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In a prospective study, 179 adult women (age range, 17-82 years) were followed up for 12 months after an index episode of community-acquired cystitis caused by Escherichia coli. Episodes of symptomatic urinary tract infection (UTI) were recorded, and urinary isolates were compared with the index episode isolate; 147 UTI episodes were detected during the follow-up. Of these episodes, 131 were classified as recurrences occurring at least 1 month after the index episode; 44% of the patients had recurrences. A history of UTI increased the risk of recurrence; only 11.8% of the 17 patients without previous episodes of UTI had at least one recurrence, while 47.5% of those with previous episodes had at least one recurrence (OR, 6.8; univariate logistic regression). E. coli caused 78% of the recurrent episodes. Phenotypic and genotypic analysis of E. coli strains showed that one-third of the recurrences were caused by the index episode strain, which could persist and cause recurrences throughout the 1-year follow-up period. The prevalence of adhesins or other identified virulence factors for UTI among the recurrence strains was identical to that among the index episode strains. The presence of these factors did not affect the risk of recurrence but did increase the likelihood that the index episode strain would persist and cause recurrent episodes of UTI.

Type 1 fimbriae are heteropolymeric surface organelles responsible for the D-mannose-sensitive (MS) adhesion of Escherichia coli. We recently reported that variation of receptor specificity of type 1 fimbriae can result solely from minor alterations in the structure of the gene for the FimH adhesin subunit. To further study the relationship between allelic variation of the fimH gene and adhesive properties of type 1 fimbriae, the fimH genes from five additional strains were cloned and used to complement the FimH deletion in E. coli KB18. When the parental and recombinant strains were tested for adhesion to immobilized mannan, a wide quantitative range in the ability of bacteria to adhere was noted. The differences in adhesion do not appear to be due to differences in the levels of fimbriation or relative levels of incorporation of FimH, because these parameters were similar in low-adhesion and high-adhesion strains. The nucleotide sequence for each of the fimH genes was determined. Analysis of deduced FimH sequences allowed identification of two sequence homology groups, based on the presence of Asn-70 and Ser-78 or Ser-70 and Asn-78 residues. The consensus sequences for each group conferred very low adhesion activity, and this low-adhesion phenotype predominated among a group of 43 fecal isolates. Strains isolated from a different host niche, the urinary tract, expressed type 1 fimbriae that conferred an increased level of adhesion. The results presented here strongly suggest that the quantitative variations in MS adhesion are due primarily to structural differences in the FimH adhesin. The observed differences in MS adhesion among populations of E. coli isolated from different host niches call additional attention to the possibility that phenotypic variants of FimH may play a functional role in population dynamics.Adhesion of bacteria to mucosal surfaces is thought to play an important role in both normal ecologic and pathogenic processes (4, 12). Type 1 fimbriae (9) or pili (6, 7) are the most common adhesive organelles expressed by Escherichia coli and other enterobacteria. The only known function of these structures is that they are responsible for the D-mannose-sensitive (MS) adhesion of E. coli to cells (31-34). Type 1 fimbriae are composed primarily of the structural subunit, FimA, and minor amounts of at least three ancillary subunits, FimF, FimG, and FimH (16,19,20,35). The 30-kDa FimH subunit represents the MS adhesin (2, 13-15, 17, 20, 21, 26, 30, 42, 45).We have recently shown that allelic variants of the highly conserved fimH gene (3) encode FimH subunits that confer distinct functional phenotypes (42). We proposed using the designations M, MF, and MFP phenotypes to distinguish strains that bound to yeast mannan (MN); to both MN and human plasma fibronectin (FN); or to MN, FN, and synthetic peptides, respectively (42). The present report extends our previous studies to show that FimH subunits are also capable of conferring broad quantitative differences in the ability of type 1 fimbriated strains ...

The genus Yersinia has been used as a model system to study pathogen evolution. Using whole-genome sequencing of all Yersinia species, we delineate the gene complement of the whole genus and define patterns of virulence evolution. Multiple distinct ecological specializations appear to have split pathogenic strains from environmental, nonpathogenic lineages. This split demonstrates that contrary to hypotheses that all pathogenic Yersinia species share a recent common pathogenic ancestor, they have evolved independently but followed parallel evolutionary paths in acquiring the same virulence determinants as well as becoming progressively more limited metabolically. Shared virulence determinants are limited to the virulence plasmid pYV and the attachment invasion locus ail. These acquisitions, together with genomic variations in metabolic pathways, have resulted in the parallel emergence of related pathogens displaying an increasingly specialized lifestyle with a spectrum of virulence potential, an emerging theme in the evolution of other important human pathogens.genomics metabolic streamlining | pathoadaptation | Enterobacteriaceae B acterial species are defined on the basis of phenotypic characteristics, such as cellular morphology and biochemical characteristics, as well as DNA-DNA hybridization and 16S rRNA comparison. Using high-throughput whole-genome approaches we can now move beyond classic methods and develop population frameworks to reconstruct accurate inter-and intraspecies relationships and gain insights into the complex patterns of gene flux that define different taxonomic groups.Bacterial whole-genome sequencing has revealed enormous heterogeneity in gene content, even between members of the same species. From a bacterial perspective the acquisition of new genes provides the flexibility to adapt and exploit novel niches and opportunities. From a human perspective, integration of genes by bacteria has been directly linked to the emergence of new pathogenic clones, often from formerly harmless lineages (1, 2). In addition to gene gain, gene loss is also strongly associated with host restriction in acutely pathogenic bacterial species, such as Yersinia pestis and Salmonella enterica serovars, including Salmonella Typhi (3-5), where gene loss can remove functions unnecessary in the new niche (6). These specialist pathogens show a much higher frequency of functional gene loss than closely related host generalist pathogens, such as Yersinia pseudotuberculosis (7).Previous Yersinia genome studies (8, 9) have examined the evolution of pathogenicity by comparing strains from a selection of species or species subtypes within the genus, limiting our understanding of the evolutionary context of individual species. The majority of the Yersinia species are found in the environment and do not cause disease in mammals. Three species are known as human pathogens: the plague bacillus Y. pestis and the enteropathogens Yersinia enterocolitica and Y. pseudotuberculosis. SignificanceOur past understanding of pathogen evo...

BackgroundDiarrhea is the most frequent health problem among children in developing countries. This study investigated the bacterial and viral etiology and related clinical and epidemiological factors in children with acute diarrhea in Ouagadougou, Burkina Faso.MethodsStool specimens were collected from 283 children under 5 years of age visiting hospital due to acute diarrhea and from 60 healthy controls of similar age. Pathogens were investigated by using conventional culture techniques, PCR and immunochromatographic testing. Salmonella and Shigella strains were serotyped and their susceptibility to 23 antimicrobial agents was determined by the agar dilution method.ResultsAt least one pathogen was detected in 64% of the 283 patients and in 8% of the 60 controls (p < 0.001). Rotavirus was found in 30% of the patients, followed by diarrheagenic Escherichia coli (24%), Salmonella enterica ssp. enterica (9%), Shigella spp. (6%), adenovirus (5%) and Campylobacter spp. (2%). Multiple pathogens were found in 11% of the patients and in 2% of the controls (p = 0.028). Viruses were found mainly in children of ≤ 2 years of age, whereas bacteria were equally prevalent among all the age groups. Viral infections occurred mostly during the cool dry season and the bacterial infections during the rainy season. Fever (64%) and vomiting (61%) were the most common symptoms associated with diarrhea. Only one Salmonella strain was resistant to nalidixic acid and ciprofloxacin. Of the Shigella strains, one was resistant to nalidixic acid but 81% to trimethoprim- sulfamethoxazole, 63% to streptomycin and 50% to ampicillin. Most of all the other Salmonella and Shigella strains were sensitive to all antimicrobials tested.ConclusionRotaviruses and diarrheal E. coli were the most predominant pathogens associated with acute diarrhea in Burkinabe children. Constant antimicrobial surveillance is warranted to observe for the emergence of enteric bacteria resistant to antimicrobials that are important in treatment also of severe infections.