Equine Protozoal Myeloencephalitis (EPM)

Veterinary advice should be sought before applying any treatment or vaccine.

Equine Protozoal Myeloencephalitis (EPM)

Equine Protozoal Myeloencephalopathy

Equine protozoal myeloencephalitis (EPM) is a common neurologic disease of horses. The disease is endemic in horses living in North and South America. It is caused by the protozoan parasite, Sarcocystis neurona and less commonly Neospora hughesi. All horses are thought to be susceptible to EPM, however not all horses that are infected show clinical signs of disease. Surveys indicate that for every one horse that shows clinical signs of EPM, more than 100 horses around the United States have been exposed to S. neurona infection. In horses infected with S. neurona, the sporozoites enter the endothelial cells and replicate asexually, developing into tachyzoites, which then migrate to the animal's central nervous system. Here they slowly replicate and gradually take over the nervous system.

Clinical signs of EPM are quite varied, ranging from acute to chronic, as they depend on the severity and location of the lesions that develop in the brain, brain stem or spinal cord. Initial, early signs observed in horses with EPM often include stumbling, abnormal gait, ataxia, weakness, abnormal upper airway function, difficulty swallowing, and sometimes seizures. As the disease progresses, affected horses may have difficulty standing up, walking, or swallowing, head tilt, and facial nerve paralysis. Progression of the disease varies widely from several hours to several years. Sometimes clinical signs stabilize in the infected horses for a couple of days to weeks, prior to relapsing.

How EPM is Diagnosed


Your veterinarian will initially perform a through neurological exam on the horse, in order to evaluate all components that make up the horse's nervous system, including the brain stem, brain, and spinal cord. If the veterinarian detects neurological defects, the next step will usually include diagnostic testing for EPM. There are a number of different diagnostic tests available for EPM, which will require blood or spinal fluid. The blood tests results will only confirm that the horse has been exposed to S. neurona. This doesn't necessarily mean that S. neurona has infiltrated into the horse's nervous system. In order to confirm the presence of S. neurona in the nervous system is through testing the horse's spinal fluid, which is obtained by a board-certified internal medicine specialist through a procedure known as a cerebral spinal fluid (CSF) tap.

Transmission


Horses become infected with S. neurona by eating pasture grass, feed, hay or water that has been contaminated with feces or urine from an infected opossum. Opossums serve as the definite host for S. neurona and are a major source of infection for horses. Infected horses are not able to infect other horses and intermediate hosts are incapable of infecting horses.

The definite host and complete life cycle of N. hughesi is yet to be identified, and as such, how horses become infected is unknown. However, a related species, N. caninum uses mammals from the Canidae family as a definite host, which includes domestic dogs, raccoons, foxes, jackals, dingoes, coyotes, and wolves. Recent studies show that N. hughesi is able to be transmitted transplacentally in horses.

Incubation Period


Many horses do not show clinical signs of EPM for months to years after infection. Many horses may have been exposed to S. neurona but never develop any clinical signs of EPM.

Geographical reach


Horses living in North and South America are more at risk of infection with S. neurona and/or N. hughesi, especially horses in the United States, Brazil, and Argentina.

Symptoms

Gait abnormalities
Ataxia
Weakness
Seizures
Head tilt
Facial paralysis
Difficulty swallowing
Blindness
Muscle atrophy
Cranial nerve signs

Diagnosis

  • History
  • Clinical signs
  • Neurological exam
  • CSF Fluid Analysis
  • IFAT Panel
  • EPM Western Blot

Treatment

TherapiesDetails
FDA-approved anticoccidial drugsPonazuril (Marquis®), Diclazuril (Protazil®), and Sulfiadiazine/Pyrimethamine (ReBalance®)Reed et al., 2016
Biological response modifiersLevamisole (1 mg/kg PO q12h for the first 2 wks of antiprotozoal treatment and for the 1st week of each month thereafter), killed Propionibacterium acnes (Eqstim™), mycobacterial wall extract (Equimune® IV), inactivated parapox ovis virus (Zylexis), and transfer factor (4Life® Trasfer Factor)Reed et al., 2016
Oroquin-10A 10-day dose of oral paste medication
Supportive therapyNonsteroidal anti-inflammatory drugs, corticosteroids (0.1 mg/kg of dexamethasone once or twice a day), dimethyl sulfoxide (1 g/kg as a 10% solution IV or by nasogastric tube once or twice a day), and vitamin E (20 IU/kg daily per os)Reed et al., 2016
AntioxidantsAdministered orally in feed
Physical therapy
Nitazoxanide (NTZ)
Toltrazuril

Prevention

  • Biosecurity
  • Reduce exposure to opossum scat in and around horse pastures and barns
  • Reduce stress level in horses
  • Do not feed horses off of the ground
  • Prevent wildlife from accessing horse pastures, barns, paddocks, and stalls.
  • Provide horses with a fresh water source
  • Intermittent use of coccidiostatic and coccidiocidal drugs
  • Administering daily low dose diclazuril (0.5 mg/kg orally, once a day)

Prognosis

The annual incidence of EPM in the United States is approximately 14 cases per 10 000 horses. The reported case fatality rate is about 7% (NAHMS 2001).

Scientific Research

General Overviews

Clinical Trials

Age Range

Younger horses (3 to 4 years of age) have a higher risk of developing the disease.

Risk Factors

  • Stressful events, such as heavy training, transport, surgery, poor diet, or recovering from an injury.
  • Presence of opossums on the premises
  • Concurrent disease
  • Male Standardbred horses are more at risk of infection.
  • Horses living near wooded areas
  • Improper storage of feed
  • Racehorses and show horses

Seasonality

WinterSpringSummerAutumn