Fig 6.

Attenuation of the uvrD1 and uvrA uvrD1 mutant strains in mouse models of infection. Growth and survival of the uvrD1 and uvrA uvrD1 strains were compared with the wild type and a uvrA mutant following infection of BALB/c mice as detailed in Materials and Methods. (A and B) Infection by the aerosol route; CFU were enumerated from the lungs and spleens of five mice for each time point. The data for the uvrA uvrD1 mutant were significantly different from the corresponding values for the wild type (P < 0.001), the uvrA mutant (P < 0.001), and the urvD1 mutant (P < 0.01) at all time points in the lungs and at each time point after day 50 in the spleens. The data for the uvrD1 mutant were significantly different from those for the wild type in both organs at each time point after day 50 (P < 0.001). (C and D) Infection by the intravenous route; additional strains in which the urvD1 and uvrA uvrD1 mutants were complemented with uvrD1 were included in the analysis. Bacterial loads were determined from the lungs and spleens of four mice for each time point. The data for the uvrA uvrD1 mutant were significantly different from the corresponding values for the wild type (P < 0.001), the uvrA mutant (P < 0.001), the urvD1 mutant (P < 0.01), and both the complemented strains (P < 0.001) at all time points in both organs. The data for the uvrD1 mutant were significantly different from those for the wild type and its complemented strain in both organs from day 42 onwards (P < 0.01). In each case the mutant strains showed similar phenotypes in a second independent experiment; the results shown are the means, and the error bars represent standard deviations.