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Infection and Immunity, February 2008, p. 695-703, Vol. 76, No. 2
0019-9567/08/$08.00+0     doi:10.1128/IAI.01215-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Molecular Basis of Commensalism in the Urinary Tract: Low Virulence or Virulence Attenuation?{triangledown} ,{dagger}

Jaroslaw Zdziarski,1 Catharina Svanborg,2 Björn Wullt,3 Jörg Hacker,1 and Ulrich Dobrindt1*

Institut für Molekulare Infektionsbiologie, Julius-Maximilians-Universität Würzburg, Röntgenring 11, 97070 Würzburg, Germany,1 Institute of Laboratory Medicine, Department of Microbiology, Immunology and Glycobiology, Lund University, 22362 Lund, Sweden,2 Department of Urology, Lund University Hospital, 22185 Lund, Sweden3

Received 4 September 2007/ Returned for modification 2 November 2007/ Accepted 13 November 2007

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, and the molecular basis of their low virulence therefore remains unclear. This study examined whether ABU strains might 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 was examined with the E. coli pathoarray. Two groups of strains could be distinguished. Several ABU strains were shown by multilocus 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 nonvirulent and resemble commensal strains. We propose that virulence attenuation might constitute a general mechanism for mucosal pathogens to evolve toward commensalism.


* Corresponding author. Mailing address: Institut für Molekulare Infektionsbiologie, Röntgenring 11, D-97070 Würzburg, Germany. Phone: 49 (0)931 312155. Fax: 49 (0)931 312578. E-mail: ulrich.dobrindt{at}mail.uni-wuerzburg.de

{triangledown} Published ahead of print on 26 November 2007.

{dagger} Supplemental material for this article may be found at http://iai.asm.org/.

Editor: A. J. Bäumler


Infection and Immunity, February 2008, p. 695-703, Vol. 76, No. 2
0019-9567/08/$08.00+0     doi:10.1128/IAI.01215-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.







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