Relationship between Escherichia coli Strains Causing Acute Cystitis in Women and the Fecal E. coli Population of the Host

Abstract

Previous epidemiological assessments of the prevalence versus special-pathogenicity hypothesis for urinary tract infection (UTI) pathogenesis in women may have been confounded by underlying host population differences between women with UTI and healthy controls and have not considered the clonal complexity of the fecal Escherichia coli population of the host. In the present study, 42 women with acute uncomplicated cystitis served as their own controls for an analysis of the causative E. coli strain and the concurrent intestinal E. coli population. Clonality among the urine isolate and 30 fecal colonies per subject was assessed by repetitiveelement PCR and macrorestriction analysis. Each unique clone underwent PCR-based phylotyping and virulence genotyping. Molecular analysis resolved 109 unique clones (4 urine-only, 38 urine-fecal, and 67 fecal-only clones). Urine clones exhibited a significantly higher prevalence of group B2 than fecal-only clones (69% versus 10%; P < 0.001) and higher aggregate virulence scores (mean, 6.2 versus 2.9; P < 0.001). In multilevel regression models for predicting urine clone status, significant positive predictors included group B2, 10 individual virulence traits, the aggregate virulence score, fecal dominance, relative fecal abundance, and (unique to the present study) a pauciclonal fecal sample. In summary, within the fecal E. coli populations of women with acute cystitis, pauciclonality, clonal dominance, virulence, and group B2 status are closely intertwined. Phylogenetic group B2 status and/or associated virulence factors may promote fecal abundance and pauciclonality, thereby contributing to upstream steps in UTI pathogenesis. This relationship suggests a possible reconciliation of the prevalence and special-pathogenicity hypotheses.Urinary tract infection (UTI), one of the most frequent types of bacterial infection in women, is usually due to Escherichia coli (1). Despite considerable study, the pathogenesis of UTI remains poorly understood. The host's fecal (and, in women, vaginal) flora is the most common immediate source for the infecting E. coli strain (22, 26). However, uncertainty remains regarding to what extent the causative strains represent simply the most prevalent fecal/vaginal E. coli clones within the host population or the affected individuals (the prevalence hypothesis) (24) or, instead, represent a distinctive, highly selected subset of the fecal/vaginal E. coli population with enhanced virulence potential (the special-pathogenicity hypothesis) (18).Favoring the prevalence hypothesis, in acute E. coli UTI, the urine strain tends to be the host's predominant fecal strain (4,18,26). Favoring the special-pathogenicity hypothesis, acutephase UTI isolates usually exhibit more virulence factors than fecal isolates from healthy hosts and derive predominantly from phylogenetic groups B2 and D (versus groups A and B1 for fecal strains) (6,13,27). However, such comparisons may be confounded by between-population host differences, since women who develop UTIs tend to...

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