Host-pathogen relationships among Escherichia coli isolates recovered from men with febrile urinary tract infection

James R. Johnson, Flemming Scheutz, Peter Ulleryd, Michael A. Kuskowski, Timothy T. O'Bryan, Torsten Sandberg

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26 Scopus citations


Background. Host-pathogen relationships in men with febrile urinary tract infection (FUTI) are poorly understood. Methods. Phylogenetic background, extended virulence genotypes, and serotypes were determined for 70 Escherichia coli isolates recovered from urine samples obtained from men with FUTI for comparison with available data for 70 E. coli rectal isolates recovered from uninfected men. Bacterial traits were assessed in relation to underlying host characteristics (age, compromise status, and history of urinary tract infection) and acute manifestations (bacteremia, flank pain, and serum prostate-specific antigen [PSA] level). Results. Compared with rectal isolates, FUTI isolates exhibited a significantly higher prevalence of virulence-associated phylogenetic groups, serotypes, and extraintestinal virulence genes. The latter included traditional prostatitis-associated traits (e.g., hemolysin and cytotoxic necrotizing factor), as well as unconventional traits, such as outer membrane protease T. These bacterial traits occurred largely independent of host age, urological compromise status, urinary tract infection history, and acute manifestations. However, certain traits were less prevalent in association with use of urinary tract instrumentation and significantly predicted elevated PSA levels. Conclusions. Considerable virulence capability may be required for an E. coli strain to cause FUTI in men, regardless of whether most compromising conditions are present. Bacterial traits that promote prostatic invasion may be relevant for the pathogenesis of FUTI, even among men without classic manifestations of acute prostatitis.

Original languageEnglish (US)
Pages (from-to)813-822
Number of pages10
JournalClinical Infectious Diseases
Issue number6
StatePublished - Mar 15 2005

Bibliographical note

Funding Information:
Financial support. This material is based on work supported by the Office of Research and Development, Medical Research Service, Department of Veterans Affairs (J.R.J.); National Institutes of Health (grant DK-47504; to J.R.J.); National Research Initiative Competitive Grants Program/ US Department of Agriculture (grant 00-35212-9408; to J.R.J.); the Scandinavian Society for Anitmicrobial Chemotherapy (T.S.); and the Medical Society of Göteborg (P.U.).

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