Changes

Outbeak prediction to date has been inaccurate, implying that other, unidentified factors may be in operation.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>  However, some epidemic requirements are beyond question.  Adequate amounts of infective virus, sufficent vectors, infected sylvatic hosts and susceptible terminal hosts, and finally, appropriate reservoirs, are all crucial.<ref>Sellers, R.F (1980) Weather, host and vector: their interplay in the spread of insect-borne animal virus diseases, ''J Hyg (Lond)'', 85:65-102.  In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>

Outbeak prediction to date has been inaccurate, implying that other, unidentified factors may be in operation.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>  However, some epidemic requirements are beyond question.  Adequate amounts of infective virus, sufficent vectors, infected sylvatic hosts and susceptible terminal hosts, and finally, appropriate reservoirs, are all crucial.<ref>Sellers, R.F (1980) Weather, host and vector: their interplay in the spread of insect-borne animal virus diseases, ''J Hyg (Lond)'', 85:65-102.  In: Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>

==Pathogenesis==

==Pathogenesis<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>==

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.

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.<ref name="again">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial found at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/100900.htm&word=Equine%2cencephalitis, accessed July 2010</ref> 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==

Unvaccinated adult horses and other equids (for VEE in donkeys [[Venezuelan Equine Encephalomyelitis (VEE) - Donkey|see here]]) are at risk in areas with suitable vectors.  Vaccinated horses can still develop the disease, particularly if they are young or old.

Unvaccinated adult horses and other equids (for '''VEE in donkeys''' [[Venezuelan Equine Encephalomyelitis (VEE) - Donkey|'''see here''']]) are at risk in areas with suitable vectors.  Vaccinated horses can still develop the disease, particularly if they are young or old.

==Clinical Signs==

==Clinical Signs==

Worse in unvaccinated horses.  Neurological signs may be assymmetrical.   

Worse in unvaccinated horses.<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref> Neurological signs may be assymmetrical.<ref name="again">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial found at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/100900.htm&word=Equine%2cencephalitis, accessed July 2010</ref>  

===EEE and WEE===

===EEE and WEE===

====Clinical Pathology====

====Clinical Pathology====

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).<ref name="multiple">Bertone, J.J (2010) Viral Encephalitis in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), ''Saunders'', Chapter 12</ref>

===Post-mortem findings===

===Post-mortem findings===