Changes

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

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

====Laboratory Tests====

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

A combination of complement fixation (CF), haemagglutination inhibition (HAI) and cross-serum neutralization assays supports the acquisition of a positive diagnosis.  A 4-fold increase in antibody (Ab) titre in convlescent sera is quoted for diagnosis but this test lacks sensitivity.  The presence of viral Abs within 24hours of the initial viraemia typically precedes clinical signs.  Ab titre increases sharply then deteriorates over 6 months.  Samples taken when clinical signs appear are likely to miss the Ab peak and may thus demonstrate a decreasing titre.  A single sample demonstrating an increased titre using HAI, CF and neutralizing Ab can provide a presumptive diagnosis.

A combination of complement fixation (CF), haemagglutination inhibition (HAI) and cross-serum neutralization assays supports the acquisition of a positive diagnosis.  A 4-fold increase in antibody (Ab) titre in convlescent sera is quoted for diagnosis but this test lacks sensitivity.  The presence of viral Abs within 24hours of the initial viraemia typically precedes clinical signs.  Ab titre increases sharply then deteriorates over 6 months.  Samples taken when clinical signs appear are likely to miss the Ab peak and may thus demonstrate a decreasing titre.  A single sample demonstrating an increased titre using HAI, CF and neutralizing Ab can provide a presumptive diagnosis.

Maternal-derived Ab may interfere with diagnosis in foals.  The serum half-life of colostral Ab in foals is around 20days.

Maternal-derived Ab may interfere with diagnosis in foals.  The serum half-life of colostral Ab in foals is around 20days.

====Clinical Pathology====

=====Clinical Pathology=====

Changes in cerebrospinal fluid (CSF) include increased cellularity (50-400 mononuclear cells per microlitre) and protein concentration (100-200mg/dl)

Changes in cerebrospinal fluid (CSF) include increased cellularity (50-400 mononuclear cells per microlitre) and protein concentration (100-200mg/dl)

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

=====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.

The brain and spinal cord are typically grossly normal, but vascular congestion and discolouration of the CNS may be seen.  Histologically the entire brain is affected by nonseptic mononuclear cell and neutrophilic inflammation.  Severe lesions are noted in the cerebral cortex, thalamus and hypothalamus.  Mononuclear meningitis, neuronal degeneration, gliosis and perivascular cuffing with mononuclear cell and neutrophilic infiltration are evident.  Immunohistochemistry can be diagnostic.  Liquefactive necrosis and haemorrhage of the cerebral cortex, atrophy of the pancreatic acinar cells and hyperplasia of the pancreatic duct cells commonly occur with VEE.  

The brain and spinal cord are typically grossly normal, but vascular congestion and discolouration of the CNS may be seen.  Histologically the entire brain is affected by nonseptic mononuclear cell and neutrophilic inflammation.  Severe lesions are noted in the cerebral cortex, thalamus and hypothalamus.  Mononuclear meningitis, neuronal degeneration, gliosis and perivascular cuffing with mononuclear cell and neutrophilic infiltration are evident.  Immunohistochemistry can be diagnostic.  Liquefactive necrosis and haemorrhage of the cerebral cortex, atrophy of the pancreatic acinar cells and hyperplasia of the pancreatic duct cells commonly occur with VEE.