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      Dissemination of ST274 Klebsiella pneumoniae epidemic clone in newborn and adult hospital settings harbouring SHV-2A or CTX-M-15 type extended spectrum β-lactamases-producing known plasmids

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          Abstract

          Molecular epidemiology and genetic features of an extended-spectrum β-lactamase (ESBL) producing Klebsiella pneumoniae epidemic clone (KP-EC) with elevated ciprofloxacin MIC (minimum inhibitory concentration) values from multiple nosocomial outbreaks and sporadic cases between 2006 and 2008 in Hungary were investigated.

          As a result of continuous monitoring of ESBL-producing KP-ECs, 27 isolates collected from five healthcare facilities were selected for macrorestriction profile analysis by PFGE (pulsed field gel electrophoresis). Of these, 12 strains were isolated from adult inpatients, while 15 strains were from newborns. The MIC values for several antibiotics were determined by agar dilution technique. Molecular typing was further performed by PCR (polymerase chain reaction) and sequencing of several antibiotic resistance genes, plasmid profile analysis, transfer of resistance determinants and multilocus sequence typing (MLST).

          All isolates showed moderate resistance to ciprofloxacin (MICs ranged from 0.5 to 8 mg L −1). PFGE revealed the existence of only one genetic cluster defined as EC IV. PstI digestion of plasmid DNA revealed two highly diverse restriction patterns in “adult” and “newborn” isolates corresponding to plasmids from the Hungarian Epidemic Clone and plasmids isolated from a neonatal nosocomial outbreak in 1998, respectively. Sequence analysis of b-lactamase genes from plasmids of 14 selected isolates detected bla SHV-2a in strains isolated exclusively from newborns and bla CTX-M-15 in strains isolated exclusively from adult inpatients. MLST established that strains of the PFGE cluster belonged to a novel sequence type ST274.

          ESBL-producing K. pneumoniae isolates belonging to the novel sequence type ST274 appeared in the newborn and adult hospital settings in Hungary and acquired SHV-2a or CTX-M-15 type enzymes, respectively. Thus, a new antimicrobial resistance strategy for successful conformation to distinct hospital settings was found.

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          The worldwide emergence of plasmid-mediated quinolone resistance.

          Ari Robicsek, George Jacoby, David Hooper (2006)
          Fluoroquinolone resistance is emerging in gram-negative pathogens worldwide. The traditional understanding that quinolone resistance is acquired only through mutation and transmitted only vertically does not entirely account for the relative ease with which resistance develops in exquisitely susceptible organisms, or for the very strong association between resistance to quinolones and to other agents. The recent discovery of plasmid-mediated horizontally transferable genes encoding quinolone resistance might shed light on these phenomena. The Qnr proteins, capable of protecting DNA gyrase from quinolones, have homologues in water-dwelling bacteria, and seem to have been in circulation for some time, having achieved global distribution in a variety of plasmid environments and bacterial genera. AAC(6')-Ib-cr, a variant aminoglycoside acetyltransferase capable of modifying ciprofloxacin and reducing its activity, seems to have emerged more recently, but might be even more prevalent than the Qnr proteins. Both mechanisms provide low-level quinolone resistance that facilitates the emergence of higher-level resistance in the presence of quinolones at therapeutic levels. Much remains to be understood about these genes, but their insidious promotion of substantial resistance, their horizontal spread, and their co-selection with other resistance elements indicate that a more cautious approach to quinolone use and a reconsideration of clinical breakpoints are needed.
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            Identification and characterization of inhibitors of multidrug resistance efflux pumps in Pseudomonas aeruginosa: novel agents for combination therapy.

            O Lomovskaya, M Warren, A. Lee … (2001)
            Whole-cell assays were implemented to search for efflux pump inhibitors (EPIs) of the three multidrug resistance efflux pumps (MexAB-OprM, MexCD-OprJ, MexEF-OprN) that contribute to fluoroquinolone resistance in clinical isolates of Pseudomonas aeruginosa. Secondary assays were developed to identify lead compounds with exquisite activities as inhibitors. A broad-spectrum EPI which is active against all three known Mex efflux pumps from P. aeruginosa and their close Escherichia coli efflux pump homolog (AcrAB-TolC) was discovered. When this compound, MC-207,110, was used, the intrinsic resistance of P. aeruginosa to fluoroquinolones was decreased significantly (eightfold for levofloxacin). Acquired resistance due to the overexpression of efflux pumps was also decreased (32- to 64-fold reduction in the MIC of levofloxacin). Similarly, 32- to 64-fold reductions in MICs in the presence of MC-207,110 were observed for strains with overexpressed efflux pumps and various target mutations that confer resistance to levofloxacin (e.g., gyrA and parC). We also compared the frequencies of emergence of levofloxacin-resistant variants in the wild-type strain at four times the MIC of levofloxacin (1 microg/ml) when it was used either alone or in combination with EPI. In the case of levofloxacin alone, the frequency was approximately 10(-7) CFU/ml. In contrast, with an EPI, the frequency was below the level of detection (<10(-11)). In summary, we have demonstrated that inhibition of efflux pumps (i) decreased the level of intrinsic resistance significantly, (ii) reversed acquired resistance, and (iii) resulted in a decreased frequency of emergence of P. aeruginosa strains that are highly resistant to fluoroquinolones.
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              Increasing prevalence of ESBL-producing Enterobacteriaceae in Europe.

              Francisco Cantón, F. Baquero, T Coque (2008)
              Extended-spectrum beta-lactamases (ESBLs) have been increasingly reported in Europe since their first description in 1983. During the 1990s, they were described mainly as members of the TEM- and SHV-beta-lactamase families in Klebsiella pneumoniae causing nosocomial outbreaks. Nowadays, they are mostly found in Escherichia coli that cause community-acquired infections and with increasing frequency contain CTX-M enzymes. Dissemination of specific clones or clonal groups and epidemic plasmids in community and nosocomial settings has been the main reason for the increase in most of the widespread ESBLs belonging to the TEM (TEM-24, TEM-4, TEM-52), SHV (SHV-5, SHV-12) and CTX-M (CTX-M-9, CTX-M-3, CTX-M-14 or CTX-M-15) families in Europe. Co-selection with other resistances, especially to fluoroquinolones, aminoglycosides and sulfonamides, seems to have contributed to the problem. The emergence of epidemic clones harbouring several beta-lactamases simultaneously (ESBLs, metallo-beta-lactamases or cephamycinases) and of new mechanisms of resistance to fluoroquinolones and aminoglycosides warrants future surveillance studies.
              Article 0 comments Cited 119 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (publisher-id): 1886
                Journal ID (MPID): 122234
                Title: European Journal of Microbiology and Immunology
                Abbreviated Title: EuJMI
                Publisher: Akadémiai Kiadó, co-published with Springer Science+Business Media B.V., Formerly Kluwer Academic Publishers B.V.
                ISSN (Print): 2062-509X
                ISSN (Electronic): 2062-8633
                Publication date (Print): 1 September 2011
                Volume: 1
                Issue: 3
                Pages: 223-227
                Affiliations
                [ 1 ] Department of Phage Typing and Molecular Epidemiology, National Center for Epidemiology, Gyáli út 2-6, H-1097, Budapest, Hungary
                [ 2 ] Department of Bacteriology, National Center for Epidemiology, Gyáli út 2-6, H-1097, Budapest, Hungary
                [ 3 ] 1st Department of Pediatrics, Semmelweis University, Bókay János u. 53-54, H-1083, Budapest, Hungary
                [ 4 ] “Jávorszky Ödön” Hospital, Argenti Döme tér 1-3, H-2600, Vác, Hungary
                [ 5 ] Institute of Medical Microbiology, Semmelweis University, Nagyvárad tér 4, H-1089, Budapest, Hungary
                Author notes
                Article
                Other ID: 6
                DOI: 10.1556/eujmi.1.2011.3.6
                PMC ID: 3906618
                PubMed ID: 24516728
                SO-VID: f4094e85-8378-4f36-8b4d-f10b6bbcd5d2
                History
                Date received : 28 June 2011
                Date accepted : 1 July 2011
                Categories
                Subject: Original Articles

                ScienceOpen disciplines: Medicine,Immunology,Health & Social care,Microbiology & Virology,Infectious disease & Microbiology
                Keywords: clonal spread, Klebsiella pneumoniae ,allodemic plasmid,MLST
                Data availability:
                ScienceOpen disciplines: Medicine, Immunology, Health & Social care, Microbiology & Virology, Infectious disease & Microbiology
                Keywords: clonal spread, Klebsiella pneumoniae , allodemic plasmid, MLST

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