EQUINE PROTOZOAL MYELOENCEPHALITISHISTORY · EPIDEMIOLOGY · DIAGNOSIS · TREATMENT · HISTORYEquine protozoal myeloencephalitis or "EPM" is an infectious disease of horses caused by a microscopic protozoan parasite which has been named Sarcocystis neurona. In the 1960's horses were displaying the symptoms of EPM although the disease was named focal or segmental myelitis/encephalitis. In the early discovery of the disease the cause was unknown. In 1974 a protozoan parasite was seen in affected neural tissues obtained from EPM-affectd horses. It was at this time the disease was first referred to as EPM, but the actual protozaon was not identified. In the late 1970's and early 1980's, evidence was accumulating to suggest that the EPM-protozoan parasite belonged to the Sarcocystis group. In the late 1980's the causative organism of EPM was isolated in the laboratory and determined to be a previously undescribed species of Sarcocystis; it was named Sarcocystis neurona. After the parasite was isolated in the laboratory, it was possible to develope some accurate diagnostic tests for EPM. One of the mysteries about Sarcocystis neurona had been it's life cycle. After it was determined that the parasite was in the Sarcocystis group, a search for possible definitive hosts was undertaken. Logical candidate species included the racoon, the opossum, and the skunk. These animals were considered because they are not found beyond the Americas. EPM has only been seen in the Americas. The only horses outside of the Americas with the disease had previously been living in the Americas. There is convincing evidence that the definitive parasite host is the opossum. Like other Sarcocystis in order to complete its life-cycle the parasite cycles between opossum(definitive host) and wild birds(intermediate host). The horse is a dead-end or aberrant host. This protozoan can cause severe life-threatening disease in some of its natural intermediate hosts, such as budgerigars, but may cause few clinical signs in others, such as pigeons. In the normal life cycle, the parasite is ingested(fecal-oral transmission)in the form of a sporocyst by the bird, undergoes asexual reproduction in the blood vessels of the liver, lungs and muscles and then encysts in the bird's muscle tissue, without traveling to the central nervous system. When the tissue of the dead bird 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 parasite for months. Horses represent the aberrant host of this protozoan. 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 intracellulary in neurons, without forming tissue cysts. Horses cannot transmit the organism to other horses, or even to opossum. Horses probably eat the opossum sporocysts inadvertently while eating grass, hay or grain. EPIDEMIOLOGYExposure of horses to EPM occurs at an average rate of about 50%. It is impossible to predict which exposed horses will develop the disease on a full blown scale. Some horses with active disease may be able to clear the organism without treatment. Currently the only approach to control EPM is early detection of incoordination, abnormal gait or other neurological disorders, definitive diagnosis of the the disease by cerebrospinal fluid analysis, and appropriate treatment. The disease can require a minimum of two weeks and up to two years to develop from the time of exposure to the development of marked clinical signs. 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 unable to combat the organism sufficiently to prevent the development of clinical signs. DIAGNOSISThis disease should be suspected whenever horses develop signs of neurological disease which cannot be readily explained by other previous events. It must be remembered that EPM can produce any neurological abnormality or combination of abnormalities. The best test involves the collection of a spinal fluid sample which is tested for antibodies against Sarcocystis neurona; this test is the Western Immunoblot. This test relies on the fact that, during active EPM, antibodies are being produced against Saracocystis neurona within the spine and brain. A positive spinal fluid Western Immunoblot test result is strong evidence that EPM may be the problem IF THE TESTED HORSE IS TRULY DEMONSTRATING SIGNS OF NEUROLOGICAL DYSFUNTION. TREATMENTThe current method of treatment is potentiated sulfonamides in combination pyrimethamine, an antimalarial medication. The efficacy of the treatment as indicated by short term survival and response to therapy has been reported to only be 55% to 60%. A new therapy (Diclazuril) has been receiving a lot of interest lately and has been under study by the University of Missouri. This new compound is a triaxine derivative that has been used as a coccidiostat in other countries for a number of years. The compound should not be toxic to mammals, however toxicity studies have not been completed to date. The treatment period is much shorter and less costly. This compound has been used primarily in horses that have relapsed after the standard therapy with resonably good success. OTHER EPM WEB SITESTITAN-An Actual EPM Case |