Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, CA 95616, USA.
Prev Vet Med. 2011 Nov 1;102(2):107-11. doi: 10.1016/j.prevetmed.2011.04.005. Epub 2011 May 12.
Bluetongue is an arthropod-transmitted viral disease of ruminants and certain other animals that was recognized and described more than 100 years ago in southern Africa. Bluetongue virus (BTV) infection of ruminants and vector Culicoides insects is enzootic throughout tropical and temperate regions of the world; however, there have been drastic recent regional alterations in the global distribution of BTV infection, particularly in Europe since 1998. Multiple novel BTV serotypes also have been detected since 1998 in the south-eastern United States, apparently encroaching from the adjacent Caribbean ecosystem, and novel serotypes of BTV have been identified recently in other historically enzootic regions of the world, including the Middle East and Australia. It has been proposed, but certainly not proven, that global climate change is responsible for these events. BTV infection of ruminants is often subclinical, but outbreaks of severe disease occur with regular frequency especially at the upper and lower limits of the virus' global range where infection is highly seasonal - occurring in the late summer and autumn. Bluetongue disease results from vascular injury, likely through a process analogous to that of human hemorrhagic viral fevers in which production of vasoactive mediators from virus-infected macrophages and dendritic cells results in enhanced endothelial paracellular permeability with subsequent vascular leakage and hypovolemic shock.
蓝舌病是一种由节肢动物传播的反刍动物和某些其他动物的病毒性疾病,100 多年前在南非被认识和描述。蓝舌病病毒(BTV)感染反刍动物和媒介库蠓昆虫在世界热带和温带地区呈地方性流行;然而,自 1998 年以来,BTV 感染的全球分布在最近发生了剧烈的区域变化,特别是在欧洲。自 1998 年以来,在美国东南部也检测到了多种新型 BTV 血清型,显然是从相邻的加勒比生态系统入侵的,最近在世界上其他历史上地方性流行的地区,包括中东和澳大利亚,也发现了新型 BTV 血清型。有人提出,但尚未得到证实,全球气候变化是造成这些事件的原因。BTV 感染反刍动物通常是亚临床的,但严重疾病的爆发经常发生,尤其是在病毒全球范围的上限和下限,感染具有高度季节性——发生在夏末和秋季。蓝舌病是由血管损伤引起的,可能通过类似于人类出血性病毒性发热的过程,病毒感染的巨噬细胞和树突状细胞产生血管活性介质,导致内皮细胞旁通透性增强,随后发生血管渗漏和低血容量性休克。