Equine Herpesvirus 1 Myeloencephalopathy
Multifocal hemorrhagic myeloencepha-lopathy with
leptomeningealvasculitis can be caused by Equine Herpesvirus
Type 1 (EHV-1) and, although outbreaks are still rare, the
frequency of occurrence has been increasing. The virus has
a worldwide distribution and outbreaks can have up to 40%
morbidity and 90% mortality.
There are four distinct herpesviruses known to
cause disease in horses; EHV-1 (equine abortion virus), EHV-2
(equine cytomegalovirus), EHV-3 (equine coital exanthema virus)
and EHV-4 (equine rhinopneumonitis virus). It was once thought
that EHV-1 and 4 were a single virus able to produce early
neonatal death, abortive, respiratory, and neurologic disease.
However, it has recently been shown that there are two distinct
viruses with only 20% corresponding DNA sequences and substantial
antigenic site differences. Transmission of the virus occurs
by direct contact, inhalation of contaminated aerosol secretions,
and fomites. It can maintain environmental infectiveness
for up to 14 days, and up to 42 days on suitable vectors,
such as horse hair. The predisposition for the outbreak of
the neurologic form of EHV-1 infection is not well understood,
but often presents in association with outbreaks of abortion
and respiratory disease. While any animal is capable of contracting
the disease, pregnant mares in the first two trimesters of
gestation seem to have an increased risk. After replicating
in the respiratory epithelium and disseminating to lymphoid
tissue, the virus is spread systemically via infected monocytes
and lymphocytes. In the short duration of viremia, replication
occurs in vascular endothelial cells. The vasculitis of arterioles
in the brain and spinal cord are responsible for the clinical
signs, which are often an acute onset of symmetrical ataxia
and paresis. Neurologic signs progress rapidly for about
2 days, then stabilize. Because the lesions of the spinal
cord are more likely to cause clinical signs, neurologic deficits
are more predominant in the hindlimbs with many cases showing
caudaequina syndrome (urinary incontinence, hypotonia of tail
and anus).
A current theory surrounding EHV-1 myeloencephalopathy
is the belief that the disease may be due to immune-complex
induced vasculitis rather than direct viral infection. This
is supported by the resemblance of the characteristic vascular
lesions to type III hypersensitivity, and the presence of
immune complexes correlating to high levels of antibody at
the onset of clinical signs. This theory is by no means absolute,
as various flaws exist in attempts to prove it experimentally.
Antemortem diagnosis of EHV-1 myeloencephalopathy
is often unsuccessful. Cerebrospinal fluid evaluation often
reveals xanthochromia (due to denatured heme pigment), elevated
protein (>80 mg/dl, and as high as 300 mg/dl), yet a normal
nucleated cell count (<8 cells/ul). It should be noted
that EHV-1 can alter the blood brain barrier and when serum
concentration of equine protozoalmyeloencephalitis (EPM) antibody
is high there may be a passage of EPM antibodies into the
CSF, causing a horse to falsely test positive to EPM. IgG
index and albumin quotient assessments can be used to detect
such invalid diagnoses. Isolation of the virus from CSF can
be difficult due to the short viremic stage, and isolation
from other tissues such as blood (collected with sodium citrate)
or respiratory tract (collected by nasopharyngeal swab) may
be helpful. Polymerase chain reaction (PCR) technique of
tissue samples shows promise for increased sensitivity for
diagnosis compared to virus isolation. Paired serum virus
antibody titer taken at onset and 2-3 weeks later is diagnostic
with a fourfold or greater increase. Also, a single serum
titer of approximately 1:400 may be indicative of the disease.
Postmortem histopathology of horses suspected of EHV-1 myeloencephalopathy
should include brain, spinal cord, spleen, thyroid and lung.
Again, virus isolation is often unsuccessful. Immunofluorescent
antibody testing of brain and spinal cord can be more sensitive,
but false-negatives have occurred. Another promising technique
is indirect immuno-peroxidase method using light microscopy
of various tissues of affected animals.
Since there is no specific antiviral treatment,
supportive care is the main therapy. Because of the suspected
immune-mediated component, corticosteroids may be helpful
as well as non-steroidal anti-inflammatories. Precaution
should be used when caudaequina syndrome is present to prevent
a ruptured bladder or constipation due to eliminatory dysfunction.
Rectal examination, fecal softeners and urinary catheterization
may be indicated. Prognosis corresponds to clinical signs,
and progression to recumbency usually has a high mortality
rate with survivors taking months to years to recover. If
recumbency does not present in the first 3-5 days, prognosis
is improved, but recovery may take several months with no
guarantee of return to normal gait or eliminatory functions.
- by Lisa Wisz, Class of 1999
- edited by Jason Baldwin, DVM
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