Molecular characterization of OXA-48 carbapenemase-producing Klebsiella pneumoniae strains after a carbapenem resistance increase in Catalonia

Argente, M. Pilar; Miró, Elisenda; Martí, Carmina; Vilamala, Ana; Alonso-Tarrés, Carles; Ballester, Frédéric; Calderón, Ana Belén Mayo; Gallés, C; Gasós, Asunción; Mirelis, Beatriz; Morta, M.; Olsina, Montserrat; Sauca, Goretti; Sierra, Montserrat; Rivera, Alba; Navarro, Ferrán

doi:10.1016/j.eimc.2018.02.003

Cited by 15 publications

(18 citation statements)

References 29 publications

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“…Thus, this mechanism was found in only 6 (1 E. coli, 4 K. pneumoniae, and 1 Klebsiella species isolates) out of 420 Gram-negative microorganisms tested (338 clinical isolates from 19 countries and a series of laboratory strains carrying different plasmids), with all 6 having been collected in 1994 in Alabama (13). In the subsequent years, this qnr determinant as well as new qnr variants (Table 5) were increasingly detected worldwide in different microorganisms, mainly Enterobacteriaceae (138,(293)(294)(295)(296)(297) and a few isolates of Aeromonadaceae (297-300), Moraxellaceae (301) Pseudomonadaceae (206,302), and Vibrionaceae (175,303,304), among others ( Fig. 5).…”

Section: Qnrmentioning

confidence: 99%

Transferable Mechanisms of Quinolone Resistance from 1998 Onward

Ruiz

2019

Clin Microbiol Rev

115

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SUMMARY While the description of resistance to quinolones is almost as old as these antimicrobial agents themselves, transferable mechanisms of quinolone resistance (TMQR) remained absent from the scenario for more than 36 years, appearing first as sporadic events and afterward as epidemics. In 1998, the first TMQR was soundly described, that is, QnrA. The presence of QnrA was almost anecdotal for years, but in the middle of the first decade of the 21st century, there was an explosion of TMQR descriptions, which definitively changed the epidemiology of quinolone resistance. Currently, 3 different clinically relevant mechanisms of quinolone resistance are encoded within mobile elements: (i) target protection, which is mediated by 7 different families of Qnr (QnrA, QnrB, QnrC, QnrD, QnrE, QnrS, and QnrVC), which overall account for more than 100 recognized alleles; (ii) antibiotic efflux, which is mediated by 2 main transferable efflux pumps (QepA and OqxAB), which together account for more than 30 alleles, and a series of other efflux pumps (e.g., QacBIII), which at present have been sporadically described; and (iii) antibiotic modification, which is mediated by the enzymes AAC(6′)Ib-cr, from which different alleles have been claimed, as well as CrpP, a newly described phosphorylase.

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Section: Qnrmentioning

confidence: 99%

Transferable Mechanisms of Quinolone Resistance from 1998 Onward

Ruiz

2019

Clin Microbiol Rev

115

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“…Thirty-seven OXA-48-producing K. pneumoniae isolates were selected from a previous study collection from 2012 and eight Catalan hospitals, including representative isolates of each MLST and PFGE profile, and antimicrobial resistance profile (Argente et al, 2019). These isolates were previously typed by PFGE (Argente et al, 2019) and MLST following the Institut Pasteur seven-gene MLST scheme 1 (Diancourt et al, 2005). Information on phenotypic resistance and genotyping results from PCR and Sanger sequencing is summarized in Table 1.…”

Section: Sample Collectionmentioning

confidence: 99%

“…The objective of this work was to investigate the molecular epidemiology of a well-characterized collection of OXA-48producing K. pneumoniae -the dissemination of which occurred in eight hospitals in Catalonia in 2012 (Argente et al, 2019)using different WGS-based typing methods and to compare them with classical MLST and PFGE. We used the following WGSbased typing methods: (i) core-genome MLST (cgMLST), based on two different schemes, SeqSphere+ and BIGSdb-Kp (Snitkin et al, 2012); (ii) whole-genome MLST (wgMLST), based on the SeqSphere+ scheme (Zhou et al, 2016); and (iii) core-genome single nucleotide polymorphism (cgSNP) analysis.…”

Section: Introductionmentioning

confidence: 99%

Core/Whole Genome Multilocus Sequence Typing and Core Genome SNP-Based Typing of OXA-48-Producing Klebsiella pneumoniae Clinical Isolates From Spain

Miró

Rossen²,

Chlebowicz

et al. 2020

Front. Microbiol.

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Whole-genome sequencing (WGS)-based typing methods have emerged as promising and highly discriminative epidemiological tools. In this study, we combined geneby-gene allele calling and core genome single nucleotide polymorphism (cgSNP) approaches to investigate the genetic relatedness of a well-characterized collection of OXA-48-producing Klebsiella pneumoniae isolates. We included isolates from the predominant sequence type ST405 (n = 31) OXA-48-producing K. pneumoniae clone and isolates from ST101 (n = 3), ST14 (n = 1), ST17 (n = 1), and ST1233 (n = 1), obtained from eight Catalan hospitals. Core-genome multilocus sequence typing (cgMLST) schemes from Institut Pasteur's BIGSdb-Kp (634 genes) and SeqSphere+ (2,365 genes), and a SeqSphere+ whole-genome MLST (wgMLST) scheme (4,891 genes) were used. Allele differences or allelic mismatches and the genetic distance, as the proportion of allele differences, were used to interpret the results from a gene-bygene approach, whereas the number of SNPs was used for the cgSNP analysis. We observed between 0-10 and 0-14 allele differences among the predominant ST405 using cgMLST and wgMLST from SeqSphere+, respectively, and <2 allelic mismatches when using Institut Pasteur's BIGSdb-Kp cgMLST scheme. For ST101, we observed 14 and 54 allele differences when using cgMLST and wgMLST SeqSphere+, respectively, and 2-5 allelic mismatches for BIGSdb-Kp cgMLST. A low genetic distance (<0.0035, a previously established threshold for epidemiological link) was generally in concordance with a low number of allele differences (<8) when using the SeqSphere+ cgMLST scheme. The cgSNP analysis showed 6-29 SNPs in isolates with identical allelic SeqSphere+ cgMLST profiles and 16-61 cgSNPs among ST405 isolates. Furthermore,

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“…Several plasmids carrying ARGs have been characterized, most of them recovered from clinically relevant bacteria (11)(12)(13)(14). In contrast, there is limited information on plasmids in the commensal microbiota of healthy humans without a selection bias for antimicrobial-resistant bacteria.…”

mentioning

confidence: 99%

“…S2 in the supplemental material). Moreover, some of the most 2AmpCs (11) n ϭ 5; 3.5% n ϭ 5; 5.0% n ϭ 1; 1.0% bla CMY-2 (5) bla CMY-2 (4) frequently reported STs worldwide (ST2, ST12, ST26, and ST36) (36) were only found in E. coli from healthy humans. The detection of many newly assigned STs in the clinical isolates and a scarce number of the most reported STs suggest that the latter may have been overreported due to their involvement in ARG dissemination, resulting in an epidemiological bias.…”

mentioning

confidence: 99%

Comparison of Commensal and Clinical Isolates for Diversity of Plasmids in Escherichia coli and Klebsiella pneumoniae

Rodríguez-Navarro

Miró

Brown-Jaque

et al. 2020

Antimicrob Agents Chemother

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In this study, the plasmid content of clinical and commensal strains was analyzed and compared. The replicon profile was similar in both populations, except for L, M, A/C, and N (detected only in clinical strains) and HI1 (only in commensal strains). Although I1 and F were the most frequent replicons, only IncI1, sequence type 12 (ST12) was associated with blaCMY-2 in both populations. In contrast, the widespread resistant IncF plasmids were not linked to a single epidemic plasmid.

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Molecular characterization of OXA-48 carbapenemase-producing Klebsiella pneumoniae strains after a carbapenem resistance increase in Catalonia

Cited by 15 publications

References 29 publications

Transferable Mechanisms of Quinolone Resistance from 1998 Onward

Transferable Mechanisms of Quinolone Resistance from 1998 Onward

Core/Whole Genome Multilocus Sequence Typing and Core Genome SNP-Based Typing of OXA-48-Producing Klebsiella pneumoniae Clinical Isolates From Spain

Comparison of Commensal and Clinical Isolates for Diversity of Plasmids in Escherichia coli and Klebsiella pneumoniae

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