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→Pathogenesis
When a BTV-infected midge takes a blood meal from a ruminant host, innoculated virus spreads from the skin to replicate in the regional lymph nodes, tonsils and spleen<sup>11</sup>. A secondary cell-associated viraemia then carries the virus to many tissues where further replication occurs in macrophages and endothelial cells. In the process of reproducing, bluetongue virus causes endothelial cell injury and necrosis<sup>10</sup> which can increase vascular permeability to cause oedema. Endothelial damage can also give thrombosis, leading to tissue infarction. In sheep and deer a consumptive coagulopathy may occur<sup>2</sup>.
When a BTV-infected midge takes a blood meal from a ruminant host, innoculated virus spreads from the skin to replicate in the regional lymph nodes, tonsils and spleen<sup>11</sup>. A secondary cell-associated viraemia then carries the virus to many tissues where further replication occurs in macrophages and endothelial cells. In the process of reproducing, bluetongue virus causes endothelial cell injury and necrosis<sup>10</sup> which can increase vascular permeability to cause oedema. Endothelial damage can also give thrombosis, leading to tissue infarction. In sheep and deer a consumptive coagulopathy may occur<sup>2</sup>.
Several factors can influence the presentation of disease. Firstly, each virus strain is associated with its own particular virulence and thus clinical manifestation<sup>10</sup>. Host factors are also important: breed<sup>12, 13</sup>, stress, nutritional status and age<sup>13, 14</sup> can all affect bluetongue presentation.
==Diagnosis==
==Diagnosis==