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FINAL   DIAGNOSIS: 
Ataxia with Equine Herpes Virus
Type 1 Infection in a Horse

History:  A Thorough-bred mare, reportedly 17.5 years old, was submitted dead for necropsy to the Purdue Animal Disease Diagnostic Laboratory.  The history included marked asymmetric ataxia for approximately four months.  The animal did not respond to treatment for equine protozoal myeloencephalitis (EPM) and was euthanized.  The owner reported herpes virus infection earlier in the year.

Gross Findings: Scattered petechial hemorrhages were seen in sections of  spinal cord at the level of T17-L3, predominantly in the ventral and ventrolateral funiculi.  The surrounding parenchyma was occasionally soft, with gray discoloration.  The brain was grossly normal.

Histopathologic Findings: The main lesions in the spinal cord consisted of wallerian-like degeneration accompanied by non-suppurative myelitis with vasculitis.  The degenerative lesions were present in all the sections examined, accompanied by minimal inflammatory lesions, with the caudal thoracic and cranial lumbar segments being the most severely affected, accompanied by multifocal hemorrhage.  Multifocal non-suppurative encephalitis was observed in all sections of brain examined except  the frontal cerebral cortex.

Discussion: The inflammatory reaction in  sections of spinal cord from this animal was centered on blood vessels, occasionally accompanied by hemorrhage. These lesions are highly suggestive of a primary vasculitis with secondary ischemic injury to the neuroparenchyma.  Immunohistochemistry revealed a positive staining for equine herpes virus-1 (EHV-1) antigen in smooth muscle cells of spinal arterioles, arteries, and veins.  PCR for West Nile virus on a sample of spinal cord was negative.  These results, as well as the reported previous infection by this virus, are highly suggestive of EHV-1 infection.

  Herpes virus infection is ubiquitous in horses, and most animals are infected by the first year of life.  Neurologic disease is an uncommon sequela to EHV-1 infection in horses and is usually, but not invariably, associated with a recent history of fever, abortion, or respiratory disease in the affected animal or herdmates. Myeloencephalopathy due to EHV-1 is commonly an epizootic disease, but may affect single animals in a herd.  Pregnant or lactating mares may be more susceptible, although stallions, geldings, and foals have also been affected with this disease.

  Natural EHV-1 infection is acquired via inhalation or ingestion of virus that is shed primarily from the nasopharynx.  The incubation period for signs of neurologic disease after experimental and natural infection with EHV-1 is 6-10 days.  This form of EHV-1 infection can occur at any time of the year, but the highest incidence is in the late winter, spring, and early summer, perhaps reflecting the seasonal occurrence of abortigenic EHV-1 infections during the same months.  Neurologic signs are of abrupt onset, and horses may be found recumbent as the first evidence of the disease. Clinical signs most often reflect spinal cord lesions; ataxia and paresis of the pelvic limbs are common, and passive dribbling of urine is a characteristic feature.  Signs may be mild and transient as recovery or compensation occurs with minimal lesions.  With severe lesions, recumbency occurs in 12-24 hours from the onset of neurological signs.  Sometimes ascending paralysis is observed and animals may die in coma or convulsion or be euthanized because of secondary complications.  Morbidity rates ranging from less than 1% to almost 90% of exposed individuals and mortality rates ranging from 0.5-43% of in-contact horses have been reported.

  The pathogenesis involves viral endotheliotropism and associated vasculitis and thrombosis in the central nervous system with resultant ischemia and myelomalacia.  Immune mechanisms have been implicated, but immunohistochemical demonstration of EHV-1 antigen in neurons of affected horses and association of myeloencephalopathy with certain EHV-1 strains indicate that primary viral neurotropism might also occur.  EHV-1 has been reported to maintain a latent state in lymphoid tissues, leukocytes, and trigeminal ganglia.  Reactivation of latent EHV-1 infection after stress situations has been reported as a possible source of infection.

  The cerebrospinal fluid from affected animals is often xanthochromic with elevated protein but normal numbers of cells (i.e., virtually none).  During the early stage of the infection, there is a cell-associated viremia, and virus may be isolated from the buffy coat in affected horses; however, failure to isolate EHV-1 does not rule out the diagnosis.  A 4-fold increase in serum neutralizing antibody titer is considered diagnostic for EHV-1 infection, and a single high titer (greater than 1:256) also suggests recent natural infection.  PCR in whole blood, nasopharyngeal swabs, lymphoid tissues, and trigeminal ganglia is another valuable technique in supporting a diagnosis of EHV-1 myeloencephalopathy, but decreased or absent viral shedding due to stage of infection, previous vaccination, or viral latency might affect the viral DNA detection.  Postmortem examination, including spinal cord histopathology and immunohistochemistry, are recommended to confirm the diagnosis of EHV-1 myelo-encephalopathy.

  No specific treatment of equine herpes myeloencephalopathy is currently available; thus,  management of horses with this condition is directed toward supportive nursing, nutritional care, and reduction of central nervous system inflammation.  Treatment with the antiviral agent acyclovir has been recommended.  Further studies are required, however, to evaluate the thera-peutic efficacy of antiviral agents in the treatment of neurologic disease associated with EHV-1.

  There is currently no known method to reliably prevent the neurologic form of EHV-1 infection.  None of the EHV-1 or EHV-4 vaccines currently available carry a claim that they prevent EHV-1 myelo-encephalopathy, and the disease has been observed in horses vaccinated regularly at 3-4 month intervals with inactivated and modified live vaccines.  Nevertheless, it is recommended to maintain appropriate vaccination procedures in an attempt to reduce the incidence of the other manifestations of EHV-1 infection and reduce the magnitude of challenge experienced by in-contact horses.  This may indirectly help prevent EHV-1 myeloencephalopathy.

  This case emphasizes that EHV-1 infection, although of rare occurrence, has to be considered as a possible cause for gait abnormalities affecting single or multiple horses on the premises, in addition to other viral myeloencephalitides, including West Nile virus, rabies virus, and togaviral encephalomyelitis, as well as equine protozoal myeloencephalitis, wobbler syndrome, cervical vertebral fracture, degenerative myelopathy, and a variety of plant and chemical intoxications.

-by Dr. Ingeborg Langohr, ADDL Graduate    Student

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