Experimental oral infection of bluetongue virus serotype 8 in type I interferon receptor-deficient mice.
Ten sheep were inoculated with bluetongue virus (BTV) serotype 17. Six of the sheep had been vaccinated before challenge exposure, 4 sheep served as nonvaccinated challenge-exposed controls, and 2 additional sheep served as nonvaccinated, nonchallenge-exposed, contact controls. Biopsy specimens (oral labial mucosa and skin) were obtained periodically after challenge exposure. Sheep were killed 8 to 13 days after challenge exposure, and necropsy was done. Vaccination did not seem to affect the nature or severity of the lesions observed. The changes in the mucosa of the cranial portion of the digestive tract included hyperemia, edema, inflammation, petechiae, erosions, ulcers, and surface encrustations. Lesions of skeletal, cardiac, and smooth muscles included hemorrhage, edema, myofiber degeneration, and necrosis. Lesions in cardiac muscles were sometimes widespread, indicating that cardiac failure may have been the major contributor to pulmonary congestion, edema, and eventual death during acute BTV infection. Damage to esophageal musculature resulted in vomiting. Hemorrhage was observed within the base of the pulmonary artery of all challenge-exposed sheep. Using immunofluorescence, bluetongue viral antigens were detected in small blood vessels of the skin, oral labial mucosa, tongue, esophagus, rumen, reticulum, urinary bladder, and pulmonary artery and in skeletal and cardiac muscles. Viral antigens were present in tissues obtained 3 to 11 days after inoculation. Ultrastructurally, changes in small-caliber blood vessels included congestion, hemorrhage, swollen degenerated endothelial cells, and occasional fibrin-platelet thrombi. Tubular structures and virus-like particles were observed within some of these endothelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)