Tiffany's Place EPM - The Silent Killer of Horses By: Virginia Rushing
What Is EPM?: The History
Equine protozoa myeloencephalitis (EPM) is a progressive neurologic
disease of horses found in both North and South America. The disease
was first identified by in 1964 by J.R. Rooney, who recognized the
protozoa in spinal cord lesions in Standardbreds (Rooney as cited in
MacKay, 1997). Similar lesions were also identified by R.Macruz in
Brazil around the same time (Macruz as cited in MacKay, 1997). Since
this time, EPM has appeared in most of the lower 48 states as well as
Panama and Canada with some "unofficial" reports from Venezuela,
Argentina, and Mexico.
When this protozoa was first isolated it was thought to be Toxoplasma
gondii, a microorganism which characteristically produces lesions.
However, in 1974, J.P.Dubey (1974) was able to culture an organism
from an infected horse and found it to be Sarcocystis (Dubey (1974) as
cited in MacKay, 1997). This genus is named for its terminal
developmental stage, sarcocyst, that is found in the striated muscle (i.e.
skeletal muscle) of the intermediate host. The organism was named
Sarcocystis neurona due to the fact that it usually develops within the
neurons (EPM Seminar, University of Missouri, 1995).
Epidemiology
EPM is present only in the Western Hemisphere. In a study presented at
the 1998 EPM workshop researchers reported the age of affected horses
ranges from two months to nineteen years with the majority (60%) being
four years or less. Thoroughbreds, Standardbreds, and Quarter Horses
are the breeds most often affected while ponies are hardly ever
represented. Currently, it is thought that the S. neurona cannot cross the
placenta so mares diagnosed with EPM are not able to pass EPM on to
their foals en vitro. However, foals have tested positive after ingesting
colostrum (mother's first milk). The youngest victim of EPM was two
months old giving rise to the theory that the minimum incubation time for
S. neurona is eight weeks (University of Kentucky EPM web site, 1998).
The Protozoa
The Sarcocystis species has an obligatory two-host life cycle. There is an
herbivorous intermediate host (prey species), most commonly birds, and a
carnivorous definitive host (predator species), isolated to be the opossum
(Fenger et al., 1995). The predator host ingests the sarcocyst which in
turn sexually reproduces in the host's intestinal cells. This reproduction
results in the formation of sporocysts which are encapsulated in oocysts.
The sporocysts are freed from their thin-walled oocysts before being
passed from the predator host within feces. There is a fecal-oral
transmission from the predator to the prey host. The infectious sporocysts
are introduced to the food and water supply of the prey host through fecal
contamination. After ingestion, the sporocyst undergoes asexual
reproduction and encysts itself in the prey host tissue (Fenger et al.,
1995). It is this tissue that is eaten by the predator host and the cycle
starts again with sexual reproduction.
The life-cycle of Sarcocystis nerona does not include the horse (Hebert,
1994). Therefore, the horse can be considered a "dead-end host"
whereby the protozoa cannot be further transmitted. Equines are infected
through fecal-oral transmission as the horse consumes contaminated food
and/or water. Instead of encysting into the tissue of the horse as S.
nerona typically does in its common prey species, the sporocysts
penetrate the bowel and migrate to the brain or spinal cord where they
undergo intercellular asexual reproduction in neurons (Fenger et al.,
1995).
There is some disagreement as to the durability of the sporocysts to the
environment. More recent studies by Dubey, Speer, and Fayer (1989)
report that the organism is a mesophile - not surviving in extremes of hot
or cold. They found the sporocysts survive best at 33% humidity and can
be killed by higher humidity or drying (Dubey, Speer, and Fayer, (1989)
as cited in MacKay, 1997). In addition to freezing and thawing, the
sporocysts have also been found to be susceptible to ultra-violet
radiation, although the organism may remain viable for up to a year
(University of Kentucky EPM web site, 1998).
Finding the definitive host of this organism was essential in mapping it's life
cycle as well as curbing its detrimental effects on the equine population.
Several wild and domestic species were studied using immunoblot testing
of serum. The most probable host species were thought to be raccoons,
skunks, and opossums as they are present solely in the Western
hemisphere. Strangely enough, the skunk was the only animal to have
Sarcocystis neurona antibodies present in its serum so was thought to be
the definitive host. However, with the implementation of DNA testing, it
was found that the genes from the opossum sporocysts shared 99.9% of
the structure of those in Sarcocystis neurona (MacKay, 1997). On the
basis of this new genetic data, researchers concluded that the opossum
was determined to be the predator host of S.neurona . The skunk, first
thought to be a link in the life cycle, was found to be a victim of the
microorganism - much like the horse. This conclusion is supported further
by geographical evidence as equine EPM cases have only been reported
in the opossum inhabited areas of North, South, and Central America.
Clinical Symptoms
An estimated 30% of the horses in the United Stated have been exposed
to S. neurona, but only a fraction of these animals ever show clinical
symptoms (Herbert, 1994). Equine protozoa myeloencephalitis presents
itself in a variety of ways, but because it effects the central nervous
system, any neurological sign may be diagnostic. Spinal cord involvement
is more common than signs of brain disease (MacKay, 1997). Horses
with EPM can present with asymmetric and symmetric truncal and limb
weakness as well as ataxia which can lead to recumbency. This
incoordination is due to asymmetric atrophy of the biceps, gluteals, and
other muscles. Other possible symptoms may be degrees of rectal,
bladder and penile paralysis which present as urine dribbling. In addition
to these internal symptoms, topically, EPM lesions may cause areas of
spontaneous sweating and/or loss of reflexes to cutaneous pressure (Cain,
1995).
Coupled with these clinical symptoms, laboratory tests are implemented
to verify diagnosis. Cerebrospinal fluid is tapped from the spinal cord and
immunoblot tested for S. neurona antibodies. There has been some
concern about the specificity of this test because of the prevalence of
positive results on clinically normal animals (MacKay, 1997). These false
positives have been attributed to a transient immune response after
exposure to the protozoa. The majority of these horses prevent the
progression of the disease to neural infection (MacKay, 1997). Those
animals that do not immunologically eliminate the S. neurona develop the
clinical abnormalities listed above.
Treatment
The key to treating EPM is arresting the parasite so that the horse can get
rid of it and like anything else, quick diagnosis and immediate therapy lead
to a successful treatment. The chemical treatment employed today has a
55-60% success rate with an approximate 28% relapse rate (Herbert,
1994). Historically, EPM affected horses were treated with anti-protozoal
drugs - mainly a combination of trimethoprim/sulfonamide and
pyrimethamine. More recently, however, the use of trimethoprim has
dropped off due to its known toxicity to humans as well as its low efficacy
rate. These chemical anti-microbial treatments are administered for at
least 90 days with some clinicians recommending placing stressed animals
on intermittent treatment to prevent relapse. Nearly 28% of treated horses
relapse with treatment being notably less successful the second time. This
figure leads to the practice of treating horses until they immunoblot test
negative (Herbert, 1994).
Along with the aggressive anti-microbial therapy, antiinflammatory and
antioxidant drugs are employed to reduce swelling. Some clinical
symptoms are due partly to the horse's inflammatory response to the toxic
protozoa. Anti-inflammatory drugs, such as DMSO, are administered
during the initial stages of anti-microbial treatment to slow the disease
progression. Vitamin E is supplemented as an anti-oxidant in order to aid
in the healing of the central nervous system.
In addition to pharmiceutical treatments, homeopathic and acupuncture
strategies have been administered. These tactics have been employed with
some reported success, but there is no scientific data as to their efficacy
(EPM Seminar, University of Missouri, 1995).
Prevention
Unfortunately, there is no vaccine to help combat the prevalence of EPM,
but some measures may be taken to minimize the risk of contraction. As
an obvious initial strategy, steps should be taken to keep opossums away
from the horses. To this end, some suggestions are to make foodstuffs
inaccessible with the aim of keeping the mouse population down to a
minimum. Another alternative is to feed heat treated grains where the
sporocysts have been killed as a result of the food processing.
Conclusion
EPM can be devastating. Having personally treated many horses that
have contracted the disease, I can attest to the helplessness an owner
feels when their once healthy horse has to be put down. As with any
microbial disease, precautions employed to reduce the chances of
contraction are worth the extra effort and expense. Especially if the
alternative is to fight the disease in full course. To this end, until there is a
vaccination, owners need to be educated about the cause and symptoms
associated with EPM. If possible, researchers should attempt to design an
inexpensive and reliable test to eliminate the false positives that currently
confuse diagnoses. Ultimately, with the existing information, early
detection and aggressive treatment are essential if infected horses are to
recover.
Endnotes:
Cain, G.L. (1995). Looking for Answers about EPM; Thoroughbred
Times , September.
Fenger, C.K., Granstrom, D.E., Langermeier, J.L., et, al. (1995).
Indentification of opossums (Didelphis virginiana) as the putative definitive
host of Sarcocystis neurona; Journal of Parasitology; 81:916.
Herbert, K. (1994). Diagnosis EPM: Not a Lost Cause ; The
BLOOD-HORSE , July.
MacKay, R. (1997). Equine Protozoal Myeloencephalitis; Selected
Neurologic and Muscular Diseases, V.13, N.1.
University of Kentucky EPM website.
University of Missouri-Columbia College of Veterinary Medicine;
Seminar on EPM; as posted on their website.
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