scholarly journals Identification of uropathogenic Escherichia coli clonal group A (CgA) in hospitalised patients

2009 ◽  
Vol 104 (5) ◽  
pp. 787-789 ◽  
Author(s):  
Rubens CS Dias ◽  
Denise V Marangoni ◽  
Lee W Riley ◽  
Beatriz M Moreira
2007 ◽  
Vol 73 (13) ◽  
pp. 4180-4184 ◽  
Author(s):  
Laura A. Boczek ◽  
Eugene W. Rice ◽  
Brian Johnston ◽  
James R. Johnson

ABSTRACT Isolates of Escherichia coli belonging to clonal group A (CGA), a recently described disseminated cause of drug-resistant urinary tract infections in humans, were present in four of seven sewage effluents collected from geographically dispersed areas of the United States. All 15 CGA isolates (1% of the 1,484 isolates analyzed) exhibited resistance to trimethoprim-sulfamethoxazole (TMP-SMZ), accounting for 19.5% of the 77 TMP-SMZ-resistant isolates. Antimicrobial resistance patterns, virulence traits, O:H serotypes, and phylogenetic groupings were compared for CGA and selected non-CGA isolates. The CGA isolates exhibited a wider diversity of resistance profiles and somatic antigens than that found in most previous characterizations of this clonal group. This is the first report of recovery from outside a human host of E. coli CGA isolates with virulence factor and antibiotic resistance profiles typical of CGA isolates from a human source. The occurrence of “human-type” CGA in wastewater effluents demonstrates a potential mode for the dissemination of this clonal group in the environment, with possible secondary transmission to new human or animal hosts.


2006 ◽  
Vol 74 (6) ◽  
pp. 3427-3436 ◽  
Author(s):  
Simon Léveillé ◽  
Mélissa Caza ◽  
James R. Johnson ◽  
Connie Clabots ◽  
Mourad Sabri ◽  
...  

ABSTRACT Virulence factors of pathogenic Escherichia coli belonging to a recently emerged and disseminated clonal group associated with urinary tract infection (UTI), provisionally designated clonal group A (CGA), have not been experimentally investigated. We used a mouse model of ascending UTI with CGA member strain UCB34 in order to identify genes of CGA that contribute to UTI. iha was identified to be expressed by strain UCB34 in the mouse kidney using selective capture of transcribed sequences. iha from strain UCB34 demonstrated a siderophore receptor phenotype when cloned in a catecholate siderophore receptor-negative E. coli K-12 strain, as shown by growth promotion experiments and uptake of 55Fe complexed to enterobactin or its linear 2, 3-dihydroxybenzoylserine (DHBS) siderophore derivatives. Siderophore-mediated growth promotion by Iha was TonB dependent. Growth and iron uptake were more marked with linear DHBS derivatives than with purified enterobactin. The reported phenotype of adherence to epithelial cells conferred by expressing iha from a multicopy cloning vector in a poorly adherent E. coli K-12 host strain was confirmed to be specific to iha, in comparison with other siderophore receptor genes. iha expression was regulated by the ferric uptake regulator Fur and by iron availability, as shown by real-time reverse transcriptase PCR. In a competitive infection experiment using the mouse UTI model, wild-type strain UCB34 significantly outcompeted an isogenic iha null mutant. Iha thus represents a Fur-regulated catecholate siderophore receptor that, uniquely, exhibits an adherence-enhancing phenotype and is the first described urovirulence factor identified in a CGA strain.


2010 ◽  
Vol 76 (24) ◽  
pp. 8281-8284 ◽  
Author(s):  
Lotte Jakobsen ◽  
Anette M. Hammerum ◽  
Niels Frimodt-Møller

ABSTRACT Escherichia coli clonal group A isolates cause infections in people. We investigated 158 phylogroup D E. coli isolates from animals, meat, and humans. Twenty-five of these isolates were of clonal group A, and 15 isolates were shown to cause infection in a mouse urinary tract infection (UTI) model. We conclude that clonal group A isolates are found in both broiler chickens and broiler chicken meat and may cause UTI in humans.


2009 ◽  
Vol 53 (7) ◽  
pp. 2733-2739 ◽  
Author(s):  
James R. Johnson ◽  
Megan Menard ◽  
Brian Johnston ◽  
Michael A. Kuskowski ◽  
Kim Nichol ◽  
...  

ABSTRACT The extent to which clonal spread contributes to emerging antimicrobial resistance in Escherichia coli is incompletely defined. To address this question within a recent, nationally representative strain collection, three established drug-resistant E. coli clonal groups (i.e., clonal group A, E. coli O15:K52:H1, and sequence type 131 [ST131]) were sought among 199 E. coli urine isolates recovered from across Canada from 2002 to 2004, with stratification by resistance to trimethoprim-sulfamethoxazole (TS) and fluoroquinolones (FQs). The isolates' clonal backgrounds, virulence genotypes, and macrorestriction profiles were assessed. The three clonal groups were found to account for 37.2% of isolates overall, but accounted for 0% of TS-susceptible (TS-S) and FQ-susceptible (FQ-S) isolates, 20% of TS-resistant (TS-R) and FQ-S isolates, 60% of TS-S and FQ-R isolates, and 68% of TS-R and FQ-R isolates (P < 0.001). E. coli ST131, the most prevalent clonal group, accounted for 23.1% of isolates overall and for 44% of the FQ-R isolates. Nearly all ST131 isolates were FQ-R (96%) but, notably, cephalosporin susceptible (98%). Although the distinctive virulence profiles of the FQ-R clonal group isolates were less extensive than those of the susceptible isolates, they were significantly more extensive than those of the other FQ-R isolates. These findings indicate that among the E. coli urine isolates studied, resistance to TS and FQs has a prominent clonal component, with the O15:K52:H1 clonal group and especially E. coli ST131 being the major contributors. These clonal groups appear to be more virulent than comparably resistant isolates, possibly contributing to their success as emerging multi-drug-resistant pathogens.


2013 ◽  
Vol 19 (7) ◽  
pp. 656-661 ◽  
Author(s):  
L. Skjøt-Rasmussen ◽  
S.S. Olsen ◽  
L. Jakobsen ◽  
K. Ejrnæs ◽  
F. Scheutz ◽  
...  

2004 ◽  
Vol 42 (6) ◽  
pp. 2618-2622 ◽  
Author(s):  
J. R. Johnson ◽  
K. Owens ◽  
A. R. Manges ◽  
L. W. Riley

2005 ◽  
Vol 41 (4) ◽  
pp. 568-568 ◽  
Author(s):  
J. R. Johnson

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