Equine neurological PCR panel
P0014 - Equine neurological PCR panel includes qualitative
detection and differentiation of:
are subject to a number of neurological disorders, most symptoms
are due to infection by Eastern Equine Encephalitis (EEE) virus,
Western Equine Encephalitis (WEE) virus, Equine Herpes Virus
type I (EHV-1), West Nile Virus (WNV), Sarcocystis neurona,
Neospora hughesi, Neospora caninum and Toxoplasma gondii (the
last four often referred to collectively as Equine Protozoal
Myeloencephalitis or EPM).
EEE and WEE
are transmitted by mosquitoes. Infected horses may exhibit
somnolence, lethargy, ataxia, incoordination, recumbency or
death. Diagnosis is based on blood or cerebrospinal fluid
testing, or by postmortem examination of the brain. There is no
treatment for these diseases and affected horses are managed
symptomatically. Although some horses recover from these
diseases, many are eventually euthanized. Vaccines are available
and are generally effective. Young foals need special attention,
as their immature immune systems cannot yet develop immunity in
response to vaccines. Mosquito control is also an important
aspect of prevention.
usually manifests as a respiratory disease, but can occasionally
mutate to a form that affects the nervous system. Infected
horses may develop symptoms such as weakness or paralysis of the
hind legs giving rise to the "dog-sitting" position, loss of
tail and anal tone, inability to urinate or defecate, urine
dribbling, cranial nerve deficits, recumbency, and death. No
specific treatment is available for EHV-1, but general
supportive therapy and care can aid recovery of affected horses.
Anti-inflammatory agents may be helpful in minimizing damage to
the spinal cord. The human drug acyclovir was used in a recent
EHV-1 outbreak in Ohio, and efficacy of this treatment seems
WNV is a
mosquito borne virus first identified in the USA in 1999. The
virus affects the horse’s central nervous system, causing a
range of symptoms including somnolence, violent behavior, toe
dragging, recumbency, hypo- or hyper-sensitivity to sound,
touch, or light, falling down on the front knees in a “prayer
position”, single limb lameness, and fever. A fever is not
always detected before neurological signs appear. Treatment is
symptomatic. Approximately 50% of horses survive the infection
and survival is not highly correlated with severity of symptoms.
An effective WNV vaccine is now available.
N. caninum, N. hughesi and T. gondii are 4 related coccidian
parasites associated with equine protozoal myeloencephalitis
(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. gondii, respectively.
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 not a
major cause of EPM in horses. Serological prevalence of N.
hughesi is also low at 6.5%. In contrast, 31.1% of horses show
serological reactivity to N. caninum and >50% of horses show
serological reactivity to 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
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.
symptoms of EPM include asymmetrical ataxia, toe dragging,
circumduction of the hind limbs, hypermetria, and less
frequently recumbency and cranial nerve deficits. In the past,
definitive diagnosis of EPM in horses was quite difficult. Since
many horses have been previously exposed to one or more of these
parasites, serological testing does not yield a definitive
diagnosis of current infection. Nearly 90% of horses in some
populations have positive antibody titers. Cerebrospinal fluid
(CSF) sample may be tested, but false positive result occurs
frequently because even a few blood cells contaminating the CSF
sample can result in false positive signal. A very clean sample
is therefore necessary.
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.
detection and identification of equine neurological viruses and
parasites is highly sensitive and specific. In particular,
PCR-based molecular techniques are more useful than
immunological methods in testing cerebrospinal fluid or brain
tissue biopsies. Furthermore, serological testing is of little
use in diagnosing active infection in an animal that has been
previously exposed to these pathogens; PCR is a more appropriate
testing technique for this application.
Help confirm the pathogen causing generalized neurological
Selection of appropriate treatment regimen
Shorten the time required to confirm a clinical
Help ensure that horse populations are free of listed
Early prevention of spread of listed neurological
Minimize personnel exposure to listed neurological
Safety monitoring of biological products that derive
Preferred samples: 0.2 ml cerebrospinal fluid, or 0.2 ml fresh or frozen brain
preferred sample: 0.2 ml whole blood in EDTA (purple top) or ACD (yellow top)
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
real time PCR and qualitative reverse
transcription coupled real time PCR