Page 1087 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition
P. 1087

1062                                       CHAPTER 10



  VetBooks.ir  10.20                                      10.21

















                                                                                       Fig. 10.21
                                                                                       A horse infected
           Fig. 10.20  Dysphagia and dementia associated with                          with EEE which
           EEE. (Photo courtesy FT Bain)                                               presented with
                                                                                       severe ataxia and
                                                                                       recumbency and
           and compulsive walking or chewing. WEE does                                 required the use of
           not usually progress beyond non-specific initial                            a sling. The horse
           signs or, less commonly, mild CNS signs such as                             eventually died.
           those above. EEE typically progresses to severe
           CNS deficits that occur secondary to diffuse cere-
           brocortical disease. Signs associated with more   Serological testing is helpful, with a four-fold rise
           severe disease in EEE include apparent blindness   in antibody titres being diagnostic.  However, a
           and circling, excitement and aggressive behaviour,   four-fold rise may not be detected because antibody
           laryngeal, pharyngeal and tongue paralysis, dys-  levels rise rapidly after infection and a delay in tak-
           phagia (Fig.  10.20) and signs of brainstem dys-  ing the acute sample frequently results in sampling
           function such as head tilt, nystagmus, strabismus   during the peak antibody titre. Another problem
           and pupil dilation (Fig. 10.21). VEE may also   frequently encountered with serological testing is
           cause inapparent infections, signs similar to those   that horses with EEE often do not live long enough
           of other encephalitis viruses, or produce signs such   for comparison of paired samples. High immuno-
           as epistaxis, pulmonary haemorrhage, oral ulcers   globulin M (IgM) titres suggest recent exposure to
           and diarrhoea that may be unrelated to CNS dam-  EEE virus and may be detected via enzyme-linked
           age. Seizures can occur with any of the alphavirus   immunosorbent  assay  (ELISA).  Definitive  ante-
           infections and sudden death may also occur despite   mortem diagnosis can also be made on the basis
           seemingly insignificant clinical signs.        of  viral  isolation  or  identification  of  viral  nucleic
                                                          acid by reverse transcription (RT-)PCR. RT-PCR
           Differential diagnosis                         is a sensitive and specific test for detection of viral
           Other viral causes of encephalitis should be consid-  nucleic  acid  in  CNS  tissue  or  CSF.  EEE,  WEE
           ered depending on the geographical incidence of   or VEE viruses can be isolated from brain tissue
           individual diseases and time of year.          of infected horses via Vero-cell culture or mouse
                                                          inoculation. Immunohistochemistry testing can
           Diagnosis                                      also be performed on brain tissue. Virus isolation
           Establishing a definitive diagnosis is important   from serum is usually unsuccessful. Other findings
           to allow implementation of control measures,   that are not specific for alphaviruses are peripheral
           but it can be challenging. Clinical signs are non-   leucocytosis and increased cellularity and elevated
           specific or similar to those of other encephalitides.   protein concentration of CSF.
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