prevention of contamination of the environment difficult; therefore, prevention of EPM can be difficult.


The opossum is a scavenger by nature and will eat anything (omnivorous). Several studies have demonstrated the presence of domestic cat, raccoon and striped skunk in the stomach contents of the opossum. Most conclude that the presence of the larger mammals was likely the result of eating carrion. In addition, based on these early reports, it appears that these are not the preferred diet of the opossum, which may be the reason why early reports have determined that 20 percent or less of the opossums excrete S. neurona sporocysts. The fact that these mammals would not be considered prey likely resulted in a different direction being studied with regard to the true intermediate hosts involved in this life cycle. 

Based on the eating habits of the opossum, prevention of EPM becomes problematic due to the excess of road-kill on the highways across the United States. The opossum will scavenge carrion to survive if other more preferred types of food are not available. Cleanup of road-kill of four of the above named species in particular would help to solve some of the EPM problems, as each of these species are able to complete the life cycle of S. neurona. However, given the fact that four species that complete the life cycle have been discovered in the last 2years, it seems likely that more species are involved in completing the life cycle and will add to the excretion of sporocysts to contaminate the environment. Preventing access of opossums to the farm or ranch environment is also difficult, particularly if food and water are in short supply. Even if hay and grain are kept stored in opossum-proof facilities, there is still no protection of grass pastures from contamination with S. neurona sporocysts. Encouragement of horse owners to pick up dead species and keep them from being eaten by opossums is one method of prevention; however, the effort to do this seems problematic. 

Recent publications describing few risk factors for EPM have delineated a few measures that could be manipulated to reduce incidence of the disease. Research from Ohio suggests that risk factors for the disease include age of the horse, occupation of the horse, season of the year, presence of woods on the premises, presence of opossums, lack of feed security, health events before diagnosis and previous cases of EPM being diagnosed on the farm. The horse factors are very difficult to manipulate; however, efforts to improve the immune status of the horse may be warranted. Unfortunately, the highest-risk occupations are racing and showing of horses. This involves transport of horses to racetracks and show events, and transport has been determined to be a risk factor for the disease as well. Other than stopping the transport of horses, which is very unlikely, improvement of immune status while in transit may be a solution. The presence of woods and opossums on the property corroborate the finding that the opossum is the definitive host and is contaminating the environment; therefore, preventing opossum access to property, or at least to the horse feed, is important in prevention. Unfortunately, removal of woods from the premises, while removing the opossum habitat, would not likely solve the problem, as the opossum has learned to adapt very well. Both theOhio and the NAHMS studies (involving horses from 28 states across the U.S.) found an increased risk for EPM in the fall season of the year. The reason for this finding was that a lot of the major horse competitions were in the fall, which also involved transport. However, perhaps it is related to the change in the opossum diet in the fall, as research has determined that the carrion involves a much bigger percentage of the opossum diet at that time. 

Recently, there has been some evidence that suggests there are triazene derivative medications that will prevent S. neurona in mice. The medication used was diclazuril, an herbicide that has been used in several species in other countries as a coccidiostat in both poultry and swine. Diclazuril has been used to treat horses that are diagnosed with EPM. Perhaps this medication as well as other similar compounds may be developed as preventative therapy in the top dress of horse rations.

Although we continue to make strides in understanding the life cycle of S. neurona, we have only a few good suggestions regarding prevention of this disease. Notwithstanding this, it is apparent that prevention of EPM should be centered on the wildlife involved in the transmission of the parasite. It is not the live wildlife that is the problem when considering the intermediate host as a cause of the disease. As far as we know, the majority of the intermediate hosts involved only play a role when they are killed or die due to disease. Therefore, picking up dead skunks, raccoons, armadillos or cats on your property and disposing the carcasses to prevent opossums from eating them may prevent many sporocysts from contaminating the environment and hence reduce the incidence of the disease. Manipulation of risk factors that are involved in the disease may also help. Whether future efforts are directed at the development of a vaccine remains to be seen.


Reviewed by Infectious Disease Committee in 2020.