Changes

====Diagnosis====

====Diagnosis====

Presumptive based on epidemiology and clinical signs.  Definitive diagnosis requires serological tests and/or post-mortem examination.  Virus isolation can be performed from blood or spinal fluid samples

Presumptive based on epidemiology and clinical signs.  Definitive diagnosis requires virus identification, serological tests and/or post-mortem examination.   

=====Laboratory Tests=====

=====(1) Laboratory Tests=====

======Virus Identification======

======Virus Identification======

Viruses can be identified by complement fixation, immunofluorescence, PCR, ELISA, or virus isolation.

Viruses can be identified by complement fixation, immunofluorescence, PCR, ELISA, or virus isolation.

CSF samples demonstrate increased cellularity (50-400 mononuclear cells/µl) and protein concentration (100-200mg/dl).

CSF samples demonstrate increased cellularity (50-400 mononuclear cells/µl) and protein concentration (100-200mg/dl).

=====Post-mortem findings=====

=====(2) Post-mortem findings=====

'''''PRECAUTION'': infective viral particles may be present in CNS and other tissues'''.

'''''PRECAUTION'': infective viral particles may be present in CNS and other tissues'''.

Gross pathological lesions of the brain and spinal cord are rarely seen in horses, although traumatic ecchymotic haemorrhages and vascular congestion of the CNS may be evident. The extent of microscopic lesions is dictated by the severity of infection and duration of neurological involvement (Walton, 1981).  Such lesions with or without immunohistochemistry may be diagnostic.  The cerebral cortex, thalamus and hypothalamus are often severely affected.  Mononuclear meningitis, neuronal degeneration, diffuse and focal gliosis and perivascular cuffing are also seen.  Histological lesions of EEE are usually present throughout the CNS, with widespread and severe neutrophilic inflammation of the grey matter.  Lesions caused by Western EEV infection are more focal and lymphocytic in nature.  VEE cases often exhibit haemorrhage and liquefactive necrosis of the cerebral cortex, but lesions are not restricted to the CNS.  In the pancreas, acinar cells atrophy and duct cells undergo hyperplasia.  There may also be damage to the liver and heart.     

Gross pathological lesions of the brain and spinal cord are rarely seen in horses, although traumatic ecchymotic haemorrhages and vascular congestion of the CNS may be evident. The extent of microscopic lesions is dictated by the severity of infection and duration of neurological involvement (Walton, 1981).  Such lesions with or without immunohistochemistry may be diagnostic.  The cerebral cortex, thalamus and hypothalamus are often severely affected.  Mononuclear meningitis, neuronal degeneration, diffuse and focal gliosis and perivascular cuffing are also seen.  Histological lesions of EEE are usually present throughout the CNS, with widespread and severe neutrophilic inflammation of the grey matter.  Lesions caused by Western EEV infection are more focal and lymphocytic in nature.  VEE cases often exhibit haemorrhage and liquefactive necrosis of the cerebral cortex, but lesions are not restricted to the CNS.  In the pancreas, acinar cells atrophy and duct cells undergo hyperplasia.  There may also be damage to the liver and heart.