Plasmid-Mediated Quinolone Resistance in Isolates Obtained in German Intensive Care Units

Jonas, Daniel E; Biehler, Klaus; Hartung, Doris; Spitzmüller, Bettina; Daschner, Franz

doi:10.1128/aac.49.2.773-775.2005

Cited by 51 publications

(33 citation statements)

References 19 publications

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“…Further, most of the qnr-positive E. cloacae isolates were frequently collected from patients admitted to ICUs, which is consistent with the reports of some previous studies (37) (38) . This result suggests that prolonged stay in ICUs, exposure to broadspectrum antibiotics, chronic underlying conditions, and the use of invasive techniques and devices might predispose patients to infections caused by the aforementioned quinolone-resistant isolates.…”

Section: Discussionsupporting

confidence: 81%

High prevalence of plasmid-mediated quinolone resistance determinants in Enterobacter cloacae isolated from hospitals of the Qazvin, Alborz, and Tehran provinces, Iran

Peymani

Farivar

Najafipour

et al. 2016

Rev. Soc. Bras. Med. Trop.

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Introduction: Plasmid-mediated quinolone resistance (PMQR) is a growing clinical concern worldwide. The main aims of this study were to detect qnr-encoding genes and to evaluate the clonal relatedness of qnr-positive Enterobacter cloacae isolates. Methods: A total of 116 E. cloacae isolates that were not susceptible to quinolone were obtained from seven hospitals in Tehran, five hospitals in Qazvin, and two hospitals in Karaj (Iran). Bacterial identification was performed using standard laboratory methods and API 20E strips. Quinolone resistance was determined using the Kirby-Bauer disk diffusion method according to the Clinical Laboratory Standards Institute (CLSI) guidelines. PCR and sequencing were employed to detect qnrA, qnrB, and qnrS genes, and clonal relatedness was assessed using the enterobacterial repetitive intergenic consensus (ERIC)-PCR method. Results: In total, 45 (38.8%) and 71 (61.2%) of isolates showed high-and low-level quinolone resistance, respectively, and qnr-encoding genes were detected in 70 (60.3%) of them. qnrB1 [45 (38.8%) isolates] was the most commonly detected gene, followed by qnrS1 [28 (24.1%) isolates] and qnrB4 [18 (15.5%) isolates] either alone or in combination with other genes. The results of the ERIC-PCR revealed that 53 (75.7%) qnr-positive isolates were genetically unrelated. Conclusions: This study describes, for the first time, the high prevalence of the qnrB1, qnrS1, and qnrB4 genes among E. cloacae isolates in Iran. The detection of qnr genes emphasizes the need for establishing tactful policies associated with infection control measures in hospital settings in Iran.

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Section: Discussionsupporting

confidence: 81%

High prevalence of plasmid-mediated quinolone resistance determinants in Enterobacter cloacae isolated from hospitals of the Qazvin, Alborz, and Tehran provinces, Iran

Peymani

Farivar

Najafipour

et al. 2016

Rev. Soc. Bras. Med. Trop.

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“…A novel quinolone resistance mechanism includes a Klebsiella pneumoniae multidrug resistance plasmid-mediated qnr gene that could be transferred horizontally (37) and has ever since been described in clinical isolates of K. pneumoniae in the United States (47,58), E. coli, Citrobacter freundii, and Enterobacter sp. in Europe and China (23,36,59), and Providencia stuartii in Egypt (60). However, until now, the qnr locus has been described only in gram negative bacteria.…”

Section: Discussionmentioning

confidence: 99%

High-Level Ciprofloxacin Resistance from Point Mutations in gyrA and parC Confined to Global Hospital-Adapted Clonal Lineage CC17 of Enterococcus faecium

et al. 2006

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To substantiate a common genetic background of ciprofloxacin-resistant Enterococcus faecium, 32 ciprofloxacin-resistant (Cip r ) and 31 ciprofloxacin-susceptible (Cip s ) isolates from outbreaks, clinical infections, surveillances, and animals from 10 different countries were genotyped by multilocus sequence typing. Additionally, susceptibilities to ampicillin and vancomycin and the presence of esp were determined and the quinolone resistance-determining regions of parC, gyrA, parB, and gyrE were sequenced. High-level Cip r (MIC > 64 g/ml) due to point mutations in the quinolone resistance-determining region was unique to a distinct hospital-adapted genetic complex in E. faecium, previously designated CC17. Low-level Cip r (MIC ‫؍‬ 4 g/ml) in non-CC17 strains is not attributable to point mutations in any subunit of the topoisomerase genes, and the mechanism of resistance remains unclear. Acquisition of mutations in parC and gyrA, leading to high-level Cip r , is, in addition to ampicillin resistance and the presence of a putative pathogenicity island, another cumulative step in hospital adaptation of CC17.Over the last two decades, enterococci have become increasingly important as nosocomial pathogens (3). These organisms are intrinsically resistant to a large number of antimicrobials and have the ability to easily acquire new resistance traits (40, 50). The emergence of nosocomial infections caused by ampicillin-, high-level aminoglycoside-, and glycopeptide-resistant Enterococcus faecium has caused clinical concern due to intraand interhospital spread and limited therapeutic options (40, 50). Glycopeptide-resistant enterococci (vancomycin-resistant enterococci [VRE]) are nowadays endemic to the United States, with ϳ30% of enterococcal infections caused by VRE (38, 43); in Europe, the epidemiology of VRE is now changing from a near absence of VRE in hospital-acquired infections at the turn of the century to a situation in which nosocomial epidemics and infections are increasingly reported (3, 13, 17). We recently described a hospital-adapted genetic subtype of E. faecium associated with epidemics and clinical infections, which has spread globally (20,32,62,65). This subpopulation belongs to a distinct genetic lineage labeled clonal complex 17 (CC17) (62) and is associated with the presence of the variant esp gene as part of a pathogenicity island (31) and resistance to ampicillin. Recently, resistance to ciprofloxacin appeared to be associated with ampicillin resistance in genotypically related E. faecium isolates from Norway (25,55,56) and Spain (7).To substantiate a common genetic background of quinoloneresistant E. faecium and association with the hospital-adapted CC17, we studied the genetic relatedness of 32 ciprofloxacinresistant and 31 ciprofloxacin-susceptible E. faecium isolates from various human and animal origins by multilocus sequence typing (MLST) and determined susceptibility to vancomycin and ampicillin and the presence of esp. Finally, we sequenced the quinolone resistance-determining regions (...

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“…Plasmid-mediated decreased susceptibility to quinolones, which was subsequently associated with the gene qnrA, was first detected in 1994 in a K. pneumoniae isolate collected in Birmingham, Alabama (43,61). However, it has recently emerged in China, Korea, and Europe, suggesting that it is likely to become much more common in the future (47,50,60,68,107). In all cases tested, the qnrA gene was found immediately downstream of ISCR1 as part of a complex class 1 integron that included the 3Ј CS duplication (Fig.…”

Section: Iscr1mentioning

confidence: 99%

IS CR Elements: Novel Gene-Capturing Systems of the 21st Century?

Toleman

Bennett

Walsh

2006

Microbiol Mol Biol Rev

529

481

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SUMMARY “Common regions” (CRs), such as Orf513, are being increasingly linked to mega-antibiotic-resistant regions. While their overall nucleotide sequences show little identity to other mobile elements, amino acid alignments indicate that they possess the key motifs of IS91-like elements, which have been linked to the mobility ent plasmids in pathogenic Escherichia coli. Further inspection reveals that they possess an IS91-like origin of replication and termination sites (terIS), and therefore CRs probably transpose via a rolling-circle replication mechanism. Accordingly, in this review we have renamed CRs as ISCRs to give a more accurate reflection of their functional properties. The genetic context surrounding ISCRs indicates that they can procure 5′ sequences via misreading of the cognate terIS, i.e., “unchecked transposition.” Clinically, the most worrying aspect of ISCRs is that they are increasingly being linked with more potent examples of resistance, i.e., metallo-β-lactamases in Pseudomonas aeruginosa and co-trimoxazole resistance in Stenotrophomonas maltophilia. Furthermore, if ISCR elements do move via “unchecked RC transposition,” as has been speculated for ISCR1, then this mechanism provides antibiotic resistance genes with a highly mobile genetic vehicle that could greatly exceed the effects of previously reported mobile genetic mechanisms. It has been hypothesized that bacteria will surprise us by extending their “genetic construction kit” to procure and evince additional DNA and, therefore, antibiotic resistance genes. It appears that ISCR elements have now firmly established themselves within that regimen.

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Plasmid-Mediated Quinolone Resistance in Isolates Obtained in German Intensive Care Units

Cited by 51 publications

References 19 publications

High prevalence of plasmid-mediated quinolone resistance determinants in Enterobacter cloacae isolated from hospitals of the Qazvin, Alborz, and Tehran provinces, Iran

High prevalence of plasmid-mediated quinolone resistance determinants in Enterobacter cloacae isolated from hospitals of the Qazvin, Alborz, and Tehran provinces, Iran

High-Level Ciprofloxacin Resistance from Point Mutations in gyrA and parC Confined to Global Hospital-Adapted Clonal Lineage CC17 of Enterococcus faecium

IS CR Elements: Novel Gene-Capturing Systems of the 21st Century?

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