Equine Protozoal Myeloencephalitis (EPM)

Table of Contents

  1. Introduction
  2. Diagnosis and Clinical Signs
  3. Laboratory Diagnosis
  4. Treatment
  5. Prevention
  6. Summary
  7. References
  8. Related Links


In some areas of North America, Equine Protozoal Myeloencephalitis (EPM) is one of the most important neurologic diseases in horses. This disease can be difficult for owners and veterinarians to diagnose and treat. The signs in individual horses range in severity and may include incoordination, weakness, spasticity and muscle loss. EPM can look like other equine neurologic diseases, including Wobbler syndrome, the neurological form of herpes virus infection (nEHV-1), rabies, West Nile virus or other equine viral encephalitis diseases, e.g., Eastern and Western equine encephalitis. Refer to the information sheet, Equine Viral Encephalitis for further information.

The primary parasite that causes the disease is the single-celled protozoal organism Sarcocystis neurona. Although identified as a protozoal disease in 1974, the specific disease-causing agent, S. neurona, was not named until 1991. Closely related parasites, Neospora spp., and particularly Neospora hughesi, have been isolated as the cause in a few cases (1,2). These organisms have a predilection for the central nervous system in horses.

Generally Sarcocystis species have a life cycle that involves predator and prey animals. In this disease, the life cycle involves the final or definitive host, the opossum (Didelphis virginiana). The opossum excretes oocysts in the stool, which develop into infective sporocysts in the environment. Intermediate hosts ingest the sporocysts where they, in turn, develop into sarcocysts in muscle tissue (3). The life cycle is complete when opossums eat infected dead intermediary hosts. Currently, the armadillo, domestic cat, skunk and raccoon have been identified as intermediary hosts pertinent to the life cycle of the disease (3). The opossum is a nocturnal animal, a scavenger by nature and eats anything, including carrion. The large number of road-killed animals in some areas may contribute to the spread of the disease.

Horses are infected incidentally when they eat feed contaminated with the feces of opossum, which contain infective sporocysts. Once the sporocysts have been ingested, they migrate from the intestinal tract into the blood stream, cross the blood/brain barrier and attack the central nervous system. The horse is considered a dead-end host for S. neurona since it cannot transmit the disease to other horses. EPM will be found most commonly in horses that reside in areas inhabited by opossums. Horses staying for short terms in endemic areas may become infected and show disease symptoms later, while resident in non-endemic areas.

Trapping data provided by the Ontario Ministry of Natural Resources (OMNR) for 1998, indicates that opossums were present in the districts of Niagara, Cambridge, Simcoe, Aylmer, Chatham, Wingham, Maple, Owen Sound and Midhurst. The highest numbers were trapped in the Chatham area. In recent years, opossums have been sited in other counties, including Wellington and Waterloo. Milder winters leading up to the winter of 2003 may have attributed to their increase in numbers and wider geographic distribution.

Diagnosis and Clinical Signs

The clinical signs of EPM are a result of direct neuronal damage early in the disease and the secondary inflammatory reaction. The signs will vary depending on the location of the lesions in the nervous system.

EPM can cripple a horse slowly or very quickly. In fact, the clinical signs may appear in weeks or up to five years or more after infection. The signs in mild cases may be limited to mild ataxia. In the most severe cases, horses may be unable to swallow or stand. If undiagnosed and untreated, the disease can cause serious and lasting neurological deficits. The disease can mimic other important neurologic diseases making diagnosis challenging, particularly in cases that develop over long periods of time.

A veterinarian should examine any horse showing neurological signs as soon as possible. The veterinarian will perform a physical examination that will include gait evaluation and neurological assessment. Other diagnostic tests, such as radiographs of the neck, may be necessary to rule out problems such as Wobbler syndrome. Refer to the information sheet Wobbler Syndrome or Cervical Vertebral Stenotic Myelopathy in Horses for more information.

In making the diagnosis of EPM, the veterinarian will consider the risk factors identified by researchers over the past decade, including (4):

  1. Age of horse - young horses (1-6 years of age) appear to be more susceptible.
  2. Occupation of horse - horses of highest risk are involved in racing or showing.
  3. Season of year - there is an increased risk in the fall of the year.
  4. Presence of woods on the premises.
  5. Presence of opossums.
  6. Inadequate feed security.
  7. Health events before diagnosis - injury or accidents that lead to immunosuppression increase risk.
  8. Horses on farms where previous cases of EPM have been diagnosed are at an increased risk.

Laboratory Diagnosis

Other neurologic diseases must be ruled out. Diagnosis of EPM is based on the presence of neurological signs plus a positive Western Blot analysis performed on cerebrospinal fluid or CSF (the fluid that bathes the brain and spinal cord). The Western Blot detects antibodies to S. neurona. A positive Western Blot performed on serum merely means that the horse has been exposed to the agent and has developed antibodies to S. neurona (5). It does not necessarily mean that the horse has the disease. False positives and false negatives can also occur when using CSF. Contamination of the CSF with as few as eight red blood cells per microliter of CSF can result in a false positive (6). The Western Blot has been used on serum to estimate the seroprevalence (rate of exposure) in normal horses to S. neurona. Studies in the United States have shown seroprevalence rates (number of horses exposed to the agent) to be between 22 and 65% (7).


Clearly, early detection means more successful treatment and prevention of further damage. However, horses can suffer permanent damage. In the past, treatments included broad-spectrum antimicrobials (e.g., sulfonamides and pyrimethamine), anti-protozoal medications (diclazuril, toltrazuril), NSAIDS (non-steroidal anti-inflammatory drugs such as phenylbutazone and flunixin meglumine), corticosteroids, dimethy-sulfoxide (DMSO), vitamin E, and folinic acid.

Marquis, (ponazuril) from Bayer HealthCare, Animal Health, is now licensed in Canada as an oral coccidiocide for the treatment of EPM. Marquis is currently the only approved drug labelled for the treatment of EPM in Canada. The product is available on the prescription of a veterinarian and is formulated and packaged in oral dosing tubes. A once-a-day treatment for a 28-day period is recommended (8).

Research is continuing into the activity of other anti-protozoal medications.


Prevention of EPM is difficult. Research is currently aimed at identifying the risk factors associated with development of the disease. In this way, horse owners can take the necessary steps to reduce a horse's exposure to the organism. A preventive program consists of wildlife management in the stable and on the farm property, especially for opossums. Opossums maintain several nest sites, including hollow trees and burrows, usually near woodlands. They do not hibernate and have a lack of tolerance for cold weather. Therefore, colder winters and deep snow will limit their range. Horse owners should:

  • Remove opossums humanely from pastures and woodlands;
  • Prevent exposure of horses to opossum feces (much easier for stabled horses);
  • Prevent opossums from entering barns, hay and grain storage areas;
  • High-pressure wash or scrub all infected areas. Disinfectants alone are ineffective for cleaning contaminated areas.

As of May, 2010, no vaccine for EPM is currently available.


Horse owners should:

  • Prevent opossums from entering horse barns and feed-storage facilities;
  • Keep grain bins tightly covered.
  • Bury any dead cats, skunks, raccoons found in and around your farm. This will prevent scavenging by opossums and the possible transmission of the disease-causing agents.
  • Arrange for a licensed trapper to remove any nuisance opossums from your property.


  1. Wobeser BK, Godson DL, Rejmanek D, Dowling P. Equine protozoal myeloencephalitis caused by Neospora hughesi in an adult horse in Saskatchewan. Can Vet J 2009; Aug, 50 (8): 851-853.
  2. Finno CJ, Packham AE, Wilson WD, Gardner IA, Conrad PA, Pusterla N. Effects of blood contamination of cerebrospinal fluid on results of indirect fluorescent antibody tests for detection of antibodies against Sarcocystis neurona and Neospora hughesi. J Vet Diag Inv 2007; 19 (3): 286-289.
  3. Saville WJ, Reed SM, Prevention of Equine Protozoal Myeloencephalitis. AAEP Proceedings 2002; 48: 181-185.
  4. Saville WJ, Reed SM, Morley PS, et al. Analysis of risk factors for the development of equine protozoal myeloencephalitis in horses. JAVMA 2000; 217: 1174-1180.
  5. Morley PS, Saville WJ. Equine protozoal myeloencephalitis: what does a positive test mean? Am Assoc Equine Pract Ann Proc 1997: 43: 1-5.
  6. Miller MM, Sweeney CR, Russell GE, Sheetz RM, Morrow JK. Effects of blood contamination of cerebral spinal fluid on western blot analysis for detection of antibodies against Sarcocystis neurona and on albumen quotient and immunoglobulin G index in horses. JAVMA 1999; 215: 67-71.
  7. Daft BM, Barr BC, Gardner IA, Read D, Bell W, Peyser KG, Ardans A, Kinde H, Morrow JK. Sensitivity and specificity of western blot testing of cerebral spinal fluid and serum for diagnosis of equine protozoal myeloencephalitis in horses with and without neurological abnormalities. JAVMA 2002; 221: 1007-1013.
  8. Personal communication, Carol Jakel DVM, Bayer Inc.

Related Links

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