MacLachlan N J, Crafford J E, Vernau W, Gardner I A, Goddard A, Guthrie A J, Venter E H
Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, CA 95616, USA.
Vet Pathol. 2008 May;45(3):310-5. doi: 10.1354/vp.45-3-310.
Sheep inoculated with a virulent South African strain of bluetongue (BT) virus serotype 4 developed severe clinical signs and lesions characteristic of fulminant BT, including coronitis, hemorrhage and ulceration of the mucosal lining of the oral cavity and forestomaches, hemorrhage in the wall of the pulmonary artery, and focally extensive necrosis of skeletal muscle, especially of the neck. At necropsy, up to 14 days after infection, the infected sheep exhibited striking pulmonary edema, edema of the subcutaneous tissues and fascial planes of the head and neck, and pleural and pericardial effusion of varying severity. A reliable model for experimental reproduction of fulminant BT in sheep will facilitate future studies to better characterize the pathogenesis of this disease, particularly as it regards the mechanisms responsible for the increased vascular permeability that characterizes BT and related orbiviral diseases such as African horse sickness.
用一种毒性很强的南非蓝舌病（BT）病毒血清型4毒株接种绵羊后，绵羊出现了暴发性蓝舌病的严重临床症状和病变，包括冠状炎、口腔和前胃黏膜内衬出血和溃疡、肺动脉壁出血以及骨骼肌局部广泛坏死，尤其是颈部骨骼肌。在尸检时，感染后长达14天，受感染的绵羊表现出明显的肺水肿、头颈部皮下组织和筋膜平面水肿以及不同程度的胸腔和心包积液。一个在绵羊身上实验性再现暴发性蓝舌病的可靠模型将有助于未来的研究，以更好地描述这种疾病的发病机制，特别是关于导致蓝舌病及相关环状病毒病（如非洲马瘟）特征性血管通透性增加的机制。
