To test the role of central metabolic pathways during an actual infection mutants were constructed in UPEC strain CFT073 to produce defects in glycolysis (pgi, phosphoglucose isomerase and tpiA, triosephosphate isomerase) [29], the Entner-Doudoroff pathway (edd, 6-phosphogluconate dehydratase) [10], the oxidative branch (gnd, 6-phosphogluconate dehydrogenase) and the non-oxidative branch (talA, transaldolase) of the pentose phosphate pathway [26], gluconeogenesis (pckA, phosphoenolpyruvate carboxykinase) [30], and the TCA cycle (sdhB, succinate dehydrogenase) [31]. This evidence concerns the gene GPI and infection.