dc.contributor.author | Isler B. | |
dc.contributor.author | Falconer C. | |
dc.contributor.author | Vatansever C. | |
dc.contributor.author | Özer B. | |
dc.contributor.author | Çınar G. | |
dc.contributor.author | Aslan A.T. | |
dc.contributor.author | Forde B. | |
dc.date.accessioned | 2024-02-04T13:30:11Z | |
dc.date.available | 2024-02-04T13:30:11Z | |
dc.date.issued | 2022 | |
dc.identifier.issn | 00222615 | |
dc.identifier.uri | https://doi.org/10.1099/jmm.0.001629 | |
dc.identifier.uri | http://hdl.handle.net/11446/4861 | |
dc.description.abstract | Introduction. Aminoglycosides are used for the treatment of carbapenemase-producing Klebsiella pneumoniae (CPK) infections. 16S rRNA methyltransferases (RMTs) confer resistance to all aminoglycosides and are often cocarried with NDM. Hypothesis/Gap Statement. There is a dart of studies looking at the aminoglycoside resistance mechanisms for invasive CPK isolates, particularly in OXA-48 endemic settings. Aim. We aimed to determine the prevalence of RMTs and their association with beta lactamases and MLSTs amongst aminoglycoside-resistant CPK bloodstream isolates in an OXA-48 endemic setting. Methodology. CPK isolates (n=181), collected as part of a multicentre cohort study, were tested for amikacin, gentamicin and tobramycin susceptibility using custom-made sensititre plates (GN2XF, Thermo Fisher Scientific). All isolates were previously subjected to whole-genome sequencing. Carbapenemases, RMTs, MLSTs and plasmid incompatibility groups were detected on the assembled genomes. Results. Of the 181 isolates, 109(60%) were resistant to all three aminoglycosides, and 96 of 109(88%) aminoglycoside-resistant isolates carried an RMT (85 ArmA, 10 RmtC, 4 RmtF1; three isolates cocarried ArmA and RmtC). Main clonal types associated with ArmA were ST2096 (49/85, 58%) and ST14 (24/85, 28%), harbouring mainly OXA-232 and OXA-48 +NDM, respectively. RmtC was cocarried with NDM (5/10) on ST395, and NDM +OXA-48 or NDM +KPC (4/10) on ST14, ST15 and ST16. All RMT producers also carried CTX-M-15, and the majority cocarried SHV-106, TEM-150 and multiple other antibiotic resistance genes. The majority of the isolates harboured a combination of IncFIB, IncH and IncL/M type plasmids. Non-NDM producing isolates remained susceptible to ceftazidime-avibactam. Conclusion. Aminoglycoside resistance amongst CPK bloodstream isolates is extremely common and mainly driven by clonal spread of ArmA carried on ST2096 and ST14, associated with OXA-232 and OXA48 +NDM carriage, respectively. © The Authors. | en_US |
dc.description.sponsorship | Pfizer: 56644459; Queensland Government | en_US |
dc.description.sponsorship | This work was supported by Pfizer Global Medical Grants (grant number 56644459). Dr Brian Forde’s research is supported by Advance Queensland Industry Research Fellowship from the Queensland Government. | en_US |
dc.language.iso | eng | en_US |
dc.publisher | Microbiology Society | en_US |
dc.relation.ispartof | Journal of Medical Microbiology | en_US |
dc.identifier.doi | 10.1099/jmm.0.001629 | |
dc.rights | info:eu-repo/semantics/closedAccess | en_US |
dc.subject | 16S rRNA methyltransferase | en_US |
dc.subject | aminoglycoside resistance | en_US |
dc.subject | ArmA | en_US |
dc.subject | bloodstream | en_US |
dc.subject | carbapenem-resistant | en_US |
dc.subject | Klebsiella pneumoniae | en_US |
dc.subject | NDM | en_US |
dc.subject | OXA-232 | en_US |
dc.subject | OXA-48 | en_US |
dc.subject | amikacin | en_US |
dc.subject | aminoglycoside | en_US |
dc.subject | avibactam plus ceftazidime | en_US |
dc.subject | beta lactamase | en_US |
dc.subject | carbapenemase | en_US |
dc.subject | colistin | en_US |
dc.subject | gentamicin | en_US |
dc.subject | methyltransferase | en_US |
dc.subject | RNA 16S | en_US |
dc.subject | tigecycline | en_US |
dc.subject | tobramycin | en_US |
dc.subject | aminoglycoside | en_US |
dc.subject | antiinfective agent | en_US |
dc.subject | bacterial protein | en_US |
dc.subject | methyltransferase | en_US |
dc.subject | RNA 16S | en_US |
dc.subject | aminoglycoside resistance | en_US |
dc.subject | antibiotic resistance | en_US |
dc.subject | antibiotic sensitivity | en_US |
dc.subject | Article | en_US |
dc.subject | bacterium isolate | en_US |
dc.subject | cohort analysis | en_US |
dc.subject | controlled study | en_US |
dc.subject | human | en_US |
dc.subject | Klebsiella pneumoniae | en_US |
dc.subject | major clinical study | en_US |
dc.subject | nonhuman | en_US |
dc.subject | observational study | en_US |
dc.subject | phylogenetic tree | en_US |
dc.subject | plasmid | en_US |
dc.subject | prevalence | en_US |
dc.subject | trimethoprim resistance | en_US |
dc.subject | Turkey (republic) | en_US |
dc.subject | whole genome sequencing | en_US |
dc.subject | carbapenem-resistant Enterobacteriaceae | en_US |
dc.subject | genetics | en_US |
dc.subject | Klebsiella infection | en_US |
dc.subject | Klebsiella pneumoniae | en_US |
dc.subject | microbial sensitivity test | en_US |
dc.subject | prevalence | en_US |
dc.subject | Aminoglycosides | en_US |
dc.subject | Anti-Bacterial Agents | en_US |
dc.subject | Bacterial Proteins | en_US |
dc.subject | beta-Lactamases | en_US |
dc.subject | Carbapenem-Resistant Enterobacteriaceae | en_US |
dc.subject | Cohort Studies | en_US |
dc.subject | Humans | en_US |
dc.subject | Klebsiella Infections | en_US |
dc.subject | Klebsiella pneumoniae | en_US |
dc.subject | Methyltransferases | en_US |
dc.subject | Microbial Sensitivity Tests | en_US |
dc.subject | Prevalence | en_US |
dc.subject | RNA, Ribosomal, 16S | en_US |
dc.title | High prevalence of ArmA-16S rRNA methyltransferase among aminoglycoside-resistant Klebsiella pneumoniae bloodstream isolates | en_US |
dc.type | article | en_US |
dc.department | DBÜ | en_US |
dc.identifier.issue | 12 | en_US |
dc.identifier.volume | 71 | en_US |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |
dc.department-temp | Isler, B., University of Queensland, Faculty of Medicine, UQ Centre for Clinical Research, Brisbane, Australia, Infection Management Services, Princess Alexandra Hospital, Brisbane, Australia; Falconer, C., University of Queensland, Faculty of Medicine, UQ Centre for Clinical Research, Brisbane, Australia; Vatansever, C., Infectious Diseases and Clinical Microbiology, School of Medicine, Koç University, Istanbul, Turkey; Özer, B., Infectious Diseases and Clinical Microbiology, School of Medicine, Koç University, Istanbul, Turkey; Çınar, G., Infectious Diseases and Clinical Microbiology, Ankara University, School of Medicine, Ankara, Turkey; Aslan, A.T., Infectious Diseases and Clinical Microbiology, Hacettepe University, School of Medicine, Ankara, Turkey; Forde, B., University of Queensland, Faculty of Medicine, UQ Centre for Clinical Research, Brisbane, Australia; Harris, P., University of Queensland, Faculty of Medicine, UQ Centre for Clinical Research, Brisbane, Australia; Şimşek, F., Infectious Diseases and Clinical Microbiology, University of Health Sciences, Ministry of Health Prof Dr Cemil Taşçıoğlu City Hospital, Istanbul, Turkey; Tülek, N., Infectious Diseases and Clinical Microbiology, Faculty of Medicine, Atilim University, Ankara, Turkey; Demirkaya, H., Infectious Diseases and Clinical Microbiology, Başkent Universi | en_US |
dc.identifier.pmid | 36748503 | en_US |
dc.identifier.scopus | 2-s2.0-85147460921 | en_US |
dc.authorscopusid | 57206274628 | |
dc.authorscopusid | 57221350758 | |
dc.authorscopusid | 57214119170 | |
dc.authorscopusid | 57210635288 | |
dc.authorscopusid | 57210793543 | |
dc.authorscopusid | 57208546633 | |
dc.authorscopusid | 35746149500 | |