Urease activity may contribute to the ability of Actinobacillus pleuropneumoniae to establish infection

• Published in: Canadian journal of veterinary research Vol. 64; no. 3; pp. 145 - 150
• Main Authors: Bosse, J.T, MacInnes, J.I
• Format: Journal Article
• Language: English
• Published: Canada 01-07-2000
• Subjects: Actinobacillus Infections - pathology; Actinobacillus Infections - veterinary; Actinobacillus pleuropneumoniae - enzymology; Actinobacillus pleuropneumoniae - genetics; Actinobacillus pleuropneumoniae - pathogenicity; Animals; Frameshift Mutation; Respiratory System - microbiology; Swine; Swine Diseases - enzymology; Swine Diseases - microbiology; Urease - metabolism
• ISSN: 0830-9000

The contribution of urease activity to the pathogenesis of Actinobacillus pleuropneumoniae was investigated using 2 different urease-negative transposon mutants of the virulent serotype 1 strain, CM5 Nalr. One mutant, cbiK::Tn10, is deficient in the uptake of nickel, a cofactor required for urease activity. The other mutant, ureG::Tn10, is unable to produce active urease due to mutation of the urease accessory gene, ureG. In aerosol challenge experiments, pigs developed acute pleuropneumonia following exposure to high doses (10(6) cfu/mL) of the parental strain, CM5 Nalr, and to the cbiK::Tn10 mutant. When low dose (10(3) cfu/mL) challenges were used, neither urease-negative mutant was able to establish infection, whereas the parental strain was able to colonize and cause lesions consistent with acute pleuropneumonia in 8 of the 20 pigs challenged. These findings suggest that urease activity may be needed for A. pleuropneumoniae to establish infection in the respiratory tract of pigs.