Pathobiology of A/Chicken/Hong Kong/220/97 (H5N1) avian influenza virus in seven Gallinaceous species
Pathobiology of A/Chicken/Hong Kong/220/97 (H5N1) avian influenza virus in seven Gallinaceous species
复制标题
DOI：
10.1354/vp.38-2-149
复制
发表时间：
2001-03-01
影响因子：
2.4
通讯作者：
Swayne, DE
中科院分区：
文献类型：
--
作者：
Perkins, LEL;Swayne, DE
源自香港的H5N1型高致病性禽流感（HPAI）病毒特有的直接从禽类传播到人类，可导致严重呼吸道疾病和人类死亡。该病毒最初是从鸡中爆发的疾病中分离出来的。在鸡、火鸡、日本鹌鹑和山鹑、珍珠鸡、野鸡和鹧鸪中调查了A/chicken/Hong Kong/ 220/97 (H5N1) （HK/220）高致病性禽流感病毒的病理生物学，在10天内造成75-100%的死亡率。抑郁症、黏液性腹泻和神经功能障碍是该病常见的临床表现。大体而言，最严重和一致的病变包括脾肿大、肺水肿和充血、肠淋巴区、浆膜表面和骨骼肌出血。组织学病变见于多个器官，其特征为渗出、出血、坏死、炎症或这些特征的组合。肺、心、脑、脾和肾上腺是最常见的受累部位，免疫组织化学在这些器官的实质组织中最常检测到病毒抗原。这些物种感染HK/220型高致病性禽流感病毒的发病机制是双重的。接种后1-2天发生的早期死亡与严重的肺水肿和充血以及病毒在血管内皮内的定位相对应。2 DPI后发生的死亡与全身生化失衡、多器官功能衰竭或这些因素的组合有关。其病理特征与其他高致病性禽流感病毒在家禽中的实验诱导相似。
Direct bird-to-human transmission, with the production of severe respiratory disease and human mortality, is unique to the Hong Kong-origin H5N1 highly pathogenic avian influenza (HPAI) virus, which was originally isolated from a disease outbreak in chickens. The pathobiology of the A/chicken/Hong Kong/ 220/97 (H5N1) (HK/220) HPAI virus was investigated in chickens, turkeys, Japanese and Bobwhite quail, guinea fowl, pheasants, and partridges, where it produced 75-100% mortality within 10 days. Depression, mucoid diarrhea, and neurologic dysfunction were common clinical manifestations of disease. Grossly, the most severe and consistent lesions included splenomegaly, pulmonary edema and congestion, and hemorrhages in enteric lymphoid areas, on serosal surfaces, and in skeletal muscle. Histologic lesions were observed in multiple organs and were characterized by exudation, hemorrhage, necrosis, inflammation, or a combination of these features. The lung, heart, brain, spleen, and adrenal glands were the most consistently affected, and viral antigen was most often detected by immunohistochemistry in the parenchyma of these organs. The pathogenesis of infection with the HK/220 HPAI virus in these species was twofold. Early mortality occurring at 1-2 days postinoculation (DPI) corresponded to severe pulmonary edema and congestion and virus localization within the vascular endothelium. Mortality occurring after 2 DPI was related to systemic biochemical imbalance, multiorgan failure, or a combination of these factors. The pathobiologic features were analogous to those experimentally induced with other HPAI viruses in domestic poultry.