EQUINE PROTOZOAL MYELOENCEPHALITIS


EPM Disease Summary  

EPM has is generally described as debilitating, but not painful to the horse.  It is not contagious between horses.  For the owner it can be elusive, confusing, frustrating, costly, and the cause of many gray hairs.

The disease is caused by one of two protozoa, Sarcocystis neurona or Neospora hughesi.  Almost all infections are caused by S. neurona, so this name is used throughout the web site.  Both infections are treated with the same drug protocols. 

The life cycle of S. neurona is dependant upon the opossum.  This makes the disease naturally occurring only where the opossum lives, North and South America.  A horse becomes infected by ingesting the protozoa in feed, hay, pasture or water contaminated with opossum feces.

© Amanda Manfredi photograph 'On the Fence'
   © Amanda Manfredi  On The Fence
In many of the infections, the horse can mount an immune defense and clear the protozoa from the blood before it crosses the blood brain barrier.  The horse may carry an antibody to the protozoa for life.  This is referred to as exposure to EPM, and is not an active infection.  Exposure to the EPM protozoa will not cause neurological symptoms.

In many of infected horses, the protozoa are able to cross the blood-brain barrier, and infect the central nervous system (CNS).  They live inside of cells in the CNS, and are not detected by the immune system.  Stressful events such as injury, extensive trailering, show schedule, pregnancy, or poor nutrition can suppress the immune system allowing the infection to flourish.  As the protozoa reproduce, they break out of the host cell, and spread to other areas in the brain or spinal column.  Protozoa activities cause lesions to form in the CNS creating the visible neurological symptoms.

Researchers cite the incubation period of EPM as weeks to two years, until outward symptoms appear.  The sooner the disease is diagnosed and treated, the better the prognosis.  Left untreated, the symptoms generally progress until the horse is recumbent, and most untreated cases end in death.

Rates of Exposure

The local opossum population rate has a significant effect on the number of horses exposed to the protozoa.  Not all opossums carry the protozoa.  Equines testing positive for Sn SAG1exposure in the United States vary by geographic location, but average around 11%.  The previous studies performed with the Western Blot test showed 50 to 90% exposure, and this is because the test cross reacts with Sarcocystis that do not cause EPM.  The old figures that only 2% of the exposed horses get EPM is incorrect.  The exact numbers are hard to determine, and are based on the strain that infects the horse.

Exposure rates can vary by barn within a geographic region.  Because exposure to the protozoa is through feed and water, it is not uncommon that a rate in a specific barn is higher than the surrounding area.  Rates of active infection in a stable could be due to a hectic show schedule – EPM is not infectious between horses.

Active Infections

Researchers do not know why some horses can effectively fight the protozoa, while others become actively infected.  Almost all breeds of horses have been infected, and all genders are susceptible.  Horses as young as six months and into their 30’s have been infected with EPM.

 After a horse has ingested the protozoa, it travels through the digestive tract, and enters the bloodstream.  If the horse’s immune system does not clear the protozoa from the blood, it can cross the blood brain barrier.  Researchers do not know with certainty how the protozoa crosses; however, theories include its ability enter leukocytes, and cross the barrier inside of these cells.  Another theory questions if the blood-brain barrier has been damaged by disease or drugs, which allows the protozoa to cross.

The protozoa live within cells (intracellular) in the CNS, reproducing very slowly.  The horse’s immune system is not able to detect protozoa while it is inside of other cells.  A stressful event is thought to trigger rapid reproduction and the protozoa begin to break out of the host cells.  They move along the CNS, and enter other cells.  There the reproduction starts again.

In the process of exiting the cell, the protozoa kill the host cell.  Areas of killed cells are lesions in the CNS.  As the lesions grow, they impede the transmission of signals from the brain to muscles, and from muscles to the brain.  Lesions in the brain can cause behavior changes in the horse.  The infection also causes inflammation, or swelling, of the CNS.  Inflammation of the CNS can be just as destructive to nerves as the infection.

As the damaged areas of the CNS increase, the horse generally finds ways of compensating for the loss of feeling in a muscle.  The immune system may fight the disease for months, with the only outward sign being a slight tiredness or occasional stumble.  The outward signs become apparent to humans when the horse can no longer compensate, and the neurologic symptoms appear.

The infection in the CNS requires remedies that can cross the blood-brain barrier to combat the protozoa.  The four drugs listed under treatment have this ability.  Other drugs or remedies may be able to kill the protozoa in the blood, but leave the active infection raging in the CNS.

New Research

New molecular tools have allowed study of S. neurona at a fine level.  35 strains have been identified, which fall into three phenotypes:  SnSAG1, SAG5, and SAG6.  SnSAG6 has only been found in Sea Otters, not in horses.  OSU used a SAG5 strain to infect horses, and had difficulty achieving active infection, and the horses showed mild transient symptoms.  National Institutes of Health is conducting studies on Sn, and has found that SnSAG1 has a 3-D crystalline structure, indicative of virulence in other species.  S. falcatula and S. fayeri may cause mild transient neurological symptoms, which could be confused with EPM.  The treatment protocol for these two Sarcocystis would be different.

December 2011

References:

AAEP Proceedings, Vol 54, 2008

Vet. Parasitol. (2010), doi:10.1016/j.vetpar.2009.12.020

 

Photograph 'Patches' LOC Patches