Changes

=====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'''.

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.   

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).  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.

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.  The extent of the lesions depends on the severity of the infection and the duration of the neurological involvement (16).

Such lesions may be diagnostic and are typified by a nonseptic infiltrate.  The cerebral cortex, thalamus and hypothalamus are severely affected.  Mononuclear meningitis, neuronal degeneration, gliosis and perivascular cuffing .  Immunohistochemistry can be diagnostic.   

Brain lesions caused by WEE virus infection are focal and have lymphocytic infiltrations. Brain lesions caused by EEE virus infection are more severe and are found throughout the grey matter. They are characterised by a larger number of neutrophils among the inflammatory cells.  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. IN VEE there may be damage to other organs such as the pancreas, liver and heart.

VEE cases often exhibit liquefactive necrosis and haemorrhage of the cerebral cortex, atrophy of the pancreatic acinar cells and hyperplasia of the pancreatic duct cells. There may also be damage to the liver and heart.

Microscopic lesions are usually found throughout the central nervous system and can be diagnostic. There is widespread evidence of a severe inflammatory response involving the grey matter. Neuronal degeneration with infiltration by polymorphonuclear leukocytes, diffuse and focal gliosis, and perivascular cuffing with lymphocytes and neutrophils are seen. Also observed are neuronophagia and liquefaction of the neuropil.  

Neuronal degeneration with infiltration by polymorphonuclear leukocytes, diffuse and focal gliosis, and perivascular cuffing with lymphocytes and neutrophils are seen. Also observed are neuronophagia and liquefaction of the neuropil.