Aspects of genome plasticity in pathogenic Escherichia coli

Bielaszewska, Martina; Dobrindt, Ulrich; Gartner, J. F.; Gallitz, Inka; Hacker, Jörg; Karch, Helge; Müller, Daniel; Schubert, Sören; Schmidt, M. Alexander; Sorsa, Liisa Johanna; Zdziarski, Jaroslaw

doi:10.1016/j.ijmm.2007.03.001

Cited by 42 publications

(27 citation statements)

References 83 publications

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“…This characteristic of group B2 can determine the relationship globally found in UPEC strains, because it concerns the most frequent biotype. We also supposed that the prevalence of group B2 among both uropathogenic and commensal E. coli isolates (21,46), found recently to be independent of VF carriage (35), would be due to a superior adaptability, perhaps corresponding to the previously named "plasticity" of the species (5,7,15). In contrast, in sites other than the bladder and the gut, the presence of B2 strains, corresponding to disease (21) and to experimental lethality (24), depends on a high level of shared virulence factors.…”

Section: Discussionmentioning

confidence: 93%

Virulence Factors in Urinary Escherichia coli Strains: Phylogenetic Background and Quinolone and Fluoroquinolone Resistance

Piatti¹,

et al. 2008

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Quinolone-and fluoroquinolone-resistant Escherichia coli strains harbor fewer virulence factors than susceptible strains. The reasons underlying this correlation are incompletely understood. We investigated the phylogenetic background, the presence of the papC, hlyA, and cnf1 (pathogenicity island II J96 -associated), fimA, iss, and iutA genes, and the presence of type 1 fimbriae, P fimbriae, and hemolysin in 243 urinary E. coli isolates resistant only to quinolones (8%), resistant to both quinolones and fluoroquinolones (51%), or susceptible to both drugs (41%). Group B2 accounted for 56% of the isolates, showing a significantly higher prevalence among fluoroquinolone-susceptible strains than among resistant strains (65% versus 50% [P ‫؍‬ 0.03]). hly and cnf1 were significantly more associated with susceptibility (P < 0.001) and with group B2 (P < 0.001 for group B2 versus groups A and D). However, within group B2, fluoroquinolone-resistant strains showed lower prevalences of papC, hlyA, and cnf1 than their susceptible counterparts (P < 0.001). In contrast, the incidence of iutA appeared higher for refractory isolates, including group B2, than for susceptible isolates (P < 0.001). Only in group B2 did fluoroquinolone-resistant strains reveal a lesser ability to agglutinate Saccharomyces cerevisiae (7%) than quinolone-resistant (87%) and susceptible (80%) isolates, despite uniform possession of fimA genes. No similar contrast emerged for expression of hemolysin and P fimbriae. Mutations conferring quinolone and fluoroquinolone resistance may thus require a particular genetic background, not strictly correlated with phylogenetic groups. More interestingly, the mutational event itself can affect the expression of type 1 fimbriae, at least in the prevalent and complex B2 strains.Urinary tract infections (UTIs) in humans are the most frequent bacterial disease, affecting both inpatients and outpatients. Especially the uncomplicated cases are mainly due to extraintestinal pathogenic Escherichia coli (ExPEC) (39). In recent years, management of UTIs has become increasingly problematic due to the emergence of resistance to first-line antibiotics among the causative bacteria, particularly among uropathogenic E. coli (UPEC) strains. This phenomenon involves quinolones (Q) and fluoroquinolones (FQ) (25), drugs of paramount importance in the treatment of several other infectious diseases. Indeed, the renal excretion of these molecules and the availability of oral and parenteral formulations have allowed them to compete with aminoglycosides and betalactams in the therapy of complicated UTIs, especially in the hospital setting. Their appropriate spectrum and good tolerability have also led to increased empirical adoption in uncomplicated infections, although their usage for these conditions in outpatients is still under debate.In E. coli, as in other gram-negative bacteria, DNA gyrase, which codifies type II DNA topoisomerases, is the main target of Q and FQ, and mutation in gyrA is the most common way to acquire resistance....

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Section: Discussionmentioning

confidence: 93%

Virulence Factors in Urinary Escherichia coli Strains: Phylogenetic Background and Quinolone and Fluoroquinolone Resistance

Piatti¹,

et al. 2008

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“…The ccdB (cytotoxic protein), malX (phosphotransferase system, pathogenicity island [PAI] associated), ompT, and the toxin-encoding astA and astA (2) genes were detected at a higher frequency in the APEC group than in commensal isolates or the "other" ExPEC group ( Table 2). The enterotoxigenic E. coli invasion protein-encod- Although the presence of the plasmid was not directly tested, the combined detection of tsh, iss, iroN, cvaC, and ompT genes as well as the aerobactin-iron acquisition system was considered an indicator of pAPEC-O2-ColV presence.…”

Section: Resultsmentioning

confidence: 99%

Pathotype and Antibiotic Resistance Gene Distributions of Escherichia coli Isolates from Broiler Chickens Raised on Antimicrobial-Supplemented Diets

Bonnet

Diarrassouba

Brousseau

et al. 2009

Appl Environ Microbiol

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The impact of feed supplementation with bambermycin, monensin, narasin, virginiamycin, chlortetracycline, penicillin, salinomycin, and bacitracin on the distribution of Escherichia coli pathotypes in broiler chickens was investigated using an E. coli virulence DNA microarray. Among 256 E. coli isolates examined, 59 (23%) were classified as potentially extraintestinal pathogenic E. coli (ExPEC), while 197 (77%) were considered commensal. Except for chlortetracycline treatment, the pathotype distribution was not significantly different among treatments (P > 0.05). Within the 59 ExPEC isolates, 44 (75%) were determined to be potentially avian pathogenic E. coli (APEC), with the remaining 15 (25%) considered potentially "other" ExPEC isolates. The distribution within phylogenetic groups showed that 52 (88%) of the ExPEC isolates belonged to groups B2 and D, with the majority of APEC isolates classified as group D and most commensal isolates (170, 86%) as group A or B1. Indirect assessment of the presence of the virulence plasmid pAPEC-O2-ColV showed a strong association of the plasmid with APEC isolates. Among the 256 isolates, 224 (88%) possessed at least one antimicrobial resistance gene, with nearly half (107, 42%) showing multiple resistance genes. The majority of resistance genes were distributed among commensal isolates. Considering that the simultaneous detection of antimicrobial resistance tet(A), sulI, and bla TEM genes and the integron class I indicated a potential presence of the resistance pAPEC-O2-R plasmid, the results revealed that 35 (14%) of the isolates, all commensals, possessed this multigene resistance plasmid. The virulence plasmid was never found in combination with the antimicrobial resistance plasmid. The presence of the ColV plasmid or the combination of iss and tsh genes in the majority of APEC isolates supports the notion that when found together, the plasmid, iss, and tsh serve as good markers for APEC. These data indicate that different resistant E. coli pathotypes can be found in broiler chickens and that the distribution of such pathotypes and certain virulence determinants could be modulated by antimicrobial agent feed supplementation.

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“…A possible explanation for these findings would be that the genomes of host-associated E. coli and Shigella strains show signs of adaptive evolution. Pathogenesis in E. coli is believed to result from the acquisition and integration of horizontally transferred virulence factors into strain-specific chromosomal pathogenic islands or from the acquisition of plasmids harboring these genetic factors (9,23,42). The comparative genome analysis of E. coli SMS-3-5 with intra-and extraintestinal E. coli isolates provides clues that at least part of the adaptation of previously sequenced E. coli strains to their host-associated lifestyles was associated with genome reduction.…”

Section: Discussionmentioning

confidence: 99%

Insights into the Environmental Resistance Gene Pool from the Genome Sequence of the Multidrug-Resistant Environmental Isolate Escherichia coli SMS-3-5

et al. 2008

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The increasing occurrence of multidrug-resistant pathogens of clinical and agricultural importance is a global public health concern. While antimicrobial use in human and veterinary medicine is known to contribute to the dissemination of antimicrobial resistance, the impact of microbial communities and mobile resistance genes from the environment in this process is not well understood. Isolated from an industrially polluted aquatic environment, Escherichia coli SMS-3-5 is resistant to a record number of antimicrobial compounds from all major classes, including two front-line fluoroquinolones (ciprofloxacin and moxifloxacin), and in many cases at record-high concentrations. To gain insights into antimicrobial resistance in environmental bacterial populations, the genome of E. coli SMS-3-5 was sequenced and compared to the genome sequences of other E. coli strains. In addition, selected genetic loci from E. coli SMS-3-5 predicted to be involved in antimicrobial resistance were phenotypically characterized. Using recombinant vector clones from shotgun sequencing libraries, resistance to tetracycline, streptomycin, and sulfonamide/trimethoprim was assigned to a single mosaic region on a 130-kb plasmid (pSMS35_130). The remaining plasmid backbone showed similarity to virulence plasmids from avian-pathogenic E. coli (APEC) strains. Individual resistance gene cassettes from pSMS35_130 are conserved among resistant bacterial isolates from multiple phylogenetic and geographic sources. Resistance to quinolones was assigned to several chromosomal loci, mostly encoding transport systems that are also present in susceptible E. coli isolates. Antimicrobial resistance in E. coli SMS-3-5 is therefore dependent both on determinants acquired from a mobile gene pool that is likely available to clinical and agricultural pathogens, as well, and on specifically adapted multidrug efflux systems. The association of antimicrobial resistance with APEC virulence genes on pSMS35_130 highlights the risk of promoting the spread of virulence through the extensive use of antibiotics.

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Aspects of genome plasticity in pathogenic Escherichia coli

Cited by 42 publications

References 83 publications

Virulence Factors in Urinary Escherichia coli Strains: Phylogenetic Background and Quinolone and Fluoroquinolone Resistance

Virulence Factors in Urinary Escherichia coli Strains: Phylogenetic Background and Quinolone and Fluoroquinolone Resistance

Pathotype and Antibiotic Resistance Gene Distributions of Escherichia coli Isolates from Broiler Chickens Raised on Antimicrobial-Supplemented Diets

Insights into the Environmental Resistance Gene Pool from the Genome Sequence of the Multidrug-Resistant Environmental Isolate Escherichia coli SMS-3-5

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