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Equine Protozoal Myeloencephalitis

September 23, 2020 4 min read

Equine Protozoal Myeloencephalitis

Of the myriad diseases that may impact the health of a horse, one of the most difficult to diagnose and successfully treat is that of Equine Protozoal Myeloencephalitis (EPM).  The single-celled organisms that cause this debilitating disease are the protozoal parasites Sarcocystis neurona and Neospora hughesi.  In 1968, veterinarians first described the condition now known as EPM, and in the 1970s, researchers first identified protozoa as the causative agent of this debilitating disease.  Sarcocystis neurona was ultimately determined to be a specific cause of EPM in the 1990s.  As there currently remains a lot unknown about Neospora, this discussion will focus primarily on the infectious pathway, clinical signs, diagnosis and treatment of Sarcocystis.

More than 50 % of all horses in the U.S. have likely been exposed to Sarcocystis, which can lead to infection with mild to severe clinical signs and can often mimic other health problems.  Of those horses exposed, approximately 1% develop clinical signs.

Sarcocystis protozoa are spread by the definitive host, the opossum, which acquires the organism from consuming the infected tissues of an intermediate host such as cats, raccoons, skunks, armadillos and potentially even otters and harbor seals.  The organism develops to the infective sporocyst stage within the opossum, and is then passed on via its feces.  Horses ingest the infected feces as they graze or consume contaminated feed or drinking water.  After the protozoa are ingested, they migrate from the intestinal tract into the bloodstream and  ultimately cross the blood-brain barrier where they attack the horse’s central nervous system.  

The extensive list of clinical signs of EPM may be acute or chronic, with severity being dependent upon the location of the parasitic lesions within the central nervous system--the brain, brain stem, or spinal cord.  Signs of infection are often asymmetrical and may include ataxia (incoordination), lameness or abnormal gates, and stiff or stilted gates.  Additionally, incoordination and weakness which are exacerbated by going up or down slopes with the head elevated is often seen.  Poor balance with a wide-based standing position,  muscle atrophy, especially along the topline and large muscles of the hind end, and occasionally the face and front end may be clinical signs.  Cranial nerve deficits such as head-tilting, paralysis of the muscles of the eyes or mouth and dysphagia (difficulty swallowing) can be seen.  Seizures, abnormal sweating, and loss of sensation along the face, neck or body, as well as behavioral changes are also possible effects of this parasitic infection.

The rate of progression and ultimately the severity of the clinical signs are ultimately dependent upon four main criteria:

How heavy the infestation is (how many organisms are ingested)

How long treatment is delayed following onset of infection

The location within the central nervous system where the organisms create lesions

Any stressful events which occur following the onset of infection

While almost every part of the U.S. has reported cases of EPM, the incidence of the disease is much lower in the western states in areas where few opossums reside.  All horses are at some risk of exposure however, due to transport of horses and feed from one part of the country to another.

Exposure to Sarcocystis Neurona can have a variety of outcomes depending upon the individual horse.  Some horses that are exposed successfully mount a strong immune response and are able to combat the disease prior to the organism establishing itself in the body.  Other horses with less efficient immune systems, those that have a preexisting infection of another organism, or that are undergoing stress can be severely debilitated.  A third category of horses may harbor the organism for months to years and eventually begin to show clinical signs at a later date.

Because the clinical signs of EPM mimic a variety of other neurologic diseases, and because there is no specific laboratory test to accurately diagnose the disease, it is often very difficult to identify the presence of the protozoa.  The most accurate method of diagnosing EPM following a thorough physical exam (including a neurologic evaluation) is via a paired analysis of blood and cerebrospinal fluid (CSF).  A positive result only indicates that the horse was exposed, not necessarily that an active infection is present.  In the presence of positive test results paired with clinical signs, treatment should be initiated immediately.

A therapeutic protocol should be devised by a veterinarian.  There are a number of FDA-approved anti-protozoal drugs available for treatment, as well as a variety of non-approved drug combinations.  The treatments generally have a duration of at least 28 days, but may last up to 3-6 months,  It is essential that the horse be closely monitored for the entire treatment period to ensure that negative side effects such as anemia do not occur.  Antiinflammatories, Vitamin E as an antioxidant, and other adjunctive treatments may be prescribed by the veterinarian.  A quality probiotic is also essential to ensure gut health and provide support to the immune system during treatment.  Minimizing environmental stress is also a key to the treatment plan.

There is unfortunately no guarantee that even an aggressive treatment plan will result in full recovery.  Approximately 60-70% of treated horses have significant to complete recovery and are able to return to normal activity; however, not all horses respond well to therapy, with up to 20% of patients suffering a relapse at some point.

Research for better diagnostic tests as well as more effective and less expensive treatment options is ongoing.  It is in every horse owner’s best interest to establish good husbandry practices in order to minimize the risk of exposure to this organism.  Keeping feed rooms and containers sealed, using feeders which minimize spillage and prevent wild animals access, cleaning up any spilled grain immediately, and ensuring that drinking water is fresh and clean are all simple preventive practices.  Ultimately maintaining healthful diet, exercise, deworming and veterinary programs for all horses in a barn will go a long way to helping reduce the risk of infection  should exposure to this organism occur.

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