Gonzalez C T, Maheswaran S K
Department of Veterinary PathoBiology, College of Veterinary Medicine, University of Minnesota, St. Paul 55108.
Br Vet J. 1993 Mar-Apr;149(2):183-93. doi: 10.1016/S0007-1935(05)80088-0.
In the pathogenesis of pneumonic pasteurellosis, there is an abrupt commensal to pathogen shift from a predominance of P. haemolytica serotype 2 (ST2) to serotype 1 (ST1) in the bovine upper respiratory tract (URT) microfloral population. This occurs following periods of stress associated with development of this disease. Data are reviewed from recent publications supporting the contention that surface-expressed ST1-specific factor(s) could be critical in mediating URT adhesion and colonization. Such factors may promote an increase in the number of ST1 organisms deposited through infective droplets into the lungs, beyond that efficiently cleared by normal lung defences. The seeding of these organisms into the lungs may provide numerous foci of infection that eventually progress into characteristic pneumonic lesions seen in the disease.
在牛巴氏杆菌肺炎的发病机制中,在与该疾病发展相关的应激期后,牛上呼吸道(URT)微生物群中会出现一种从以溶血巴氏杆菌2型(ST2)为主突然转变为1型(ST1)的共生菌到病原菌的转变。本文回顾了近期出版物中的数据,这些数据支持以下观点:表面表达的ST1特异性因子可能在介导URT黏附和定植中起关键作用。这些因子可能会促进通过感染性飞沫沉积到肺部的ST1菌数量增加,超过正常肺部防御系统有效清除的数量。这些细菌在肺部的定植可能会形成许多感染灶,最终发展为该疾病中所见的典型肺炎病变。