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Journal of Clinical Microbiology, June 2002, p. 1913-1923, Vol. 40, No. 6
0095-1137/02/$04.00+0     DOI: 10.1128/JCM.40.6.1913-1923.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Global Molecular Epidemiology of the O15:K52:H1 Extraintestinal Pathogenic Escherichia coli Clonal Group: Evidence of Distribution beyond Europe

James R. Johnson,1,2* Adam L. Stell,1,2,{dagger} Timothy T. O'Bryan,1,2 Michael Kuskowski,3,4 Bogdan Nowicki,5 Candice Johnson,6 Joel N. Maslow,7 Anil Kaul,8,{ddagger} Justine Kavle,1,2,§ and Guillem Prats10,||

Medical Service,1 Geriatric Research, Education, and Clinical Center, Minneapolis VA Medical Center,3 Departments of Medicine,2 Psychology,4 Obstetrics and Gynecology,,8 Department of Obstetrics and Gynecology, Hennepin County Medical Center,Minneapolis, Minnesota,9 Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, Texas,5 Child Health Clinic, The Childrens Hospital, and Department of Pediatrics, University of Colorado, Denver, Colorado,6 VA Medical Center and Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania,7 Departament de Microbiologia, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain,10

Received 27 December 2001/ Returned for modification 28 February 2002/ Accepted 10 March 2002

Escherichia coli O15:K52:H1 is a significant extraintestinal pathogen in Europe (G. Prats et al., J. Clin. Microbiol. 38:201-209, 2000). To search for evidence of this clonal group outside of Europe, 75 non-European E. coli isolates of serogroup O15 were compared with five members of the O15:K52:H1 clonal group from Barcelona, Spain, according to genomic background, virulence genotypes, and antimicrobial resistance profiles. Amplification phylotyping showed that 16 (21%) of the 75 non-European O15 isolates corresponded with the O15:K52:H1 clonal group. The 16 non-European O15:K52:H1 clonal group members represented diverse geographic locales. They were isolated almost exclusively from humans with extraintestinal infections and accounted for 50% of all O15 isolates from five human clinical collections studied. Most non-European clonal group members exhibited a consensus virulence factor profile that included the F16 or F7-2 papA alleles (P fimbrial structural subunit), papG allele II (P fimbrial adhesin), iha (putative adhesin siderophore), and iutA (aerobactin receptor). This resembles the virulence profiles of (i) European representatives of the O15:K52:H1 clonal group and (ii) phylogenetically related "clonal group A," a recently recognized significant contributor to trimethoprim-sulfamethoxazole resistance in the United States (A. R. Manges et al., N. Engl. J. Med. 345:1007-1013, 2001). Antimicrobial resistance profiles were variable, and resistance was inconsistently transferred by conjugation. These findings indicate that the O15:K52:H1 clonal group is broadly distributed beyond Europe, exhibits previously unrecognized phenotypic and genotypic diversity, and contributes significantly to extraintestinal infections in humans.

* Corresponding author. Mailing address: University of Minnesota Department of Medicine, Infectious Diseases (111F), VA Medical Center, One Veterans Dr., Minneapolis, MN 55417. Phone: (612) 725-2000, ext. 4185. Fax: (612) 727-5995. E-mail: johns007{at}tc.umn.edu.

{dagger} Present address: Department of Molecular Genetics and Microbiology, University of Texas at Austin, Austin, Tex.

{ddagger} Present address: Minnesota State Health Technology Advisory Committee, St. Paul, Minn.

§ Present address: School of Public Health, Johns Hopkins University, Baltimore, Md.

|| Present address: Servei de Microbiologia, Hospital de Vall d'Hebron, Barcelona, Spain.

Journal of Clinical Microbiology, June 2002, p. 1913-1923, Vol. 40, No. 6
0095-1137/02/$04.00+0     DOI: 10.1128/JCM.40.6.1913-1923.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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