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Journal of Clinical Microbiology, August 2005, p. 3895-3900, Vol. 43, No. 8
0095-1137/05/$08.00+0 doi:10.1128/JCM.43.8.3895-3900.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Phylogenetic and Pathotypic Comparison of Concurrent Urine and Rectal Escherichia coli Isolates from Men with Febrile Urinary Tract Infection
James R. Johnson,1,2*
Flemming Scheutz,3
Peter Ulleryd,4
Michael A. Kuskowski,5,6
Timothy T. O'Bryan,1,2 and
Torsten Sandberg4
Mucosal and Vaccine Research Center,1
Geriatric Research, Education, and Clinical Center, Minneapolis VA Medical Center,5
Departments of Medicine,2
Psychiatry, University of Minnesota, Minneapolis, Minnesota,6
International Escherichia coli and Klebsiella Center, Statens Seruminstitut, Copenhagen, Denmark,3
Department of Infectious Diseases, University of Göteborg, Göteborg, Sweden4
Received 27 February 2005/
Returned for modification 11 April 2005/
Accepted 18 May 2005
Among men with febrile urinary tract infection (FUTI), whether the host's fecal flora is the source for the urine strain ("fecal-urethral" hypothesis), and whether pathogenesis is driven by prevalence versus special pathogenicity, are unknown. Accordingly, pretherapy urine isolates from 65 men with FUTI were compared with concurrent rectal isolates from the same hosts according to serotype, genomic profile, phylogenetic group, and virulence genotype. The host's multiple rectal colonies included only the urine clone in 25% of subjects, the urine clone plus additional clones in 22%, and only nonurine clones in 54%. Compared with the 67 unique rectal clones, the 65 urine isolates were significantly enriched for phylogenetic group B2, virulence-associated serotypes, and specific virulence genes and contained more virulence genes (median, 10 versus 6: P < 0.001). In multivariable models, phylogenetic group B2, hlyD (hemolysin), cnf1 (cytotoxic necrotizing factor), iroN (siderophore receptor), ompT (outer membrane protease), and malX (pathogenicity island marker) most strongly predicted urine source. These findings challenge the fecal-urethral and prevalence hypotheses for FUTI pathogenesis and instead strongly support the possibility of alternate infection routes in some men and the special pathogenicity hypothesis. They also identify specific bacterial traits as potential targets for anti-FUTI interventions.
* Corresponding author. Mailing address: Infectious Diseases (111F), Minneapolis VA Medical Center, 1 Veterans Drive, Minneapolis, MN 55417. Phone: (612) 467-4185. Fax: (612) 727-5995. E-mail: johns007{at}umn.edu.
Journal of Clinical Microbiology, August 2005, p. 3895-3900, Vol. 43, No. 8
0095-1137/05/$08.00+0 doi:10.1128/JCM.43.8.3895-3900.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
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Copyright © 2005 by the American Society for Microbiology. All rights reserved.