Page 1092 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition
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Nervous system                                      1067



  VetBooks.ir  EQUINE HERPESVIRUS                        age can be affected but cases tend to be more than
          MYELOENCEPHALOPATHY
                                                         2 years old, and any sex or breed can be affected.
                                                           The onset of neurological signs usually occurs
          Definition/overview                            6–10 days after initial infection, and may be preceded
          Equine herpesvirus (EHV) myeloencephalopathy   by fever, lethargy and inappetence. The neurological
          (EHM) is a relatively common cause of CNS disease   signs relate to ischaemic damage to the white mat-
          in the horse. It has a worldwide distribution and it   ter of the spinal cord, and the severity of the signs is
          is reported that up to 80% of horses carry a latent   related to the combined effect of all of the lesions scat-
          infection. Neurological disease is an uncommon   tered along the spinal cord. Clinical signs are always
          sporadic sequela to EHV-1 infection, and outbreaks   acute and rarely progress after 2–3 days – typical for
          have been widely reported. Adult horses are more   vascular compromise. Most frequently, symmetrical
          commonly affected.                             hindlimb ataxia and paresis is reported. There can be
                                                         sacrocaudal signs such as incontinence (perhaps due
          Aetiology/pathophysiology                      to the involvement of spinal cord segments respon-
          EHV-1 is the only herpesvirus that has been consis-  sible for micturition) and also hypotonia and hypal-
          tently associated with neurological disease. Markers   gesia of the perineum, tail and anus. Cervical spinal
          of virulence and neuro-predilection have been inves-  cord lesions result in spastic tetraparesis and paraly-
          tigated and the strain with a D  genotype of the   sis similar to that seen in youngsters with OAAM.
                                      752
          DNA polymerase is more strongly associated with   Horses  with  extensive  cervical  spinal  cord  lesions
          EHM outbreaks than the G  genotype. Other      usually become recumbent and these horses are rarely
                                    752
          syndromes associated with EHV-1 include abortion   able to stand again. Horses that remain standing after
          storms, sporadic abortions in mares, neonatal death   3 days have a reasonable prognosis for recovery, which
          and respiratory disease in young horses.       may take weeks to months depending on the sever-
            Viraemia results from inhalation of virus and   ity of the CNS vascular compromise. Occasionally,
          infection of respiratory epithelium or recrudescence   horses with EHM can develop cortical, brainstem or
          of latent viral infection. The virus replicates in local   vestibular lesions and related clinical signs including
          lymph nodes and infected leucocytes are released   depression, head tilt, CN deficits and coma.
          into the circulation; cell-associated viraemia persists
          for 4–10 days post-infection. Virus is transported via  Differential diagnosis
          leucocytes to sites of secondary infection where leu-  Equine degenerative myelitis; EPM; WNV enceph-
          cocytes interact with the vascular endothelium. As a   alomyelitis; trauma; verminous meningomyelo-
          consequence of infected endothelial cells in the small   encephalitis (Halicephalobus deletrix); equine motor
          vessels in the brain and spinal cord, vasculitis and   neuron disease (EMND); cervical vertebral ste-
          thrombosis occur, which results in ischaemia and   notic myelopathy; hyperammonaemia; metabolic
          myelomalacia. Immunohistochemistry for EHV-1   derangement; spinal cord impingement secondary
          shows evidence of the antigen in the endothelium   to neoplasia; fibrocartilaginous embolic myelopathy.
          and smooth muscle cells of arterioles, arteries and
          veins of the CNS.                              Diagnosis
                                                         A presumptive diagnosis of EHM is often made in
          Clinical presentation                          horses  with  characteristic  neurological  signs.  The
          Multiple horses in a herd may be affected, although   CSF frequently has an increased total protein with
          sporadic individual cases are not uncommon. The   little change in nucleated cell count. Xanthochromia
          history sometimes includes contact with horses   (associated with red cell breakdown) is frequently
          demonstrating signs of herpesvirus respiratory   noted. Attempts to isolate the virus from the CSF
          disease (fever, depression, cough, nasal discharge).   are usually unsuccessful. CSF changes bear no cor-
          Outbreaks may occur following introduction of   relation with the severity of clinical signs and cannot
          new horses into the yard or hospital. Horses of any   be used as a prognostic indicator.
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