Equine protozoal myeloencephalitis (EPM) panel
P0017 - Ultrasensitive qualitative detection and differentiation of
by real time polymerase chain reaction.
included in P0014 - equine
protozoal myeloencephalitis (EPM) is one of the most challenging
and exasperating diseases in horses, not only for veterinary
scientists but for horse owners as well. EPM is the most
commonly diagnosed neurologic disease of horses in North America
(MacKay, 1997). It occurs when protozoal parasites infect and
invade the central nervous system. EPM infection results in
characteristic lesions in the brain and spinal cord that are
evident during necropsy. The presence of these lesions
correlates well with the clinical signs generally attributed to
EPM (ataxia, muscle atrophy, etc).
availability of molecular testing, it was almost impossible to
definitively identify the causative agent and infection status
of an affected horse. If a horse showed signs of neurologic
problems, the veterinarian began a process of elimination to
determine what was NOT causing the symptoms. Traditional EPM
tests were only effective at determining that the horse did not
have EPM. If traditional EPM test results were positive, that
only definitively revealed that the horse had been exposed in
the past to the parasites that cause EPM. Testing could not show
whether the horse had an active infection by those parasites.
EPM is a long process that should begin as soon after clinical
presentation as possible. Accurate identification of the
causative agent is critical to successful treatment. Various
anti-parasitic drugs are used and generally must be administered
for several weeks to months. With proper, quick and aggressive
treatment, 60% to 70% of horses make a significant or complete
recovery. Recently an EPM vaccine has become commercially
available under a conditional license from the USDA. Studies are
underway to determine the efficacy of the vaccine.
neurona, N. caninum, N. hughesi
T. gondii are related coccidian parasites associated
with EPM. The source of infection for
N. hughesi is
unknown, whereas opossums, dogs, and cats are the definitive
hosts for S. neurona, N.
caninum and T.
parasitic organism S.
neurona is carried by a number of hosts at different
stages of its life cycle. The opossum is the major end host and
feces from infected opossums can transmit the disease to horses.
The horse is a dead end host for
S. neurona -- i.e.
the protozoa are unable to complete their life cycle in the
horse. However, they can cause severe neurological damage during
their development within a horse’s central nervous system.
Because >50% of horses show serological reactivity to
S. neurona, antibody
testing is not very effective for detecting current infections.
recently S. neurona
was thought to be the sole cause of EPM. However, a newly
identified parasite, Neospora hughesi, has now been recognized as another cause of
this disease. Both species are challenging to treat due to the
concealment of cysts in tissue, which can result in
recrudescence of infection even after treatment. Because
infections from N. hughesi,
their lesions and the actual parasites are so similar to
S. neurona, it is
likely that some N. hughesi
infections have been mistaken in the past for
infections. However, Serological prevalence of
N. hughesi is relatively low at 6.5%
is also a recently discovered, apicomplexan, coccidial protozoan
that causes abortion in many mammals including cattle, goats,
horses and sheep. Some evidence also indicates association of
this organism with neonatal neurological and neuromuscular
disease in mammalian species including horses. 31.1% of horses
show serological reactivity to
and N. caninum are very similar in their genomic organization and
biochemical characteristics, making clinical differentiation of
the two species very difficult. Clinical differentiation of
S. neurona from N.
hughesi/caninum is also difficult, as the range of
symptoms overlap broadly. Although
N. caninum seems to
have wide serological prevalence, EPM cases are most often
attributed to S. neurona.
is prevalent in many species of domestic and wild animals (Dubey,
1993). However, a recent serological study of 276 horses in
central Wyoming (Dubey et al., 2003) indicated that the
serological prevalence of T. gondii was less than 1%, suggesting
that this parasite is a relatively infrequent cause of EPM in
PCR is the
most specific and sensitive method available for detection and
Sarcocystis neurona, Neospora hughesi, Neospora caninum
and Toxoplasma gondii.
This testing technique is vital to correctly identifying these
EPM pathogens in affected horses.
Help confirm the disease causing agent
Shorten the time required to confirm a clinical
diagnosis of EPM.
Determine proper EPM treatment regimen
Help ensure that animal populations are free of organisms
Early prevention of spread of these organisms
Minimize personnel exposure to these organisms
Safety monitoring of biological products that derive
from horses and other host animals
Dubey, J.P. (1993) Toxoplasma, Neoplasma, Sarcocystis, and other
tissue cyst-forming coccidian of human and animals. pp1-56. In:
Parasitic protozoa (Kreier, P.J. ed), vol. 6, 2nd ed., Academic
Press, Inc., San Diego, California.
Dubey, J.P. and Lindsay,
D.S. (1998) Isolation in immunodeficient mice of Sarcocystis
neurona from opossum (Didelphis virginiana) faeces, and its
differentiation from Sarcocystis falcatula. Int. J. Parasitol.
Dubey, J.P., Lindsay, D.S., Saville, W.J.A.,
Reed, S.M., Granstrom, D.E. and Speer, C.A. (2001) A review of
Sarcocystis neurona and equine protozoal myeloencephalitis
(EPM). Vet. Parasitol. 95: 89–131.
Fenger, C.K., Granstrom,
D.E., Langemeier, J.L. and Stamper, S. (1997) Epizootic of
equine protozoal myeloencephalitis on a farm. J. Am. Vet. Med.
Assoc 210: 923–927.
NAHMS (2001). Equine Protozoal
Myeloencephalitis (EPM) in the US. APHIS:VS, CEAH, National
Animal Health Monitoring System. USDA, Fort Collins, CO.
Saville, W.J.A., Reed, S.M., Granstrom, D.E., Hinchcliff, K.W.,
Kohn, C.W., Wittum, T.E. and Stamper, S. (1997) Prevalence of
serum antibodies to Sarcocystis neurona in horses residing in
Ohio. J. Am. Vet. Med. Assoc. 210:519–524.
Stich, R.W., Dubey, J.P., Reed, S.M., Njoku, C.J., Lindsay,
D.S., Schmall, L.M., Johnson, G.K., LaFave, B.M. and Saville,
W.J. (2003) Epidemiology of Sarcocystis neurona infections in
domestic cats (Felis domesticus) and its association with equine
protozoal myeloencephalitis (EPM) case farms and feral cats from
a mobile spay and neuter clinic. Vet Parasitol. 117:239-49.
Specimen requirements: 0.2 ml whole blood in EDTA (purple top) or ACD (yellow top)
tube, or 0.2 ml cerebrospinal fluid, or 0.2 ml fresh, frozen or
fixed brain tissue.
types other than those listed here, please call to confirm
specimen acceptability and shipping instructions.
specimen types, if there will be a delay in shipping, or during
very warm weather, refrigerate specimens until shipped and ship
with a cold pack unless more stringent shipping requirements are
specified. Frozen specimens should be shipped so as to remain
frozen in transit. See shipping
instructions for more information.
3 business days
Qualitative real time PCR