Changes

==Pathogenesis==

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virs then seconarily replicated in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acqure PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistance of infection occurs despite this. The fact that virus replicates in pigs for such a long time contributes to the maintenance of infection within a herd.

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virs then seconarily replicated in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acqure PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistance of infection occurs despite this.

==Diagnosis==

==Diagnosis==