EPM in Horses
Equine protozoal myeloencephalitis (EPM) is the most prevalent cause of neurologic disease of horses in the Americas (North, Central and South America). It is an extremely serious disease that can be difficult to diagnose due to the fact that its presentation often mimics other equine health disorders.
It is estimated that over half of the horses in the U.S. have been exposed to Sarcocystis neurona, the protozoal parasite that causes EPM. This takes place as a result of horses ingesting food or water that has been contaminated with feces from the opossum (Didelphis virginiana), the definitive host of S. neurona. The feces of the opossum contain the infective sporocysts of the protozoan. Thus, in areas where the opossum is common, approximately 50% of horses will be seropositive for S. neurona, indicating exposure to the organism.1
In less than 1% of exposures, the ingested sporocysts migrate from the horse’s intestinal tract into the bloodstream and cross the blood/brain barrier, causing disease by attacking the horse’s central nervous system.2 The S. neurona protozoa cannot be transmitted from one horse to another.
A few cases of EPM have been associated with N. hughesi, another protozoal parasite, rather than S. neurona. The life cycle, natural hosts, and modes of transmission of N. hughesi are poorly understood; affected horses may not show clinical signs, or may display clinical signs consistent with those caused by S. neurona. Infection with N. hughesi has also been associated with abortions and neuromuscular disease. Transmission from N. hughesi-infected broodmares to their offspring has been reported, but few offspring develop clinical signs in these instances.1
Both S. neurona and N. hughesi are members of the phylum Apicomplexa, a group of pathogens that are found worldwide, and include the protozoa that cause malaria and toxoplasmosis (the zoonotic disease notorious for putting human pregnancies at risk for premature birth and birth defects, and most commonly when pregnant women are exposed to infected cat feces).3
EPM Symptoms
The onset of EPM can be slow or sudden. If left untreated, it can cause devastating and permanent neurological damage. The clinical signs of EPM can vary greatly, and are typically asymmetrical (presenting differently on either side of the horse). It is believed that these signs are contingent upon the location and severity of the lesions that develop in the brain, brain stem or spinal cord.1 These signs can include:
- Ataxia (poor coordination), spasticity (stiff, jerking movements), lameness or an abnormal gait
- Weakness that tends to worsen under exercise
- Muscle atrophy
- Paralysis of muscles of the eyes, face or mouth (evidenced by drooping eyes, ears or lips)
- Difficulty swallowing
- Seizures
- Excessive sweating;
- Loss of sensation
- Head tilt and poor balance
The literature holds that several factors can influence the progression of clinical cases of EPM, with extent of the infection, length of time infected, area of infection (within the brain or spinal cord) and external stressors.1,3 Almost every region in the continental U.S. has reported cases of EPM, however, the incidence of clinical cases is much lower in areas with small opossum populations, such as the southwestern United States.
As indicated above, very few horses exposed to the S. neurona protozoa will develop clinical disease. Most horses appear to mount an effective immune response and are able to eradicate the protozoa before they gain a foothold.3 Some horses succumb rapidly to the debilitating effects of EPM, while others can harbor the parasite for months or years and subsequently develop symptoms slowly or quickly.
Given the popularity of horses in the Americas and the numerous industries which depend on the participation of horses to varying degrees, researchers and veterinarians have committed to discovering as much as possible about S. neurona—how the protozoan affects the horse and physiological responses to the parasite—so that can more effective methods of diagnosis and treatments may be developed. In addition to this, researchers are examining how coinfections with other pathogens might influence the development of EPM.
Finally, researchers are carefully examining why most horses in the Americas have been exposed to S. neurona, yet just a tiny fraction of these horses develop the disease. Their belief is that solving this riddle might reveal the mechanism by which clinical infections might be prevented. Practicing equine veterinarians often see cases of horses that relapse within a few months of therapy, while others seem to completely recover. Many of these veterinarians strongly believe that there is a direct connection with the initial immune response to the S. neurona protozoan.3
EPM Diagnosis
Apart from the difficult-to-interpret symptoms, diagnosing EPM is difficult because there is no specific assay for the disease.2 The veterinarian will first conduct a thorough physical examination to assess the horse's general health and identify any suspicious signs. If the veterinarian suspects EPM, they may order blood and cerebrospinal fluid (CSF) analysis.1,3 Cerebrospinal fluid is collected via a needle inserted into the spinal canal at the lower back or at the poll.1 There are risks associated with this procedure that should be discussed with the veterinarian ahead of time; a positive blood test only means the horse has been exposed to the parasite, not that it has or will develop clinical disease.
Cerebrospinal fluid can also be tested for the S. neurona organism, though any contamination of the sample with blood can lead to a false positive result. CSF can be safely collected from a standing horse, but sample contamination is more likely. Unfortunately, CSF in normal horses has also been found to contain antibodies to S. neurona.4 Thus, positive CSF tests can be difficult to interpret with certainty.
EPM Prevention
Since horses are usually exposed to S. neurona via ingesting feed or water containing opossum feces, reducing the chances of opossum feces being present in food and water sources is critical. Making stables and feeding areas less hospitable to opossums is a prudent measure, as well as preventing them from accessing feed and water if they do gain access. No animal feed should be left out in areas in which horses are housed, and open feed bags and garbage should be kept in closed, secure containers.4 Fallen fruit and waste food items are extremely attractive to opossums, so areas frequented by horses should be regularly policed for such items. Outbuildings on the property can also serve as attractive hiding places for opossums and other nuisance animals. Opossums themselves can also be trapped and relocated if these fail to discourage them from frequenting a particular location.1,4
EPM Treatment
Vitamin E supplementation is also frequently recommended by equine veterinarians for horses diagnosed with EPM. This vitamin is important for healthy nerve function, and it also serves as an antioxidant to reduce free-radical damage. These medications can be obtained in combination through veterinary compounding pharmacies in concentrations that are optimal for the treatment and prevention of EPM in horses, and are generally available in paste and injectable forms.
1Reed, S. M., Furr, M., Howe, D. K., Johnson, A. L., MacKay, R. J., Morrow, J. K., Pusterla, N., & Witonsky, S. (2016). Equine Protozoal Myeloencephalitis: An Updated Consensus Statement with a Focus on Parasite Biology, Diagnosis, Treatment, and Prevention. Journal of veterinary internal medicine, 30(2), 491–502.
2MacKay, R., et. al. Equine Protozoal Myeloencephalitis, Veterinary Clinics of North America: Equine Practice, Volume 16, Issue 3, 2000, Pages 405-425.
3Dubey, J.P. & Lindsay, David & Saville, William & Reed, Stephen & Granstrom, David & Speer, C.A.. (2001). A review of Sarcocystis neurona and equine protozoal myeloencephalitis (EPM). Veterinary parasitology. 95. 89-131. 10.1016/S0304-4017(00)00384-8.
4Alderman, L., DVM. EPM and How to Prevent it. (2016) In: irongateequne.com. https://www.irongateequine.com/education/epm-and-...
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