This is the first reported case of high-level extended-spectrum cephalosporin-resistant N. gonorrhoeae transmission. The molecular typing and MDR genotype suggest possible European spread of this strain, highlighting the need for surveillance and the importance of testing the susceptibility of N. gonorrhoeae to extended-spectrum cephalosporins.

To ascertain whether on animal farms there reside extended-spectrum ␤-lactamase (ESBL) and plasmidic class C ␤-lactamase-producing Escherichia coli isolates potentially pathogenic for humans, phylogenetic analyses, pulsed-field gel electrophoresis (PFGE) typing, serotyping, and virulence genotyping were performed for 86 isolates from poultry (57 isolates) and pig (29 isolates) farms. E. coli isolates from poultry farms carried genes encoding enzymes of the CTX-M-9 group as well as CMY-2, whereas those from pig farms mainly carried genes encoding CTX-M-1 enzymes. Poultry and pig isolates differed significantly in their phylogenetic group assignments, with phylogroup A predominating in pig isolates and phylogroup D predominating in avian isolates. Among the 86 farm isolates, 23 (26.7%) carried two or more virulence genes typical of extraintestinal pathogenic E. coli (ExPEC). Of these, 20 were isolated from poultry farms and only 3 from pig farms. Ten of the 23 isolates belonged to the classic human ExPEC serotypes O2:H6, O2:HNM, O2:H7, O15:H1, and O25:H4. Despite the high diversity of serotypes and pulsotypes detected among the 86 farm isolates, 13 PFGE clusters were identified. Four of these clusters contained isolates with two or more virulence genes, and two clusters exhibited the classic human ExPEC serotypes O2:HNM (ST10) and O2:H6 (ST115). Although O2:HNM and O2:H6 isolates of human and animal origins differed with respect to their virulence genes and PFGE pulsotypes, the O2:HNM isolates from pigs showed the same sequence type (ST10) as those from humans. The single avian O15:H1 isolate was compared with human clinical isolates of this serotype. Although all were found to belong to phylogroup D and shared the same virulence gene profile, they differed in their sequence types (ST362-avian and ST393-human) and PFGE pulsotypes. Noteworthy was the detection, for the first time, in poultry farms of the clonal groups O25b:H4-ST131-B2, producing CTX-M-9, and O25a-ST648-D, producing CTX-M-32. The virulence genes and PFGE profiles of these two groups were very similar to those of clinical human isolates. While further studies are required to determine the true zoonotic potential of these clonal groups, our results emphasize the zoonotic risk posed especially by poultry farms, but also by pig farms, as reservoirs of ESBL-and CMY-2-encoding E. coli.

Uropathogenic isolates of Escherichia coli (UPEC) contain blocks of DNA, termed pathogenicity islands (PAIs), that contribute to their virulence. Two multiplex PCR assays were developed to detect eight PAI markers among 50 commensal E. coli and 100 UPEC isolates. In total, 40% of commensal isolates and 93% of UPEC carried PAIs. Despite this difference, the distribution of various PAIs showed the same pattern in both groups, with the most prevalent being PAI IV(536) (38% commensal vs. 89% UPEC), followed by PAI I(CFT073) (26% vs. 73%), PAI II(CFT073) (14% vs. 46%), PAI II(J96) (8% vs. 34%), PAI I(536) (8% vs. 33%) and PAI II(536) (4% vs. 20%). PAI III(536) was detected only in UPEC (2%), while PAI I(J96) was not detected in any isolate. Although the mean number of PAIs per isolate was higher among UPEC (2.97) than in commensal (0.98) isolates, there were no statistical differences among group B2 E. coli from the two origins; however, commensal isolates from groups D and B1 appeared to be less virulent than pathogenic isolates. Regardless of their phylogenetic group, nearly all the commensal and UPEC isolates with the same number of PAIs had the same PAI combinations. Although group B2 E. coli are uncommon among commensal intestinal flora, they are highly virulent when present, suggesting that the intestinal flora may act as a reservoir for bacteria that can cause urinary tract infection.

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...

E. coli isolates resistant to quinolones, trimethoprim/sulfamethoxazole and especially fluoroquinolones were associated with reductions in virulence traits and shifts to non-B2 phylogenetic groups. Moreover, fluoroquinolone resistance usually occurred in low-virulence E. coli group A isolates rather than in isolates from groups B2 and D which had lost virulence traits. CGA accounted for 23% of trimethoprim/sulfamethoxazole-resistant E. coli producing pyelonephritis.

To gain insight into the mechanisms by which Lactobacillus blocks the adherence of uropathogens to vaginal epithelial cells and inhibits their growth, 15 Lactobacillus strains and 22 uropathogens were studied. Lactobacilli from hemagglutination group III, identified as Lactobacillus crispatus, showed greater capacity to block uropathogen adherence than those from hemagglutination groups II and I (61.9%, 49.5%, and 52.6% of blockage, respectively). Pseudomonas aeruginosa PA5 and Klebsiella pneumoniae KP7 were the uropathogens most susceptible to blockage, and Staphylococcus aureus SA11 and Proteus mirabilis PM1 were the most resistant. Lactobacillus inhibited uropathogen growth better in liquid assays; the 3 Lactobacillus groups showed similar inhibitory power (72.3%, 71.9%, and 74.2% of light transmittance). P. aeruginosa PA5 was the most inhibited, and Enterococcus species E15 was the least inhibited. There is considerable variation among Lactobacillus strains regarding their adherence to uroepithelium, blockage of uropathogen attachment, and inhibition of uropathogen growth. Although these properties are independent, they may coincide and therefore allow for these strains to balance the vaginal ecosystem and to make them useful as probiotics.

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To clarify whether prevalence or special pathogenicity is more important in determining urinary tract infection (UTI) causation, we compared the biotype, phylogenetic group, and virulence genes of Escherichia coli urine strains from 11 women with acute lower UTI with those of the host's dominant intestinal E. coli strain(s). Twenty-one unique E. coli clones were identified. For three women, the single faecal clone identified was also the host's urine clone, whereas for eight women faecal samples yielded 1 or 2 distinct non-urine clones (total, n = 10), either with (n = 3) or without (n = 5) the concurrent urine clone. The eight urine clones from the latter eight women exhibited significantly greater inferred virulence, according to virulence gene content and phylogenetic background, than did the hosts' 10 corresponding 'faecal only' clones. In contrast, the three urine clones that were detected as the host's sole faecal clone exhibited significantly lower inferred virulence than the other eight urine clones, and were statistically indistinguishable from the 10 'faecal only' clones. In conclusion, special pathogenicity is an important determinant of UTI pathogenesis in women, although prevalence may occasionally allow less virulent strains to cause UTI.