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Infect. Immun. doi:10.1128/IAI.01215-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Molecular basis of commensalism in the urinary tract: low virulence or virulence attenuation?

Julius-Maximilians-Universität Würzburg, Institut für Molekulare Infektionsbiologie, Röntgenring 11, 97070 Würzburg, Germany; Institute of Laboratory Medicine, Department of Microbiology, Immunology and Glycobiology, Lund University, 22362 Lund, Sweden; Department of Urology, Lund University Hospital, 22185 Lund, Sweden

^* To whom correspondence should be addressed. Email: ulrich.dobrindt{at}mail.uni-wuerzburg.de.

	Abstract

In some patients Escherichia coli strains establish significant bacteriuria without causing symptoms of urinary tract infection (UTI). These asymptomatic bacteriuria (ABU) strains have been shown to express fewer virulence factors than the uropathogenic E. coli (UPEC) strains that cause severe, symptomatic UTI. Paradoxically, ABU strains carry many typical UPEC virulence genes, however, and the molecular basis of their low virulence therefore remains unclear. This study examined if ABU strains may evolve from UPEC by genome loss and virulence gene attenuation. The presence of conserved E. coli K-12 genes was examined using an E. coli K-12 strain MG1655-specific DNA array and the distribution of UPEC virulence-related genes with the E. coli pathoarray. Two groups of strains could be distinguished. Several ABU strains were shown by multi locus sequence typing and by comparative genomic analyses to be related to UPEC but to have smaller genome sizes. There were significant alterations in essential virulence genes, including reductive evolution by point mutations, DNA rearrangements and deletions. Other strains were unrelated to UPEC and lacked most of the virulence-associated genes. The results suggest that some ABU strains arise from virulent strains by attenuation of virulence genes while others are non-virulent and resemble commensal strains. We propose that virulence attenuation might constitute a general mechanism for mucosal pathogens to evolve towards commensalism.