Changes

====Description====

====Description====

'''NOTIFIABLE''' and '''ZOONOTIC''' infectious mosquito-borne disease of equidae.  The same virus strains can cause serious human disease as well as infecting poultry and other farmed birds including quail, ostriches and emus (ratites).  The disease is not directly contagious between horses and man.

'''NOTIFIABLE''' and '''ZOONOTIC''' infectious mosquito-borne disease of equidae affecting the central nervous system (CNS). 

 

 

Viraemia during the acute phase of EEE and WEE.  Incubation period of 1-3weeks after experimental infection with EEE or WEE.  Incubtion often shorter with EEE.  Central nervous system (CNS) replication within a week

====Aetiology====

====Aetiology====

[[Equine Encephalitis Virus|see this page for details of the causal pathogen]]

[[Equine Encephalitis Virus|see this page for details of the causal pathogens]].  The same virus strains can infect poultry and other farmed birds including quail and ratites.  Some strains are potential agents of biowarfare or bioterrorism (Steele and Twenhafel, 2010).

potential agents of biowarfare or bioterrorism

====Epidemiology====

====Epidemiology====

=====Seasonal Incidence=====

=====Seasonal Incidence=====

The diseases occur largely during the height of the vector season.  In temperate climates, case numbers peak in June to November.  In warm climates, where the vector season is longer, the disease period is prolonged.  Global warming may promote more cold climate outbreaks.

The disease is not directly contagious between horses and humans but occurs sporadically in both species from mid-summer to late autumn - during the height of the vector season.  In temperate climates, case numbers peak in June to November.  In warm climates, where the vector season is longer, the disease period is prolonged.  Global warming may promote more cold climate outbreaks.

=====Epidemics=====

=====Epidemics=====

Prerequisites for epidemics to occur include adequate and adjacent numbers of reservoir animals, sufficient quantities of virulent virus, infected intermediate hosts, insect vectors and susceptiple horse and human populations.  Outbeak prediction has been inaccurate, implyingf that other, unidentified factors may be important.

Prerequisites for epidemics to occur include adequate and adjacent numbers of reservoir animals, sufficient quantities of virulent virus, infected intermediate hosts, insect vectors and susceptiple horse and human populations.  Outbeak prediction has been inaccurate, implyingf that other, unidentified factors may be important.

====Pathogenesis====

====Pathogenesis====

After inoculation into an equine host, viruses multiply in the muscle, enter the lymphatic circulation and localize in lymph nodes.  Viral replication occurs in macrophages and neutrophils with subsequent shedding and significant clearance of viral particles.  No further clinical signs develop if clearance is successful but neutralizing Abs are still produced.  Viral immunological avoidance mechanisms include erythrocyte and leukocyte absorption.  After incomplete elimination, residual virus infects endothelial cells and concentrates in highly vascular organs such as the liver and spleen.  In these organs, viral replication produces circulating virus.  The second viraemic period is typically associated with early clinical signs.  CNS infection occurs within 3-5 days.

After inoculation into an equine host, viruses multiply in the muscle, enter the lymphatic circulation and localize in lymph nodes.  Viral replication occurs in macrophages and neutrophils with subsequent shedding and significant clearance of viral particles.  No further clinical signs develop if clearance is successful but neutralizing Abs are still produced.  Viral immunological avoidance mechanisms include erythrocyte and leukocyte absorption.  After incomplete elimination, residual virus infects endothelial cells and concentrates in highly vascular organs such as the liver and spleen.  In these organs, viral replication produces circulating virus.  The second viraemic period is typically associated with early clinical signs.  CNS infection occurs within 3-5 days.