The membrane transporter PotE is required for virulence in avian pathogenic Escherichia coli (APEC)

Over the last few years, polyamines have been described as key-signal of virulence in pathogenic bacteria. In the current study, we investigated whether the knockout of genes related to polyamine biosynthesis and putrescine transport affected the virulence of an avian pathogenic E. coli (APEC) strain. One-week-old White Leghorn chickens were infected intratracheally with mutants in polyamine biosynthesis (Delta speB/C and Delta speD/E) and transport genes (Delta potE) of a well-characterized APEC strain of ST117 (O83: H4). All polyamine mutants and the wild-type strain were able to infect chicken; however, we observed significantly fewer lesions in the lungs of the chickens infected with the polyamine mutants in comparison with chicken infected with the wild-type. Results derived from histology of infected lungs detected significantly fewer lesions in the lung of birds infected within particular the putrescine transport mutant (Delta potE). A decrease in colonization levels was observed in the liver and spleen of birds infected with the putrescine biosynthesis mutant Delta speB/C, and likewise, a decrease of the colonization levels of all organs from birds infected with the Delta potE was detected. Together, our data demonstrate that the deletion of polyamine genes, and in particular the PotE membrane protein, attenuates the virulence of APEC during infection of chickens.