Intestinal carriage of Escherichia coli in prepubertal girls without a history of urinary tract infection was examined by collecting weekly stools and periurethral and urine samples over 3 to 4 weeks of study. Dominant and minor clones were defined by grouping 28 E. coli isolates into clonal types. Multiple enteric clones of E. coli, which changed week to week, were found in the 13 girls during the study (median, 3 clones/girl; range, 1 to 16 clones/girl). Dominance of an enteric clone did not predict persistence in the stool. In only 10 (34%) of the 29 episodes in which a dominant clone present in one weekly sample could have been detected the following week did it persist as the dominant clone in the next weekly sample. In 5 (17%) of the 29 episodes, a dominant clone found in one weekly sample was classified as a minor clone the next week. Both dominant and minor clones were observed to colonize the urinary tract. However, when colonization of the periurethra or bladder urine occurred, it was brief and often did not reflect the dominant stool flora from the same week. In fact, in only 40% of episodes was a clone that was detected either on the periurethra or in the urine also recovered from the stool the same week. Our findings suggest that the intestinal flora of healthy girls is multiclonal with frequent fluctuations in composition.Escherichia coli organisms infecting the urinary tract are thought to originate in the intestinal flora. There are two theories that attempt to explain infection of the urinary tract with E. coli derived from the intestine (12). The prevalence theory holds that the numerically dominant fecal strain is most likely to infect the urinary tract. The special-pathogenicity theory holds that a special subset of the intestinal microflora expressing specific virulence markers is most likely to infect the urinary tract. Virulence markers have been defined based on their higher frequency in E. coli isolates from patients with urinary tract infection (UTI) than among the dominant fecal strains of the UTI patient (5, 8, 13) or of healthy controls (6,7,18). Support for either theory relies on examination of the dominant strain in the stool at the time infection of the urinary tract occurs. Drawing conclusions from comparison of strains infecting the urinary tract to the dominant strain in stool is predicated on the notion that the dominant strain in an individual's stool is stable over time. The stability of dominant clones and the frequency of transfer of dominant clones to the urinary tract in healthy controls are therefore important background information for interpreting findings in patients with UTI.Few studies have examined carriage of dominant clones in the intestines of healthy controls (3,4,16). In the present study, we examined the intestinal carriage of E.coli in healthy girls without the confounding variables of antibiotic pressure, estrogenization, or sexual activity. For this, stool, periurethral, and urine samples were obtained weekly from prepubertal females. Dominant and minor ...

Typical enteropathogenic Escherichia coli (EPEC) strains produce bundle-forming pili (BFP), type IVB fimbriae that have been implicated in EPEC virulence, antigenicity, autoaggregation, and localized adherence to epithelial cells (LA). BFP are polymers of bundlin, a pilin protein that is encoded by the bfpA gene found on a large EPEC plasmid. Striking sequence variation has previously been observed among type IV pilin genes of other gram-negative bacterial pathogens (e.g., Pseudomonas and Neisseria spp.). In contrast, the established sequences of bfpA genes from two distantly related prototype EPEC strains vary by only a single base pair. To determine whether bundlin sequences vary more extensively, we used PCR to amplify the bfpA genes from 19 EPEC strains chosen for their various serotypes and sites and years of isolation. Eight different bfpA alleles were identified by sequencing of the PCR products. These alleles can be classified into two major groups. The ␣ group contains three alleles derived from strains carrying O55, O86, O111, O119, O127, or O128 somatic antigens. The ␤ group contains five alleles derived from strains carrying O55, O110, O128ab, O142, or nontypeable antigens. Sequence comparisons show that bundlin has highly conserved and variable regions, with most of the variation occurring in the C-terminal two-thirds of the protein. The results of multilocus enzyme electrophoresis support the hypothesis that bfpA sequences have spread horizontally across distantly related clonal lineages. Strains with divergent bundlin sequences express bundlin protein, produce BFP, and carry out autoaggregation and LA. However, four strains lack most or all of these phenotypes despite having an intact bfpA gene. These results have important implications for our understanding of bundlin structure, transmission of the bfp gene cluster among EPEC strains, and the role of bundlin variation in the evasion of host immune system responses.Enteropathogenic Escherichia coli (EPEC) is one of several pathovars of E. coli capable of causing diarrhea (45). While human EPEC infections, which are manifest primarily in infants, were once commonplace in industrialized nations (56), they are now identified primarily in developing countries (10). EPEC strains possess distinct virulence factors not found in most E. coli strains (45). Typical EPEC strains produce bundleforming pili (BFP), long, flexible, rope-like structures composed of intertwining fibers (19). Based on protein sequence analysis and morphology, BFP belong to the type IV group of fimbriae or pili found on a variety of gram-negative bacteria, many of which are human, animal, or plant pathogens (67, 70, 77). BFP have recently been shown to elicit an antibody response in natural infections (37, 38, 53) and a modest response in experimentally infected adults (13). BFP are required for two phenotypes of EPEC that can be studied in vitro and probably play a role in colonization in vivo. The first is autoaggregation, which is the ability of EPEC to reversibly form multicellu...