Proceedings from the Grayson Jockey Club Research Foundation, published in Equine Care Watch, a Communications of Project TRC.
EPM is a debilitating neurologic disease of horses. It can affect the brain, brainstem, spinal cord or any combination of these three areas of the central nervous system. Clinical signs may suggest focal or multifocal disease, which means the disease may affect a very small (focal) part of the central nervous system (CNS) or may parts of the CNS (multifocal). Therefore the disease may present itself with a variety of different clinical signs, dependant on the location of the damage caused by the organism within the CNS. There is no vaccine currently available.
Lifecycle:
Although EPM has been recognized since the 1970's, it was not until,1991 that the organism (protozoan parasite) was cultured from a horse and given the name Sarcocysitis neurona. The horse is a dead-end aberrant host, as infectious forms of the parasite are not passed from horse to horse or from horse to the definitive or true intermediate hosts. Recent investigation indicates that opossum faeces (definitive host) are the source of the infection for horses. Opossums acquire the infection by eating infected birds (intermediate hosts). Most infections would come from contaminated pasture, hay, grain, and water with opossum faeces. Contamination of feed and water with opossum faeces may occur indirectly through other mechanisms such as birds and insects. Control of the parasite to prevent infection of horses will be a daunting task because of the wide distribution of definitive and intermediate hosts in the environment of horses. Relocation of opossums away from horses, water, bedding and feed storage environments may be beneficial to reduce exposure.
EPM occurs in much of North America. Surveys conducted in central Kentucky, one county in Pennsylvania and the entire states of Ohio and Oregon have revealed that approximately 50% of the horses have been exposed to this parasite. We know that a positive serum test indicates exposure to the parasite, not necessarily the presence of disease, the incidence of which is much lower. In the studies that looked at the distribution of seropositive cases geographically, it was found that climatic factors may affect exposure rates, i.e., an increase of freezing days was associated with a decrease in numbers of horses exposed to the parasite. A similar effect of very hot environments may also decrease the survival of the infective stages of the protozoan parasites and lessen exposure to horses. EPM appears to have a sporadic distribution, although outbreaks have been reported on farms in Kentucky, Ohio, Indiana, Michigan, and Florida.
Clinical Signs:
EPM is a progressive disease, which if not treated may eventually lead to death. Any horse that is demonstrating neurological abnormalities may have EPM. The clinical signs are dependent on the location of the organism within the central nervous system. EPM can affect a horse of any age, breed, or sex. The youngest horse reported affected was two months of age, and the eldest in its 30s. Clinical signs may be triggered or worsened by physiologic stress or the administration of corticosteroids. Clinical signs of the disease include weakness, malposition of a limb, muscle atrophy, spinal ataxia or "wobbling" head tilt with asymmetry of the face (eyelid, ear, lip). A severely EPM-affected horse may be down and unable to rise. Lameness not traceable to orthopedic disease or any combination of the above signs may occur in early or less severe infections. Other unusual signs may occur.
In most cases, affected horses are bright and alert with a normal appetite although some horses are dysphagic (unable to eat) and may act as if they are choked, with feed material coming from their nose. Hematological and biochemical blood values are usually in the normal range. Sometimes a horse may have more than one disease, e.g., both EPM and cervical stenotic myelopathy ("wobbler"). It is important to realize that all neurological disease in horses is not EPM and a complete workup by your veterinarian is needed in many cases to arrive at a specific diagnosis of the problem.
Diagnosis:
Diagnosis of EPM is based on clinical signs and on testing of the horse's cerebrospinal fluid (CSF). Originally, the diagnosis was based on the presence of antibodies to Sarcocysitis neurona in serum. We know now that a positive serum test cannot be used to make a diagnosis, but simply indicates exposure to the parasite, not necessarily the presence of the disease. Cerebrospinal fluid testing is now believed to be the most useful test to assist in the diagnosis of this disease in the live horse. The western blot test of CSF detects antibodies that the horse has formed against the parasite. The presence of these antibodies in the CSF of horses with neurologic signs usually indicates active disease. However if blood contaminates the CSF sample, a false positive test may result. Positive CSF tests among horses without neurologic signs have occurred, however, the significance of these findings has not been determined. If the test is negative, and the horse is exhibiting clinical signs, the horse may still have the disease. In some cases, a second test (PCR) may be able to detect
very small amounts of parasite DNA (parts of the parasite's genetic make-up), and may assist in the diagnosis. However, we consider the PCR test most useful as a research tool. It is recommended that the PCR test only be used in conjunction with the western blot. There is only one commercial laboratory performing these tests and [it] is located at the University of Kentucky. Acupuncture is not recognized as an accurate diagnostic test.
Therapy:
Treatment of horses with EPM is expensive. The average range of treatment is 90 to 120 days, and may exceed six months in some instances. The appropriate length of treatment and the method to determine adequate treatment duration are unknown. The current approaches to treatment for EPM include pyrimethamine in combination with a sulfonamide antimicrobial with or without trimethoprim. These medications should be administered one hour prior to feeding hay. The EPM Workshop Participants recommend frequent, periodic, veterinary neurologic examinations during the treatment period. Discontinuation of therapy may be based on administration of medications 30 days beyond the plateau of clinical improvement. An alternative approach to determining discontinuing of therapy is disappearance of antibody to the protozoa from the CSF. Suboptimal dosing of intermittent therapy has no proven efficacy.
Adverse side effects of therapy may include anemia, abortion, diarrhea, and low white blood cell counts. Both medications for treatment of EPM inhibit folic acid metabolism. Supplementation with folic acid (40 mg orally, once a day) may help prevent adverse side effects. Folic acid should not be administered at the same time as the antimicrobial drugs. In cases with severe neurologic signs, nonsteroidal anti-inflammatory treatment medications and DMSO may be added to the treatment regimen.
Prognosis:
It would appear that early detection and therapy increase the chance of successful treatment is highly variable; many treated horses return to their original level of function, however, some may not respond completely. It is also estimated that approximately 10% of the cases relapse after treatment is discontinued. Some horses are currently on medication indefinitely.