Preferential Use of Central Metabolism In Vivo Reveals a Nutritional Basis for Polymicrobial Infection
Figure 4
Contribution of the TCA cycle and gluconeogenesis during UTI.
Competitive indices (CI) were determined following co-challenge infections of female CBA/J mice with a 1∶1 ratio of either wild-type (A) E. coli CFT073 or (B) P. mirabilis HI4320 and their respective mutants in the following genes: sdhB, succinate dehydrogenase; fumC, fumarate hydratase; frdA, fumarate reductase; and pckA, phosphoenolpyruvate carboxykinase. E. coli was cultured from bladders and kidneys at 48 hpi. P. mirabilis was cultured from organs at 7 dpi. Each dot represents bladder (closed symbols) and kidneys (open symbols) from an individual animal. Bars indicate the median CI. Significant differences in colonization (*P<0.05) were determined by the Wilcoxon signed-rank test. A CI<1 indicates a fitness defect. Growth of (C, E) E. coli CFT073 and (D, F) P. mirabilis HI4320 wild-type and mutant strains in: sdhB, fumC, frdA, and pckA in LB medium (C, D) or defined medium containing 0.2% glucose (E, F) as the carbon source. A representative growth curve is shown for each panel.