Equine Protozoal Myeloencephalitis (EPM): Back by Popular Demand

There is no end to the requests that I get to repost my EPM website.  In response to the requests, I have revamped the site and decided to post it here.  This current installment is the introduction, and clinical signs, diagnosis and treatment will follow over the next few weeks.  Keep checking back for the next installment.

He may stumble once or twice. At first you didn't think much of it, but now it's getting worse. He's not lame, just not the same. Or your yearling colt seems to be really clumsy. He drags his hind toes, but maybe its just a stage he's going through. Maybe your trail mare is starting to be a little unsure over the terrain. Or worse, your horse is stumbling, tripping or falling, worse behind. It could be the development of a lameness, or it could be something else.  

Equine Protozoal Myeloencephalitis (EPM) is an infection of the brain or spinal cord of horses that is most commonly insidious in onset with nebulous clinical signs. However, because the organism can affect any part of the central nervous system, clinical signs can vary widely. The neurologic signs that it causes are most commonly asymmetric incoordination (ataxia), weakness and spasticity, although they may mimic almost any neurologic condition. Clinical signs among horses with EPM include a wide array of symptoms that may result from primary or secondary problems. Some of the signs cannot be distinguished from other problems, such as lameness. Airway abnormalities, such as laryngeal hemiplegia (paralyzed flaps), dorsal displacement of the soft palate (snoring), or airway noise of undetermined origin may result from protozoa infecting the nerves which innervate the throat. Apparent lameness, particularly atypical lameness or slight gait asymmetry of the rear limbs are commonly caused by EPM. Focal muscle atrophy, or even generalized muscle atrophy or loss of condition may result. Secondary signs also occur with neurologic disease. Upward fixation of the patella (locking up of the stifle) is among the most common findings among horses with neurologic disease. Another common side effect of EPM is back soreness, which can be severe. Even typical racing injuries may ultimately be caused by EPM, because horses which are uncoordinated are much more likely to "take a bad step" in racing or training. Therefore, any horse with these signs should be carefully evaluated by your veterinarian for the presence of neurologic disease.

EPM was originally identified as a fatal neurologic disease of horses by Dr. Jim Rooney in the 1960s, who saw the characteristic inflammatory lesions in the spinal cord of horses. Protozoa were first identified in the lesions of affected horses in 1974. The protozoa was identified as being similar to other members of the genus Sarcocystis by Dr. JP Dubey, a senior researcher at the USDA, who named it Sarcocystis neurona in 1990. In 1996, my research identified the opossum as the definitive host and source of infection to horses of S. neurona. Over the next several years, I worked with several pharmaceutical companies worked to develop anti-protozoal treatments.

Like other species of Sarcocystis, S. neurona has a two host life cycle. The definitive host (opossum) consumes the muscle tissue of the intermediate host (skunks, raccoons, armadillos) containing protozoal cysts. The protozoa enter the intestinal cells and undergo sexual reproduction in the intestinal cells of the definitive host, forming the infective sporocysts which are passed in the feces of the definitive host. These sporocysts are ingested by the intermediate host, where they hatch in the intestines and pass into the bloodstream. In the intermediate host (skunks, raccoons, armadillos), the protozoa undergoes asexual reproduction in the blood vessels of the liver, lungs and muscles and then encysts in the intermediate host's muscle tissue, without traveling to the central nervous system. When this tissue is eaten by the opossum, the organism undergoes sexual reproduction in the intestinal cells, and forms the infective sporocysts, which are passed in the feces. The opossum does not become sick, but may shed the parasites for months.

Horses represent an aberrant host of S. neurona. Sporocysts are ingested, but never encyst in the tissues of the horse. Instead, they migrate to the central nervous system, where they continue to undergo asexual reproduction intracellularly in neurons, without forming tissue cysts. Horses cannot transmit the organism to other horses, or even to opossums. Horses probably eat the opossum sporocysts inadvertently while eating grass, hay or grain.

In one of my research studies, I was able to reproduce the disease by feeding opossum-derived sporocysts to horses. The horses had detectable serum antibodies at about 3 weeks after infection, and all of the horses that ultimately developed EPM had spinal fluid antibodies about a week later. Those that did not develop EPM never had antibodies in the spinal fluid, even as long as 4 months later.

This disease may be preventable by some simple measures. Anything that may attract opossums into barns should be tightly covered, or put away, especially at night. This includes cat food, garbage and grain. Opossums are particularly fond of cat and dog food. Feed should not be left out at night for the morning, or even during the day to attract birds. The opossum population should be kept under control on farms and stables, where possible. Mesh wire or chain link fencing with "hot wire" around the outside may keep opossums out, since they can climb, but they do not dig. The processes of steam-crimping and pelleting grain kills off the sporocysts, so using processed grains can also decrease the exposure to EPM.

Exposure of horses to EPM occurs at an average rate of about 50%, but approaches 80-90% among some groups of horses. It is impossible to predict which exposed horses will develop fulminant disease. Some horses with active disease may be able to clear the organism without treatment. Currently, the only approach to control of EPM is early detection of incoordination, gait or other abnormalities, definitive diagnosis of the disease by cerebrospinal fluid (CSF) analysis, and appropriate treatment. The disease probably requires a minimum of two weeks and up to two years to develop from the time of exposure to the development of marked clinical signs. Exposure rates (but not disease rates) for different farms or training facilities may vary from zero to 100% of the horses at a given location. Premises with very high seroprevalence appear also to have a high prevalence of clinical disease. Most horses probably ingest the sporocysts, mount an immune response, and clear the organisms before they reach the central nervous system. Alternatively, they may be persistently infected in the central nervous system, but are able to combat the organism sufficiently to prevent the development of clinical signs. There is no "dormant" stage, and there is no "remission.".