Pathogenicity Islands of Intestinal E. coli

2002 ◽  
pp. 31-48 ◽  
Author(s):  
A. G. Torres ◽  
J. B. Kaper
Keyword(s):  
Pathogenicity Islands ◽  
E Coli

Pathogenicity Islands of Uropathogence E. Coli and Evolution of Virulence

2005 ◽  
pp. 25-32 ◽  
Author(s):  
Gabriele Blum-Oehler ◽  
Ulrich Dobrindt ◽  
Britta Janke ◽  
Gábor Nagy ◽  
Katharine Piechaczek ◽  
...  
Keyword(s):  
Pathogenicity Islands ◽  
E Coli ◽  
Evolution Of Virulence

scholarly journals Genetic Structure and Distribution of Four Pathogenicity Islands (PAI I536 to PAI IV536) of Uropathogenic Escherichia coli Strain 536

2002 ◽  
Vol 70 (11) ◽  
pp. 6365-6372 ◽  
Author(s):  
Ulrich Dobrindt ◽  
Gabriele Blum-Oehler ◽  
Gabor Nagy ◽  
György Schneider ◽  
André Johann ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Genetic Structure ◽  
Dna Sequences ◽  
Coli Strain ◽  
Open Reading Frames ◽  
Pathogenicity Islands ◽  
Virulence Determinants ◽  
Core Element ◽  
E Coli ◽  
Virulence Potential

ABSTRACT For the uropathogenic Escherichia coli strain 536 (O6:K15:H31), the DNA sequences of three pathogenicity islands (PAIs) (PAI I536 to PAI III536) and their flanking regions (about 270 kb) were determined to further characterize the virulence potential of this strain. PAI I536 to PAI III536 exhibit features typical of PAIs, such as (i) association with tRNA-encoding genes; (ii) G+C content differing from that of the host genome; (iii) flanking repeat structures; (iv) a mosaic-like structure comprising a multitude of functional, truncated, and nonfunctional putative open reading frames (ORFs) with known or unknown functions; and (v) the presence of many fragments of mobile genetic elements. PAI I536 to PAI III536 range between 68 and 102 kb in size. Although these islands contain several ORFs and known virulence determinants described for PAIs of other extraintestinal pathogenic E. coli (ExPEC) isolates, they also consist of as-yet-unidentified ORFs encoding putative virulence factors. The genetic structure of PAI IV536, which represents the core element of the so-called high-pathogenicity island encoding a siderophore system initially identified in pathogenic yersiniae, was further characterized by sample sequencing. For the first time, multiple PAI sequences (PAI I536 to PAI IV536) in uropathogenic E. coli were studied and their presence in several wild-type E. coli isolates was extensively investigated. The results obtained suggest that these PAIs or at least large fragments thereof are detectable in other pathogenic E. coli isolates. These results support our view that the acquisition of large DNA regions, such as PAIs, by horizontal gene transfer is an important factor for the evolution of bacterial pathogens.

scholarly journals A subset of mucosa-associated Escherichia coli isolates from patients with colon cancer, but not Crohn's disease, share pathogenicity islands with urinary pathogenic E. coli

Microbiology ◽  
2008 ◽  
Vol 154 (2) ◽  
pp. 571-583 ◽  
Author(s):  
Christina Bronowski ◽  
Shirley L. Smith ◽  
Kyoko Yokota ◽  
John E. Corkill ◽  
Helen M. Martin ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Colon Cancer ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Pathogenicity Islands ◽  
E Coli

scholarly journals Molecular Profiling of Shiga Toxin-Producing Escherichia coli and Enteropathogenic E. coli Strains Isolated from French Coastal Environments

2016 ◽  
Vol 82 (13) ◽  
pp. 3913-3927 ◽  
Author(s):  
C. Balière ◽  
A. Rincé ◽  
S. Delannoy ◽  
P. Fach ◽  
M. Gourmelon
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Virulence Gene ◽  
Coastal Environment ◽  
Pathogenicity Islands ◽  
Content Type ◽  
E Coli ◽  
Gene Profiles ◽  
Genes Encoding ◽  
High Level

ABSTRACTShiga toxin-producingEscherichia coli(STEC) and enteropathogenicE. coli(EPEC) strains may be responsible for food-borne infections in humans. Twenty-eight STEC and 75 EPEC strains previously isolated from French shellfish-harvesting areas and their watersheds and belonging to 68 distinguishable serotypes were characterized in this study. High-throughput real-time PCR was used to search for the presence of 75E. colivirulence-associated gene targets, and genes encoding Shiga toxin (stx) and intimin (eae) were subtyped using PCR tests and DNA sequencing, respectively. The results showed a high level of diversity between strains, with 17 unique virulence gene profiles for STEC and 56 for EPEC. Seven STEC and 15 EPEC strains were found to display a large number or a particular combination of genetic markers of virulence and the presence ofstxand/oreaevariants, suggesting their potential pathogenicity for humans. Among these, an O26:H11stx1aeae-β1 strain was associated with a large number of virulence-associated genes (n= 47), including genes carried on the locus of enterocyte effacement (LEE) or other pathogenicity islands, such as OI-122, OI-71, OI-43/48, OI-50, OI-57, and the high-pathogenicity island (HPI). One O91:H21 STEC strain containing 4stxvariants (stx1a,stx2a,stx2c, andstx2d) was found to possess genes associated with pathogenicity islands OI-122, OI-43/48, and OI-15. Among EPEC strains harboring a large number of virulence genes (n, 34 to 50), eight belonged to serotype O26:H11, O103:H2, O103:H25, O145:H28, O157:H7, or O153:H2.IMPORTANCEThe speciesE. coliincludes a wide variety of strains, some of which may be responsible for severe infections. This study, a molecular risk assessment study ofE. colistrains isolated from the coastal environment, was conducted to evaluate the potential risk for shellfish consumers. This report describes the characterization of virulence gene profiles andstx/eaepolymorphisms ofE. coliisolates and clearly highlights the finding that the majority of strains isolated from coastal environment are potentially weakly pathogenic, while some are likely to be more pathogenic.

scholarly journals Instability of Pathogenicity Islands in Uropathogenic Escherichia coli 536

2004 ◽  
Vol 186 (10) ◽  
pp. 3086-3096 ◽  
Author(s):  
Barbara Middendorf ◽  
Bianca Hochhut ◽  
Kristina Leipold ◽  
Ulrich Dobrindt ◽  
Gabriele Blum-Oehler ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Direct Repeat ◽  
Pathogenicity Islands ◽  
Site Specific ◽  
Site Specific Recombination ◽  
E Coli ◽  
Specific Pcr ◽  
Specific Pcr Assay ◽  
Derivatives Of ◽  
Specific Sequences

ABSTRACT The uropathogenic Escherichia coli strain 536 carries at least five genetic elements on its chromosome that meet all criteria characteristic of pathogenicity islands (PAIs). One main feature of these distinct DNA regions is their instability. We applied the so-called island-probing approach and individually labeled all five PAIs of E. coli 536 with the counterselectable marker sacB to evaluate the frequency of PAI-negative colonies under the influence of different environmental conditions. Furthermore, we investigated the boundaries of these PAIs. According to our experiments, PAI II536 and PAI III536 were the most unstable islands followed by PAI I536 and PAI V536, whereas PAI IV536 was stable. In addition, we found that deletion of PAI II536 and PAI III536 was induced by several environmental stimuli. Whereas excision of PAI I536, PAI II536, and PAI V536 was based on site-specific recombination between short direct repeat sequences at their boundaries, PAI III536 was deleted either by site-specific recombination or by homologous recombination between two IS100-specific sequences. In all cases, deletion is thought to lead to the formation of nonreplicative circular intermediates. Such extrachromosomal derivatives of PAI II536 and PAI III536 were detected by a specific PCR assay. Our data indicate that the genome content of uropathogenic E. coli can be modulated by deletion of PAIs.

scholarly journals Horizontally acquired papGII-containing pathogenicity islands underlie the emergence of invasive uropathogenic Escherichia coli lineages

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Michael Biggel ◽  
Basil B. Xavier ◽  
James R. Johnson ◽  
Karen L. Nielsen ◽  
Niels Frimodt-Møller ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Bacterial Infections ◽  
Large Scale ◽  
Asymptomatic Bacteriuria ◽  
Pathogenicity Islands ◽  
Phylogenomic Analysis ◽  
E Coli ◽  
Non Invasive ◽  
Genome Wide ◽  
A Genome

AbstractEscherichia coli is the leading cause of urinary tract infection, one of the most common bacterial infections in humans. Despite this, a genomic perspective is lacking regarding the phylogenetic distribution of isolates associated with different clinical syndromes. Here, we present a large-scale phylogenomic analysis of a spatiotemporally and clinically diverse set of 907 E. coli isolates, including 722 uropathogenic E. coli (UPEC) isolates. A genome-wide association approach identifies the (P-fimbriae-encoding) papGII locus as the key feature distinguishing invasive UPEC, defined as isolates associated with severe UTI, i.e., kidney infection (pyelonephritis) or urinary-source bacteremia, from non-invasive UPEC, defined as isolates associated with asymptomatic bacteriuria or bladder infection (cystitis). Within the E. coli population, distinct invasive UPEC lineages emerged through repeated horizontal acquisition of diverse papGII-containing pathogenicity islands. Our findings elucidate the molecular determinants of severe UTI and have implications for the early detection of this pathogen.

scholarly journals Quinolones Induce Partial or Total Loss of Pathogenicity Islands in Uropathogenic Escherichia coli by SOS-Dependent or -Independent Pathways, Respectively

2006 ◽  
Vol 50 (2) ◽  
pp. 649-653 ◽  
Author(s):  
S. M. Soto ◽  
M. T. Jimenez de Anta ◽  
J. Vila
Keyword(s):  
Escherichia Coli ◽  
Virulence Factors ◽  
Reca Protein ◽  
Total Loss ◽  
Pathogenicity Islands ◽  
E Coli ◽  
Cytotoxic Necrotizing Factor ◽  
Tract Infections ◽  
Cytotoxic Necrotizing Factor 1

ABSTRACT Escherichia coli is the most common microorganism causing urinary tract infections. Quinolone-resistant E. coli strains have fewer virulence factors than quinolone-susceptible strains. Several urovirulence genes are located in pathogenicity islands (PAIs). We investigated the capacity of quinolones to induce loss of virulence factors such as hemolysin, cytotoxic necrotizing factor 1, P fimbriae, and autotransporter Sat included in PAIs in three uropathogenic E. coli strains. In a multistep selection, all strains lost hemolytic capacity at between 1 and 4 passages when they were incubated with subinhibitory concentrations of ciprofloxacin, showing a partial or total loss of the PAI containing the hly (hemolysin) and cnf-1 (cytotoxic necrotizing factor 1) genes. RecA− mutants were obtained from the two E. coli strains with partial or total loss of the PAI. The inactivation of the RecA protein affected only the partial loss of the PAI induced by quinolones. No spontaneous loss of PAIs was observed on incubation in the absence of quinolones in either the wild-type or mutant E. coli strains. Quinolones induce partial or total loss of PAIs in vitro in uropathogenic E. coli by SOS-dependent or -independent pathways, respectively.

scholarly journals Comparative Analysis of Virulence Genes, Genetic Diversity, and Phylogeny of Commensal and Enterotoxigenic Escherichia coli Isolates from Weaned Pigs

2006 ◽  
Vol 73 (1) ◽  
pp. 83-91 ◽  
Author(s):  
Xi-Yang Wu ◽  
Toni Chapman ◽  
Darren J. Trott ◽  
Karl Bettelheim ◽  
Thuy N. Do ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Clustering Analysis ◽  
Virulence Genes ◽  
Geographical Origin ◽  
Virulence Gene ◽  
Dna Fingerprint ◽  
Enterotoxigenic Escherichia Coli ◽  
Pathogenicity Islands ◽  
E Coli ◽  
Postweaning Diarrhea

ABSTRACT If the acquisition of virulence genes (VGs) for pathogenicity were not solely acquired through horizontal gene transfers of pathogenicity islands, transposons, and phages, then clonal clusters of enterotoxigenic Escherichia coli (ETEC) would contain few or even none of the VGs found in strains responsible for extraintestinal infections. To evaluate this possibility, 47 postweaning diarrhea (PWD) ETEC strains from different geographical origins and 158 commensal E. coli isolates from the gastrointestinal tracts of eight group-housed healthy pigs were screened for 36 extraintestinal and 18 enteric VGs using multiplex PCR assays. Of 36 extraintestinal VGs, only 8 were detected (fimH, traT, fyuA, hlyA, kpsMtII, k5, iha, and ompT) in the ETEC collection. Among these, hlyA (α-hemolysin) and iha (nonhemagglutinating adhesin) occurred significantly more frequently among the ETEC isolates than in the commensal isolates. Clustering analysis based on the VG profiles separated commensal and ETEC isolates and even differentiated serogroup O141 from O149. On the other hand, pulsed-field gel electrophoresis (PFGE) successfully clustered ETEC isolates according to both serotype and geographical origin. In contrast, the commensal isolates were heterogeneous with respect to both serotype and DNA fingerprint. This study has validated the use of VG profiling to examine pathogenic relationships between porcine ETEC isolates. The clonal relationships of these isolates can be further clarified by PFGE fingerprinting. The presence of extraintestinal VGs in porcine ETEC confirmed the hypothesis that individual virulence gene acquisitions can occur concurrently against a background of horizontal gene transfers of pathogenicity islands. Over time, this could enable specific clonotypes to respond to host selection pressure and to evolve into new strains with increased virulence.

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