Equine protozoal myeloencephalitis (EPM) is a parasitic infection of horses caused by Sarcocystis neurona that can result in devastating neurologic disease. Infection with S. neurona can also cause a neuromuscular disease that doesn't result in destruction of neurological tissues, and this is treatable. Diagnosis and treatment of EPM require a distinction between EPM and non-brain associated S. neurona infections, sarcocystosis.
EPM has a poor prognosis for getting a horse back to use if parasites occupy the brain and spinal cord (CNS). The damage isn't reversible. However, we realized that neuroinflammation can result in clinical signs that look like EPM. The parasite didn't ever get into the central nervous system. Signs were caused by the inflammation from the parasite infection. When we treated the inflammation and the parasitic infection, the horses got better. We found that sarcocystosis is a highly treatable disease.
Equine protozoal myeloencephalitis is a clinical diagnosis made by a veterinarian. The disease EPM means that parasites are in the brain tissues. Detection of antibodies against Sarcocystis neurona enhance the probability that the infection is due to neurona. Lameness and other causes of neurological disease should be excluded, for the most part these are treatable diseases. EPM is rare in horses. However, Sarcocystis infections that result in antibody but not parasite entry into the CNS are common.
Sarcocystis neurona causes infections in horses. The horse is an unnatural host for the parasite. An infection results in immune responses. Infections are usually resolved without clinical signs!
Some horses do get clinical signs associated with S. neurona infections. Three clinically relevant EPM issues are the pathogenesis of disease in the horse (does the parasite get into the central nervous system), diagnosis (what do the diagnostic tests indicate), and treatment of the inflammatory component of disease.
Sensitive molecular based studies showed that the opossum was the definitive host of S. neurona. These same techniques later confounded diagnostic tests, the methods were just too sensitive! It is generally accepted that horses are dead end or aberrant hosts because sarcocysts (cysts in muscles are the end result of infections) from S. neurona have not been identified in horse muscle tissue. The horse is an natural host for Sarcocystis fayeri, this organism completes it's life cycle forming cysts in horses muscles. Both organisms can make horses ataxic or wobbly, but these infections are treatable.
None of the experiments using challenge models (from infectious material derived from opossum feces) result in merozoites in the CNS. The entire set of S. neurona horse-challenge experiments did prove inflammation was the cause of clinical signs. We showed that a (autologous leukocyte-merozoite challenge model) parasite can result in brain infections. A likely method of travel from the gut to the brain is by hitching a ride in a leukocyte, the gist of our model. The effects of inflammation in the merozoite model are clinically relevant because inflammation is a treatable part of the disease syndrome.
The presumptive diagnosis of EPM is based on detection of antibody to certain antigens of S. neurona in a horse with clinical signs of neuromuscular disease. Major surface antigens (SAG’s) have taken a central role in commercially available tests. It is important to understand the differences in SAG’s and the information they provide. The horse responds to infection using both immunity (antibody) and inflammation (innate immunity mediated through cytokines). Inflammation is a key issue in the disease process but had played no role in disease management until the use of CRP testing.
Normal anti-inflammatory agents, NSAID's, don't treat the right inflammatory pathway stimulated by Sarcocystis. The inflammation is treatable with the right drugs. Successful outcome in horses with "EPM" is correctly diagnosing the disease and treating for the treatable.