A primer on the neurological disease and best practices for prevention and treatment
By ELLE GIBBS
Equine Protozoal Myeloencephalitis, referred to as EPM, is a term that is often brought up in the equine community. Unfortunately, the abbreviation for this neurological disease is misapplied and misunderstood by many riders and owners.
The cause of EMP is Sarcocystis neurona, an apicomplexan protozoan, which is transferred mostly by opossums to horses through fecal matter. It is believed that all horses are susceptible to developing EPM and some researchers have found that in America 15% to 89% of horses have been in contact with the protozoan depending on their geographic region.
Interestingly, most cases only involve one horse, limiting the assumption that horses can spread the disease to each other. EPM works by altering the central nervous system (CNS) of a horse, causing a wide range of clinical signs that can make it difficult to differentiate the disease from other neurological disorders or traumas.
Even though EPM is classified as a rare disease, lack of diagnosis and treatment for affected horses can be life-ending. EPM is not a general term that should be taken lightly around the barn. It is the responsibility of owners and riders to pay attention to their horse’s behavior and activity, not only to display good horsemanship but also to make sure challenging diseases to diagnose, like EPM, do not go untreated. The following article provides an outline of the causes, symptoms, treatments, and preventative care for Equine Protozoal Myeloencephalitis.
Parasite Pathway and Transmission
One of the most challenging aspects of preventing and treating EPM is tracking the various transmission and internal pathways of S. neurona. Sarcocystis neurona survives by alternating between a definitive and intermediate host. The opossum is considered a main definitive host while other species like horses, cats, and skunks act as intermediate carriers of the parasite.
The opossum is currently the only animal known to be able to transmit S. neurona to horses. The cycle of transmittance begins after an opossum consumes tissue infected by S. neurona from a prior intermediate host. The parasite then undergoes sexual reproduction in the intestinal tract of the opossum to produce copies that get released into the environment through feces.
An intermediate host, like a horse, encounters fecal matter by some form of contamination of feed, water, or housing environment. Once inside of the horse, the parasite can infect any portion of the central nervous system and cause lesions (damage to tissue) on the brain, spinal cord, or brain stem. S. neurona can attack multiple areas of the CNS, which is why there is a vast range of disease symptoms. Although S. neurona is most associated with EPM, another protozoan, Neospora hughesi, has also been identified as a causing agent. Although less common, scientists have suspected N. hughesi acts much like that of S. neurona in terms of external and internal activity.
Clinical Signs
One of the most important aspects of horse care is being able to tell when an animal is not displaying normal behavior or demonstrates a change in health that could signal an underlying veterinary issue.
Sarcocystis neurona has the ability to target and damage multiple sites of tissue across the CNS allowing the disease in horses to produce an extensive list of clinical signs. S. neurona can harm CNS tissue by causing focal discoloration (tissue discoloration), hemorrhage (loss of blood due to a damaged vessel), and malacia (softening of tissue).
Because the majority of neurological problems have a degree of overlap with the symptoms of EPM, identifying this disease is challenging and can be overlooked even by the most experienced vets. The most common target of S. neurona damage is the spinal cord with lesions on the brain stem being less frequent.
The general clinical signs associated with spinal cord damage are: ataxia (incoordination), muscle atrophy (weakness), stumbling (often confused for lameness), standing splay-footed, leaning on walls/objects for support, and hyporeflexia (decrease reflex response).
Recurring symptoms of brain stem degradation include behavioral issues, mild depression, facial nerve paralysis, head tilt, dysphagia (difficulty swallowing), lethargy, abnormal airway functioning, snoring, drooling, abnormal eye movements. Horses can also experience hyporeflexia (decrease reflex response), seizures, and death. Many horses with EPM will seem bright and have good vitals providing an extra layer of difficulty for barns to pick up on this disease.
The timeline of EPM in horses varies and does not follow a linear projection. It can take hours or even years for a horse to reach a point of recumbency (inability to stand) and most of the time this journey is in a start-stop fashion. Even though EPM is difficult to diagnose due to its vast list of symptoms, knowing the common signs of the disease can help equine caretakers be more conscious of character changes in their animals and encourage detailed analysis of abnormal behaviors displayed in the barn.
Factors Influencing EPM
Another important question to consider when facing a deathly neurological disease like EPM is: What factors exacerbate the likelihood or severity of developing this disease? Age is one factor that has shown to influence the presence of EPM in horses. A study performed at The Ohio State University concluded that young horses (1-5 years old) and older horses (>13 years old) had a statistically higher risk of developing EPM than other age categories.
Another study performed at the New Bolton Center at the University of Pennsylvania revealed that age also impacted EPM prevalence but found no correlation between the disease and either breed or gender. In addition to age, seasonal temperature has shown to influence EPM presence.
In the same Ohio State University experiment, they found that EPM cases increased three-fold in the spring and summer compared to winter months. Some possible reasons for this are the decreased activity of opossums and horse events during freezing temperatures. Dense population and high stocking densities of barns have shown a positive relationship with the presence of EPM.
An explanation for this could be the displacement of opossums due to human development causing the animals to try and find new homes closer to farms. Within the same study, it was found that a high barn population (20+ horses on a farm) caused a seven times increase in EPM cases.
This statistic poses a contradiction to the previous theory—that horses cannot transmit the parasite directly to each other—and opens up questions of whether or not the animals can pass the disease through other forms like feed and water contamination. Stress is another common factor that researchers associate with the development of EPM.
In another experiment conducted by The Ohio State University, they exposed four groups of horses to an equal number of parasites and then altered the stress induced on each group to determine whether high cortisol levels played a role in EPM development. The study concluded that the more stress a horse is exposed to, the higher the chance and more severe the development of EPM is.
Major stressors for horses include transportation, new ownership, pregnancy, illness, injury, and athletic competitions or training. Another study showed that racehorses and show horses had a higher risk of developing EPM compared with breeding and pleasure horses. The cellular understanding behind stress linked to EPM severity/development is the idea that corticosteroids limit horses’ bodies from exhibiting proper immune response to the pathogen, allowing S. neurona to enter and move throughout the animal more easily.
Diagnosis
EPM can be a life-ending disease, however, with screenings and treatment, horses gain substantial increase in the likelihood of survival. Horses that are infected with EPM and receive veterinary attention have a ten-time increase in the chance of improvement than horses without care.
Additionally, if horses show signs of improvement following treatment, then they are 50 times more likely to survive than those who show no positive progress. Common tests for EPM are general diagnosis tests, Western Immunoblot Test, SAG ELISAs, and Indirect Fluorescent antibody test (IFAT), and spinal tapings. General diagnosis tests use horse serum or cerebrospinal fluid (CSF) to detect the presence of EPM parasites. A positive result does not indicate active EPM; rather, it shows that the horse has been exposed to the parasite.
EPM is one of the most difficult neurological diseases to diagnose, so once detected, treatment and preventative action is necessary in ensuring the future safety of your horses.
Treatment and Prevention
EPM is one of the most difficult neurological diseases to diagnose, so once detected, treatment and preventative action is necessary in ensuring the future safety of your horses.
Most treatment plans for EPM include: a six-month administration of antibiotics and an antiprotozoal agent or a 28-day prescription of an antiprotozoal (like ponazuril) that may or may not need a second round of use. Other supportive care like immunomodulators and anti-inflammatory drugs can also be given to provide comfort and/or prevent worsening of neurological state.
Unfortunately, there is currently no approved vaccination on the market for EPM. Once a case is confirmed or even before parasite exposure, there needs to be adjustments made to the farm to decrease the likelihood of an/another EPM case. Three major areas of owner improvements to decrease EPM cases are: barn cleanliness and organization, population of humans and animals, and equine management and stress.
In the barn, limiting opossum and wildlife access to feeds, water, and bedding can be done by placing grain in sealed tight containers indoors, feeding and hanging water buckets off the ground, having stalls with doors that prevent passage underneath, and maintaining overall cleanliness to limit unwanted animals. Farms can also work to reduce the number of birds by cleaning out nests and eliminating bird feeders. Research has shown that birds can carry S. neurona infected sporophytes that can be passed to opossums upon death or even transmitted to horses (this needs further testing).
It has been noted insects, like cockroaches or flies, can also carry the EPM parasite, making barn tidiness and additional protection like fly spray great preventive approaches. Opossums are omnivores and consume dead animals, so picking up skunks, racoons, armadillos, or cat roadkill can decrease the initial spread of the parasite. Feeding dogs and cats in closed off areas as well as picking up any edible fallen fruit from plants or trees can decrease the presence of unwanted wildlife. Opossums near or around the property can also be relocated (although this is a highly debated moral issue).
High human population and farm density are known escalators of EPM. Building farms further from densely populated areas (acknowledged as not always an option) or spreading out the number of horses per farm could help decrease the presence of EPM. Efforts to coordinate less long-distance shipping and decreasing the number of shows visited per year could help prevent severe EPM development. Other stressful events for horses (like illness, pregnancy, or injury) should be monitored closely by owners because this is a time where horses are known to be more susceptible to the disease.
Even though there is no 100% effective preventative measure for EPM, knowing ways to decrease the likelihood of a case and how to treat current infections can improve future care and survival rate of horses.
Conclusion
Equine Protozoal Myeloencephalitis is one of the most challenging neurological diseases to diagnose and prevent. Understanding the complexity of the many transmission pathways of S. neurona and the life-altering implications it can cause a horse should encourage owners and riders to be more aware of changes in their animal’s behavior. By understanding the normal nature of your horse, you are becoming a better horseman by potentially identifying diseases, injuries, or disorders that could mean the difference between life and death of your animal.
AUTHOR BIO
Elle Gibbs is a first-year student at Cornell University where she is majoring in Biological Science as well as pursuing a minor in Economics and second minor in Animal Science. Her dream is to attend Cornell University’s College of Veterinary Medicine and pursue a career as an equine veterinarian.
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