Urease activity may contribute to the ability of Actinobacillus pleuropneumoniae to establish infection.
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.
Bossé
J T
JT
Department of Pathobiology, University of Guelph, Ontario.
MacInnes
J I
JI
D000189:Actinobacillus Infections / Q000473:pathology / Q000662:veterinary*; D016977:Actinobacillus pleuropneumoniae / Q000201:enzymology / Q000235:genetics / Q000472:pathogenicity*; D000818:Animals; D016368:Frameshift Mutation; D012137:Respiratory System / Q000382:microbiology; D013552:Swine; D013553:Swine Diseases / Q000201:enzymology / Q000382:microbiology*; D014510:Urease / Q000378:metabolism*
D014510:Urease