Equine Protozoal Myeloencephalitis
By: Dr. Philip Johnson
Read By: Pet Lovers
EPM was originally identified by J.R. Rooney in 1964. The first cases were recognized among horses returning to Kentucky from racetracks in the northeastern United States. Subsequent cases have been reported among native horses in most of the United States as well as in Canada and Mexico. At that time, it was not appreciated that the symptoms were due to a protozoan parasite, and the disease was known as "focal or segmental myelitis/encephalitis" (the cause was unknown – the disease was named for the pathologist's microscopic observations). Judging from the literature, EPM may not have been as common in those days.
In the 1970s, the protozoan parasite was seen in affected neural tissues obtained from EPM-affected horses. The disease was then described as equine protozoal myeloencephalitis for the first time, but the actual protozoan parasite was not identified. It was (incorrectly) thought that the protozoan was Toxoplasma gondii (leading to the incorrect name "equine toxoplasmosis"). Probably most, if not all, of the literature about neurological disease associated with toxoplasmosis in horses actually relates to EPM.
In the late 1970s and the early 1980s, evidence was accumulating to suggest that the protozoan parasite responsible for EPM belonged to the Sarcocystis group. In the late 1980s, the causative organism of EPM was finally isolated in the laboratory and determined to be a previously undescribed species of Sarcocystis; it was named Sarcocystis neurona. Soon after it had been isolated in the laboratory, it became possible to develop some useful diagnostic tests for EPM.
One of the persisting mysteries about Sarcocystis neurona had been its life cycle. After it was determined that the causative parasite was a Sarcocystis spp., a search for possible definitive hosts was undertaken. Logical candidate species included the raccoon, opossum and skunk. These animals were considered as possibilities because they are not found beyond the Americas, and EPM has only been described in North and South America, where these particular mammalian species exist. EPM has only been described outside of the Americas in horses that had previously been living in America. In North America, the distribution of the majority of cases of EPM almost exactly follows the population distribution of the opossum.
It has been shown that the definitive parasite host for Sarcocystis neurona is the opossum. Like other Sarcocystis spp, in order to complete its life cycle, the parasite must cycle between the opossum and an intermediate host (the intermediate host for Sarcocystis neurona is currently unknown). The horse is thought to be a dead-end or aberrant host; in other words, the horse does not transmit the disease.
Recently, in a small number of horses, EPM has been attributed to infection by Neospora hughesi (in California and Alabama), but whether Neospora hughesi is as epidemiologically important as Sarcocystis neurona has not yet been determined. In some parts of the United States where the opossum is NOT found, such as Arizona, horses that have always lived there may develop EPM and may have a positive blood test for EPM. It is possible that in those cases the disease may be associated with Neospora. Currently, it is believed that Neospora hughesi is not a very common cause of EPM in horses in the United States.
The life cycle of Sarcocystis parasites follows a well-defined life cycle. These parasites exist in two distinct forms: in one form, the parasite "lives" in the lining of the intestine of a carnivore (the "definitive" host). It reproduces at that location and passes infective sporocysts in the feces.
Recently, the carnivore host (in North America) for Sarcocystis neurona has been identified as the opossum (Didelphis virginiana). EPM is also seen in South America (associated with a different species of opossum). EPM is only seen in the Old World in those horses that have been imported from the USA.
All Sarcocystis parasites have an obligate predator-prey life cycle. Opossums are infected by eating sarcocyst-containing muscle tissue from an infected intermediate (prey) host and, after a brief prepatent period, (probably 10 days), infectious sporocysts are passed in the feces.
In order for the parasite to complete its life cycle, the intermediate host must ingest the infective sporocysts by way of a fecally contaminated food source. Once ingested, the sporocyst migrates to the skeletal muscles and can persist there (as a sarcocyst) for many years. The carnivore host (opossum) becomes infected (in its intestinal lining) by eating the skeletal muscles of the secondary host. Obviously, the secondary host has either been killed by the carnivore or has died for other reasons. Of the two classic Sarcocyst hosts, one is a predator, the other is prey.
Opossums eat almost anything, including dead birds and insects. It has been suggested that the intermediate host for Sarcocystis neurona could be a species of bird. It is not surprising that the feces of the opossum represent a rich source of nutrition for wild birds. By eating dead birds (or whatever other animal is shown to be the intermediate host), the opossum enables Sarcocystis neurona to complete its life cycle. Wild birds ingest sporocysts by eating opossum feces. Probably, neither the opossum nor the intermediate host are clinically affected in any way by the presence of a few Sarcocystis parasites – at least not seriously.
Horses may become infected with EPM by eating food material (grain, hay, grass) or drinking water (ponds, streams, water troughs) that has been contaminated by the feces of the opossum, containing infective sporocysts. The horse is infected in the same way as the intermediate host, by ingesting the infective sporocysts. However, unlike the intermediate host, in horses the infective "stages" of the parasite (merozoites are the tissue-invasive stage) migrate into the central nervous system. Even when an infected horse dies, it is unlikely that an opossum (or anything else) would ingest its brain or spinal cord; therefore, the horse is a dead-end host for this parasite. In other words, the horse is not needed for the completion of the parasite's life cycle. EPM is not contagious; Sarcocystis neurona parasites cannot be transmitted from the horse to other animals (including other horses).
Although the exact species that acts as the intermediate host for S. neurona is not currently known, numerous other species (including birds) may assist in the dispersion of infective sporocysts in the environment. Some infective sporocysts may also be passed through the intestinal tract in birds' feces unchanged. Therefore, bird droppings should also be regarded as potentially infective for horses; if this is true, birds are acting as mechanical vectors for dispersion of the infective sporocysts. It has also been suggested that certain insect species (such as cockroaches) might also aid in the mechanical dispersion of infective sporocysts.