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===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. 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.     
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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.<ref>Walton T.E (1981) Venezuelan, eastern, and western encephalomyelitis. In: ''Virus Diseases of Food Animals. A World Geography of Epidemiology and Control''. Disease Monographs, Vol. 2, Gibbs E.P.J, ed. Academic Press, New York, USA, 587-625.</ref> 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.     
    
[[Image:Venezuelan_equine_encephalitis_virus.jpg|300px|thumb|right|''' (Photomicrograph of mouse brain tissue after dying of Venezuelan Encephalitis. Reveals neural necrosis and edema.  ''Sourced from Wikimedia Commons, Copyright of the Centers for Disease Control and Prevention (CDC) Public Health Image Library (PHIL) Image #2809, 2006)'' ''']]
 
[[Image:Venezuelan_equine_encephalitis_virus.jpg|300px|thumb|right|''' (Photomicrograph of mouse brain tissue after dying of Venezuelan Encephalitis. Reveals neural necrosis and edema.  ''Sourced from Wikimedia Commons, Copyright of the Centers for Disease Control and Prevention (CDC) Public Health Image Library (PHIL) Image #2809, 2006)'' ''']]
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<references/>
 
<references/>
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Walton T.E. (1981). Venezuelan, eastern, and western encephalomyelitis. In: ''Virus Diseases of Food Animals. A World Geography of Epidemiology and Control''. Disease Monographs, Vol. 2, Gibbs E.P.J, ed. Academic Press, New York, USA, 587-625.
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