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What is EPM?
EPM is a common neurological disease seen in horses throughout the
United States. Distinct lesions in the central nervous system were
first identified in the early 1960s by Dr. J. R. Rooney. In the early
1970s, Dr. J. P. Dubey identified a protozoal parasite associated with
these lesions. The protozoa was ultimately determined to be a species
of Sarcocystis and was named Sarcocystis neurona in
the early 1990s.
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How common is the disease?
Based on the detection of antibodies in the serum of horses, it is
estimated that the exposure of horses to S. neurona occurs in
about 50% or more of horses throughout the United States. Exposure
rates can approach 80–90% in the racing horse population. The
disease is reported less frequently in the arid western areas of the
country, however, due to the mobility of the horse population, it is
still found in those areas.
It is important to realize that exposure to S. neurona does not
necessarily mean that the clinical signs of disease will occur in the
horse. It is impossible to predict which horses may display
neurological signs of the disease based simply on the presence of
serum antibodies. The presence of serum antibodies only indicates that
the horse was exposed to S. neurona. The development of
clinical signs may depend on individual stress factors, the burden of
exposure to S. neurona, or the individual's immune response to
the invading organism. The detection of antibodies in the
cerebrospinal fluid (CSF) is often associated with the development of
neurologic disease.
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How is EPM transmitted?
S. neurona has a complicated life cycle that requires two hosts
for completion. Intermediate hosts include armadillos, raccoons, cats
and skunks. Because the organism reproduces in the opossum, this
animal is considered the definitive host for S. neurona.
Until recently it was thought that horses were a dead end or
accidental host for this organism, unnecessary to its life cycle.
Recent work from Michigan State University indicates that the horse
maybe an intermediate host as well.
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After infection with S. neurona, several possibilities
may occur.
- The horse may clear the organism by mounting an immune response.
- The organism may invade the central nervous system (CNS) and
divide rapidly, causing acute neurological signs.
- The organism may invade the CNS and divide slowly, causing
progressive neurological impairment.
- Unknown mechanisms of the disease may exist that will be
understood only with continuing research.
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What are the clinical signs of EPM?
An accurate diagnosis of EPM requires professional examination by a
veterinarian because the presenting clinical signs can be quite
variable. This variability occurs because the clinical signs are
related to where lesions occur in the central nervous system.
The most common clinical signs for EPM at presentation include
asymmetric ataxia and focal muscle atrophy. Atrophy of muscles in the
gluteal, or rump, area occur most frequently. Other commonly observed
clinical signs include:
- Generalized muscular atrophy or loss of condition
- Cranial nerve dysfunction
- Weakness in the rear limbs, difficulty maintaining correct leads
or subtle alterations in performance
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Which diseases might be confused with
EPM?
EPM must be differentiated from all conditions that have similiar
clinical presentations. Conditions in the horse that must be
considered and ruled out include:
- Otitis media/interna
- Lameness, vertebral problems, musculoskeletal disorders
- Cauda equina syndrome
- Cervical vertebral stenotic myelopathy
- Equine degenerative myeloencephalopathy
- Equine herpesvirus myeloencephalitis (EHV1)
- Polyneuritis equi
- Verminous myeloencephalitis
- Rabies
- Neoplasia of the CNS
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How is EPM diagnosed?
A diagnosis of EPM starts with a horse that is displaying clinical
signs of neurological disease. The differential conditions listed
above are ruled out based on the history of the horse, physical
examination, serum biochemistry and serology. A complete neurological
examination is conducted to confirm the presence of a neurological
disorder.
The neurological examination is based on a well-defined set of
parameters, such as the checklist offered by the Modified
Mayhew scale  (10 KB). The
details found during this neurological examination help the
veterinarian more closely define the location of the lesion(s).
The presence of antibodies against S. neurona in the serum and
cerebrospinal fluid (CSF) indicates exposure to the organism. EPM is
strongly suspected in horses that present with clinical signs of
neurological disease and a positive antibody response in the CSF.
Given the limited diagnostic aids available to the veterinary
practitioner, sometimes the animal's response to treatment with drugs
shown to be effective against S. neurona is necessary to
confirm a suspicious case of EPM.
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Is there currently a way to prevent or
control exposure to S. neurona?
While it is not possible to completely prevent exposure to EPM, some
common-sense approaches to controlling the disease may be helpful.
Since the causative organism of EPM is spread by opossums, preventing
access to barns by these creatures may help. Food should not be left
out where it might attract opossums to areas where the horse resides.
The heat process involved in the production of extruded feeds will
kill sporocysts of S. neurona that might be present, however,
subsequent contamination may occur if opossums have access to the
feed.
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