Host response to bovine respiratory pathogens

• Published in: Animal health research reviews Vol. 10; no. 2; p. 141
• Main Author: Czuprynski, Charles J
• Format: Journal Article
• Language: English
• Published: England 01-12-2009
• Subjects: Animals; Bovine Respiratory Disease Complex - immunology; Bovine Respiratory Disease Complex - microbiology; Bovine Respiratory Disease Complex - virology; Cattle - immunology; Host-Pathogen Interactions - immunology; Immunity, Cellular; Mannheimia haemolytica - immunology; Pasteurella Infections - veterinary; Pasteurellaceae; Pneumonia of Calves, Enzootic - immunology
• ISSN: 1475-2654
• DOI: 10.1017/s1466252309990181

Bovine respiratory disease (BRD) involves complex interactions amongst viral and bacterial pathogens that can lead to intense pulmonary inflammation (fibrinous pleuropneumonia). Viral infection greatly increases the susceptibility of cattle to secondary infection of the lung with bacterial pathogens like Mannheimia haemolytica and Histophilus somni. The underlying reason for this viral/bacterial synergism, and the manner in which cattle respond to the virulence strategies of the bacterial pathogens, is incompletely understood. Bovine herpesvirus type 1 (BHV-1) infection of bronchial epithelial cells in vitro enhances the binding of M. haemolytica and triggers release of inflammatory mediators that attract and enhance binding of neutrophils. An exotoxin (leukotoxin) released from M. haemolytica further stimulates release of inflammatory mediators and causes leukocyte death. Cattle infected with H. somni frequently display vasculitis. Exposure of bovine endothelial cells to H. somnii or its lipooligosaccharide (LOS) increases endothelium permeability, and makes the surface of the endothelial cells pro-coagulant. These processes are amplified in the presence of platelets. The above findings demonstrate that bovine respiratory pathogens (BHV-1, M. haemolytica and H. somni) interact with leukocytes and other cells (epithelial and endothelial cells) leading to the inflammation that characterizes BRD.