MANAGING TO PREVENT EPM
since the mouse model hasn’t been the best. Now we are talking about using [intermediate hosts, such as] raccoons, cats or armadillos. Our goal is to avoid using horses, if possible. We realize that at some point we may have to go back to the horse---since it is the host we are most concerned about---but we want to use as few horses as possible to infect with the disease.”
Reed adds, “If we can develop a good model, we may go back and start over again at looking at a vaccine. The early vaccine trials did not show good success. That doesn’t mean we should give up on creating a vaccine, but if we could do something like feed a low level of an antiprotozoal drug and keep the horses from becoming infected, it would be very helpful.”
As with many diseases, the effort to combat EPM is complex and has many fronts. Nonetheless two basic questions remain to be answered: Where are horses most likely to encounter the causal organisms, and what can be done to prevent those who are infected from becoming ill?
Work is underway to better understand where exposure to the EPM parasites is greatest. “Unfortunately there is not a lot of recent data on prevalence,” says Pusterla. “Some states are ‘hot’ states, meaning higher infection rates in the horse population. There are more EPM cases in Oklahoma, Ohio, Kentucky and Texas, for instance, along with some of the Southern and Midwestern states. By contrast we see fewer cases in some of the Northern and Western states.
“To look at infection rates, we sample 100 healthy horses and see how many of them have evidence of past infection based on antibody titers,” Pusterla adds.
With no vaccine currently available, your best strategy for reducing your horse’s risk of developing equine protozoal myeloencephalitis (EPM) is to take steps to limit his exposure to the primary protozoan that causes it: Sarcocystis neurona, which is spread in the feces of the opossum. And that means trying to limit the opossums that live near your barn and pastures. Here are some steps you can take:
• Reduce potential shelter. Clear brush piles, and seal off access to crawlspaces under your sheds and other outbuildings. Keep shed and garage doors closed.
• Cut off food sources. Opossums will eat just about anything. Clean up spilled feed immediately, and keep grain in sealed containers. Use sturdy garbage cans with tight-fitting lids. Avoid leaving cat or dog food out overnight. Pick up fallen fruit from any fruit trees.
• Keep the food and water clean. Store hay and bedding in a secure shed, and throw out anything you find contaminated with droppings. Check outdoor hay feeders and water troughs frequently for signs of small animals, and clean them as needed.
• Dispose of animal carcasses quickly. Opossums ingest S. neurona by scavenging the bodies of other small animals that carryarry it—especially raccoons, cats, skunks ks and armadillos. Pick up roadkill and other dead animals you find on or near your farm.
Note: Trapping or killing opossums is not a goodood solution. If your farm is a source rce of food and shelter for them, more will come. “I have a graduate student looking at 5,200 serum samples collected from healthy horses during 2013 across the United States. The study represents 17 states in all the geographic areas, with approximately 300 animals per state. Her job is to determine seroprevalence for both S. neurona and N. hughesi. This data will give us a better idea about where the hot spots are, and what the actual infection rate might be.”
Armed with that information, a person who lived in a hot spot might be able to take additional precautions with higher risk horses, such as younger ones entering stressful training. “You’d want to monitor these horses a bit more closely,” says Pusterla.
Likewise, researchers in the coming years also hope to answer another confounding question about EPM: Why do some horses develop the disease when others exposed to the same parasite do not?
“In some states 90 percent and in many states over 50 percent of the horses in a given area will have antibodies, indicating they have been infected,” says Reed. “Yet the incidence of severe disease is much lower than that. Is the reason for this difference something about the immune function? Are the horses who develop the disease immunocompromised? There may be something unique about the immune function of those