Fig 5. Primary site initiation of bacteremia enhances resolution of splenic fitness defects and illuminates requirements of factors across phases of pathogenesis.
To model bacteremic pneumonia, mice were infected with 1x106 CFU K. pneumoniae. Competitive infections were performed with a 1:1 mixture of KPPR1 and a transposon mutant for (A) arnD, (B) purD, (C) dsbA, (D) sspA, or (E) pdxA or (F) a pdxA knockout (ΔpdxA). (G) Competitions were also performed with strains carrying the empty pACYC vector (ev) or complementation provided on pACYC for pdxA only (pACYCpdxA) or pdxA and downstream members of the operon (pACYCoperon). The log10 competitive index at 24 hours post infection is displayed for individual mice with bars representing the median and interquartile range. For all, *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001 by one-sample t test with a hypothetical value of zero; #p<0.05, ##p<0.01, ###p<0.001, ####p<0.0001 by unpaired t test. For each group, n≥10 mice in at least two independent infections.