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  • Molecular Analysis of Asymptomatic Bacteriuria Escherichia coli Strain VR50 Reveals Adaptation to the Urinary Tract by Gene Acquisition

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    Author(s)
    Beatson, Scott A
    Ben Zakour, Nouri L
    Totsika, Makrina
    Forde, Brian M
    Watts, Rebecca E
    Mabbett, Amanda N
    Szubert, Jan M
    Sarkar, Sohinee
    Phan, Minh-Duy
    Peters, Kate M
    Petty, Nicola K
    Alikhan, Nabil-Fareed
    Sullivan, Mitchell J
    Gawthorne, Jayde A
    Stanton-Cook, Mitchell
    Nguyen, Thi Khanh Nhu
    Chong, Teik Min
    Yin, Wai-Fong
    Chan, Kok-Gan
    Hancock, Viktoria
    Ussery, David W
    Ulett, Glen C
    Schembri, Mark A
    Griffith University Author(s)
    Ulett, Glen C.
    Year published
    2015
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    Abstract
    Urinary tract infections (UTIs) are among the most common infectious diseases of humans, with Escherichia coli responsible for >80% of all cases. One extreme of UTI is asymptomatic bacteriuria (ABU), which occurs as an asymptomatic carrier state that resembles commensalism. To understand the evolution and molecular mechanisms that underpin ABU, the genome of the ABU E. coli strain VR50 was sequenced. Analysis of the complete genome indicated that it most resembles E. coli K-12, with the addition of a 94-kb genomic island (GI-VR50-pheV), eight prophages, and multiple plasmids. GI-VR50-pheV has a mosaic structure and contains ...
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    Urinary tract infections (UTIs) are among the most common infectious diseases of humans, with Escherichia coli responsible for >80% of all cases. One extreme of UTI is asymptomatic bacteriuria (ABU), which occurs as an asymptomatic carrier state that resembles commensalism. To understand the evolution and molecular mechanisms that underpin ABU, the genome of the ABU E. coli strain VR50 was sequenced. Analysis of the complete genome indicated that it most resembles E. coli K-12, with the addition of a 94-kb genomic island (GI-VR50-pheV), eight prophages, and multiple plasmids. GI-VR50-pheV has a mosaic structure and contains genes encoding a number of UTI-associated virulence factors, namely, Afa (afimbrial adhesin), two autotransporter proteins (Ag43 and Sat), and aerobactin. We demonstrated that the presence of this island in VR50 confers its ability to colonize the murine bladder, as a VR50 mutant with GI-VR50-pheV deleted was attenuated in a mouse model of UTI in vivo. We established that Afa is the island-encoded factor responsible for this phenotype using two independent deletion (Afa operon and AfaE adhesin) mutants. E. coli VR50afa and VR50afaE displayed significantly decreased ability to adhere to human bladder epithelial cells. In the mouse model of UTI, VR50afa and VR50afaE displayed reduced bladder colonization compared to wild-type VR50, similar to the colonization level of the GI-VR50-pheV mutant. Our study suggests that E. coli VR50 is a commensal-like strain that has acquired fitness factors that facilitate colonization of the human bladder.
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    Journal Title
    Infection and Immunity
    Volume
    83
    Issue
    5
    DOI
    https://doi.org/10.1128/IAI.02810-14
    Copyright Statement
    © 2012 American Society for Microbiology. The attached file is reproduced here in accordance with the copyright policy of the publisher. Please refer to the journal's website for access to the definitive, published version.
    Subject
    Biological sciences
    Agricultural, veterinary and food sciences
    Biomedical and clinical sciences
    Medical bacteriology
    Publication URI
    http://hdl.handle.net/10072/155749
    Collection
    • Journal articles

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