This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Google Scholar
Right arrow Articles by Olesen, B.
Right arrow Articles by Johnson, J. R.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Olesen, B.
Right arrow Articles by Johnson, J. R.

 Previous Article  |  Next Article 

Journal of Clinical Microbiology, June 2009, p. 1857-1862, Vol. 47, No. 6
0095-1137/09/$08.00+0     doi:10.1128/JCM.00230-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Three-Decade Epidemiological Analysis of Escherichia coli O15:K52:H1{triangledown}

Bente Olesen,1,2* Flemming Scheutz,2 Megan Menard,3 Marianne N. Skov,4 Hans Jørn Kolmos,4 Michael A. Kuskowski,3 and James R. Johnson3

Department of Clinical Microbiology, Hillerød Hospital, Helsevej 2, DK-3400 Hillerød, Denmark,1 The International Escherichia and Klebsiella Centre (WHO), Statens Serum Institut, Copenhagen, Denmark,2 Veterans Affairs Medical Center and Department of Medicine, University of Minnesota, Minneapolis, Minnesota,3 Department of Clinical Microbiology, Odense University Hospital, Sdr. Boulevard 29, DK-5000 Odense C, Denmark4

Received 3 February 2009/ Returned for modification 14 March 2009/ Accepted 25 March 2009

The successful Escherichia coli O15:K52:H1 clonal group provides a case study for the emergence of multiresistant clonal groups of Enterobacteriaceae generally. Accordingly, we tested the hypotheses that, over time, the O15:K52:H1 clonal group has become increasingly (i) virulent and (ii) resistant to antibiotics. One hundred archived international E. coli O15:K52:[H1] clinical isolates from 100 unique patients (1975 to 2006) were characterized for diverse phenotypic and molecular traits. All 100 isolates derived from phylogenetic group D and, presumptively, sequence type ST393. They uniformly carried the F16 papA allele and papG allele II (P fimbria structural subunit and adhesin variants), iha (adhesin-siderophore), fimH (type 1 fimbriae), fyuA (yersiniabactin receptor), iutA (aerobactin receptor), and kpsM II (group 2 capsule); 85% to 89% of them contained a complete copy of the pap operon and ompT (outer membrane protease). Slight additional virulence profile variation was evident, particularly within a minor diarrhea-associated subset (biotype C). However, in contrast to the clonal group's fairly stable virulence profiles over the past 30+ years, during the same interval the clonal group members' antimicrobial resistance profiles increased by a mean of 2.8 units per decade (P < 0.001). Moreover, the numbers of virulence genes and resistance markers were positively associated (P = 0.046), providing evidence against antimicrobial resistance and virulence being mutually exclusive in these strains. Thus, the O15:K52:H1 clonal group has become increasingly resistant to antimicrobials while maintaining (or expanding) its virulence potential, a particularly concerning trend if other emerging multiresistant enterobacterial clonal groups follow a similar pattern.

* Corresponding author. Mailing address: Department of Clinical Microbiology, Hillerød Sygehus, Helsevej 2, DK-3400 Hillerød, Denmark. Phone: 45-4829-4379. Fax: 45-4829-4384. E-mail: benol{at}hih.regionh.dk

{triangledown} Published ahead of print on 1 April 2009.

Journal of Clinical Microbiology, June 2009, p. 1857-1862, Vol. 47, No. 6
0095-1137/09/$08.00+0     doi:10.1128/JCM.00230-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»