Abstract

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.

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