EPM: The devil is in the diagnosis

EPM: The devil is in the diagnosis

Nov 01, 2009

Photo 1: This horse was diagnosed and treated successfully for EPM but suffered severe muscle loss on the right side of the rump involving the gluteal muscles. The nerve damage to these muscles is permanent; they cannot regrow.(Photos: courtesy of Dr. Kenneth L. Marcella)
Equine protozoal myelo-encephalitis (EPM) has been a prominent neurological disease of horses for nearly 15 years. During this period, numerous bits of information have emerged about the causative organisms, their lifecycles, hosts and transmission. The veterinary community has made significant advances in the areas of treatment and rehabilitation.

The problem, however, is that EPM seems to remain as difficult to diagnose accurately as it ever was. EPM has been called "the great imitator" because it can present in many ways with varying clinical signs of differing intensities.

Photo 2: A thermography scan of a horse with an active EPM infection shows cooler (bluer) muscle on the right side of the hip and rump, indicating a reduction of nerve stimulation and resulting decrease in blood flow and activity to these muscle groups.
There are numerous tests available but even these have limitations. Currently, "there is no perfect test for EPM," says Dr. Sharon Witonsky of the Equine Field Service group at the Virginia-Maryland Regional College of Veterinary Medicine.

EPM is a disease of the central nervous system caused by protozoal organisms. The majority of cases are caused by Sarcocystis neurona but recent work has shown some horses are affected by Neospora hughesi, another protozoan closely related to Neospora caninum. Similar clinical signs are seen with both organisms. The main host for S. neurona is the opossum (the definitive host for N. hughesi is not yet known), and horses are infected through the consumption of contaminated water and/or feed and hay.

Other hosts for these protozoan organisms have been implicated as possibly contributing to this disease and include armadillos, skunks and cats. Once S. neurona or N. hughesi enter the horse, they migrate to the central nervous system and can cause inflammation and damage anywhere in the brain and spinal cord. This fact leads to the varied and often confusing array of clinical presentations of EPM.

Horses with EPM can exhibit ataxia (incoordination) that can range from subtle to profound. They can show spasticity evidenced by stiffness or lack of fluidity in movement with stilted, slow or awkward limb placement, abnormal gaits and lameness. This incoordination can become worse when the head is lifted, and the gait abnormality or weakness is accentuated when the horse is walked up or down slopes.

Because damage to the spinal cord results in a "disconnect" to peripheral nerves, muscle atrophy is seen with EPM. Again, because the damage to the cord is random based on the para-site's movement, the muscle loss seen in EPM generally is asymmetrical and can vary in location and amount.

The muscles of the hindquarters and top line seem to be the most commonly affected or noticeable, though cases involving the neck, shoulder, forelegs and even the facial muscles have been reported. Other more subtle signs also can be encountered with EPM. Paralysis of the muscles of the face, eyes or mouth can be seen with associated drooping of the ears, eyelids or lips. Horses can have difficulty swallowing or breathing due to lack of nerve stimulation to muscles of the throat, larynx and associated structures.

Horses can exhibit only mild signs like abnormal sweating, head tilt or abnormal mentation, loss of sensation in various body parts, or the signs may be severe such as seizures and collapse. It is easy to see that EPM can have a wide variety of presentations that cause the practitioner problems when trying to accurately diagnose this disease.

Other signs to consider

There are other causes of neurological signs in the horse that should always be considered and either ruled in or out when progressing through the work-up of a potential EPM case. Fortunately, many of these other conditions have very accurate tests available and usually can be diagnosed more easily then EPM.

Eastern, Western and Japanese encephalitis and equine herpes virus can cause similar clinical signs but good titer tests are available.

West Nile viral infection can mimic many EPM signs, but a simple blood titer test will provide confirmation of this diagnosis.

Botulism, lower motor neuron disease, rabies, "wobbler syndrome" and a few lesser-seen conditions such as some toxins, tumors and trauma also may present with EPM-like signs, but history, disease progression and other tests (titers, radiographs/myelogram, additional blood values) usually help the clinician differentiate between these causes of neurological disease.

This leaves EPM as a "back-door" diagnosis in many cases. Additionally, EPM has become an all-too-common diagnosis for muscle weakness, poor balance, poor performance or behavioral issues in sport horses, even without any other evidence of neurological signs.

Many times, owners, trainers and even veterinarians evaluating the weak, imbalanced or poorly performing sport horse seize upon an EPM diagnosis and initiate treatment based on vague signs and without a definitive diagnosis.

Yet here is the problem: Definitive EPM diagnosis sill remains difficult, especially in the early stages or in cases with mild, vague or subtle clinical signs.

"There is no excuse, however, for not doing a thorough physical examination and working your way through an appropriate problem list when dealing with a potential EPM case," according to Mark Chrisman, DVM, Dipl. ACVIM, of the Department of Large Animal Clinical Sciences at the Virginia-Maryland Regional College of Veterinary Medicine. This work-up should involve a complete physical exam, the importance of which cannot be overstressed, with appropriate tests for some possible alternative diagnoses as well as tests for EPM.