Changes

The pathogenesis of BTV infection has been shown to be similar in sheep and cattle, and is assumed to be similar in other species of ruminants^{7, 8, 9}. However, the severity of disease varies greatly with species and cattle in particular express very few signs.  

The pathogenesis of BTV infection has been shown to be similar in sheep and cattle, and is assumed to be similar in other species of ruminants^{7, 8, 9}. However, the severity of disease varies greatly with species and cattle in particular express very few signs.  

When a BTV-infected midge takes a blood meal from a ruminant host, innoculated virus spreads from the skin to the regional lymph nodes. After initial replication in the lymph nodes, a cell-associated viraemia carries the virus to many tissues where further replication occurs in macrophages and endothelial cells.

When a BTV-infected midge takes a blood meal from a ruminant host, innoculated virus spreads from the skin to the regional lymph nodes. After initial replication in the lymph nodes, a cell-associated viraemia 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 necrosis⁹. In turn, an increase in vascular permeability causes oedema, and thrombosis can arise which may lead to tissue infarction. A consumptive coagulopathy can occure sheep and deer².

Clinical signs and lesions in BTV-infected sheep likely reflect virus-mediated endothelial injury, as BTV replicates in endothelial cells causing cell injury and necrosis [21,26]. Similarly, white-tailed deer, which are highly susceptible to BT, develop consumptive coagulopathy as a consequence of BTV-induced damage to endothelial cells [18]. Consumptive coagulopathy in BTV-infected sheep and deer predisposes to the bleeding tendency that characterizes fulminant BT. Endothelial injury also is likely responsible for increased vascular permeability leading to edema in tissues such as the lung (pulmonary edema), and vascular thrombosis leads to tissue infarction.

Clinical signs and lesions in BTV-infected sheep likely reflect virus-mediated endothelial injury, as BTV replicates in endothelial cells causing cell injury and necrosis [21,26]. Similarly, white-tailed deer, which are highly susceptible to BT, develop consumptive coagulopathy as a consequence of BTV-induced damage to endothelial cells [18]. Consumptive coagulopathy in BTV-infected sheep and deer predisposes to the bleeding tendency that characterizes fulminant BT. Endothelial injury also is likely responsible for increased vascular permeability leading to edema in tissues such as the lung (pulmonary edema), and vascular thrombosis leads to tissue infarction.