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.
Department of Pathobiology, University of Guelph, Ontario.
J T
JT
Bossé
J I
JI
MacInnes
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