We report the characteristics of 115 extended-spectrum beta-lactamase (ESBL)-producing Escherichia coli clinical isolates, from 115 unique Danish patients, over a 1-year study interval (1 October 2008 to 30 September 2009). Forty-four (38%) of the ESBL isolates represented sequence type 131 (ST13)1, from phylogenetic group B2. The remaining 71 isolates were from phylogenetic groups D (27%), A (22%), B1 (10%), and B2 (3%). Serogroup O25 ST131 isolates (n ‫؍‬ 42; 95% of ST131) comprised 7 different K antigens, whereas two ST131 isolates were O16:K100:H5. Compared to non-ST131 isolates, ST131 isolates were associated positively with CTX-M-15 and negatively with CTX-M-1 and CTX-M-14. They also were associated positively with 11 virulence genes, including afa and dra (Dr family adhesins), the F10 papA allele (P fimbria variant), fimH (type 1 fimbriae), fyuA (yersiniabactin receptor), iha (adhesin siderophore), iutA (aerobactin receptor), kpsM II (group 2 capsules), malX (pathogenicity island marker), ompT (outer membrane protease), sat (secreted autotransporter toxin), and usp (uropathogenicity-specific protein) and negatively with hra (heat-resistant agglutinin) and iroN (salmochelin receptor). The consensus virulence gene profile (>90% prevalence) of the ST131 isolates included fimH, fyuA, malX, and usp (100% each), ompT and the F10 papA allele (95% each), and kpsM II and iutA (93% each). ST131 isolates were also positively associated with community acquisition, extraintestinal pathogenic E. coli (ExPEC) status, and the O25, K100, and H4 antigens. Thus, among ESBL E. coli isolates in Copenhagen, ST131 was the most prevalent clonal group, was community associated, and exhibited distinctive and comparatively extensive virulence profiles, plus a greater variety of capsular antigens than reported previously. E scherichia coli is the most common agent of urinary tract infection (UTI) and Gram-negative bacteremia. E. coli sequence type 131 (ST131) is a recently emerged worldwide pandemic clonal group, causing widespread antimicrobial-resistant infections (1). Although many studies have examined various aspects of E. coli ST131 in diverse locales and clinical contexts (1, 2), little is known about ST131's O:K:H serotypes, especially in relation to community versus health care site of acquisition, coresistance phenotypes, extended-spectrum beta-lactamase (ESBL) variants, and pulse-field gel electrophoresis (PFGE) types. Such data are needed to more fully understand the epidemiology of ST131 and to help guide diagnostic and preventive efforts.CTX-M-type beta-lactamases have become the dominant ESBLs worldwide during the past decade (3). The responsible bla CTX-M genes are known to be associated with conjugative plasmids and certain successful bacterial clones, notably ST131 (4).Here we assessed the prevalence of E. coli ST131 among 115 consecutive ESBL-producing E. coli isolates from 115 patients (2008)(2009) from 3 hospitals and 100 general practitioners' offices in Copenhagen, Denmark. Subsequently, we compared ST131 and ...

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Of over 200 different identified Vibrio cholerae serogroups only the O1 serogroup is consistently associated with endemic and epidemic cholera disease. The O1 serogroup has two serologically distinguishable variants, the Ogawa and Inaba serotypes, which differ only by a methyl group present on the terminal sugar of the Ogawa O-antigen but absent from Inaba strains. This methylation is catalyzed by a methyltransferase encoded by the wbeT gene, which in Inaba strains is disrupted by mutation. It is currently thought that there is little difference between the two serotypes. However, here we show, using isogenic pairs of O1 El Tor V. cholerae , that Inaba strains show significantly different patterns of gene expression and are significantly less able than the corresponding Ogawa strains to cause cholera in an infant mouse infection model. Our results suggest that changes in gene expression resulting from the loss of the wbeT gene lead to reduced virulence and possibly also reduced survival fitness outside the human host.