Changes

==Pathogenesis==

==Pathogenesis==

Upon entry to the host, viruses multiply in the muscle, enter the lymphatic circulation and localize in lymph nodes.  In macrophages and neutrophils viral replication leads to shedding and significant clearance of viral particles.  No further clinical signs develop if this clearance is successful.  Erythrocyte and leukocyte absorption are used to circumvent the immune defences of the host.  After incomplete elimination, residual virus infects endothelial cells and accumulates in highly vascular organs such as the liver and spleen.  In these organs, viral replication produces circulating virus and a second viraemic period, typically associated with early clinical signs.  Neuroinvasion and replication occurs within a week.  An incubation period of 7-21days has been demonstrated after experimental infection with Eastern or Western EEV, but the incubtion is often shorter for EEE compared with that of WEE.

Upon entry to the host, viruses multiply in the muscle, enter the lymphatic circulation and localize in lymph nodes.  In macrophages and neutrophils viral replication leads to shedding and significant clearance of viral particles.  No further clinical signs develop if this clearance is successful.  Erythrocyte and leukocyte absorption are used to circumvent the immune defences of the host.  After incomplete elimination, residual virus infects endothelial cells and accumulates in highly vascular organs such as the liver and spleen.  In these organs, viral replication produces circulating virus and a second viraemic period, typically associated with early clinical signs.  Neuroinvasion and replication occurs within a week.  An incubation period of 7-21days has been demonstrated after experimental infection with Eastern or Western EEV, but the incubation is often shorter for EEE compared with that of WEE.

==Signalment==

==Signalment==