Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8505518 | Veterinary Microbiology | 2018 | 7 Pages |
Abstract
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 (ÎspeB/C and ÎspeD/E) and transport genes (ÎpotE) 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 (ÎpotE). A decrease in colonization levels was observed in the liver and spleen of birds infected with the putrescine biosynthesis mutant ÎspeB/C, and likewise, a decrease of the colonization levels of all organs from birds infected with the ÎpotE 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.
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Authors
Priscila Regina Guerra, Ana Herrero-Fresno, Susanne Elisabeth Pors, Shahana Ahmed, Dan Wang, Ida Thøfner, Fabio Antenucci, John Elmerdahl Olsen,