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Winter 1998 Newsletter


Canine Mast Cell Tumors

Equine Herpes Virus 1 Myelo encephalopathy
Feline Heart Worm Disease
Surpulinapilosi coli
Vesicular Stomatis in the Horse
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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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