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Teicoplanin resistance in Staphylococcus haemolyticus is associated with mutations in histidine kinases VraS and WalK
V. Vimberg, JP. Cavanagh, O. Benada, O. Kofroňová, E. Hjerde, L. Zieglerová, G. Balíková Novotná,
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články
Grantová podpora
NV15-28807A
MZ0
CEP - Centrální evidence projektů
- MeSH
- antibakteriální látky farmakologie MeSH
- bakteriální léková rezistence genetika MeSH
- DNA bakterií genetika MeSH
- fenotyp MeSH
- genom bakteriální genetika MeSH
- histidinkinasa genetika MeSH
- jednonukleotidový polymorfismus genetika MeSH
- lidé MeSH
- rezistence na vankomycin genetika MeSH
- sekvence nukleotidů MeSH
- sekvenční analýza DNA MeSH
- stafylokokové infekce mikrobiologie MeSH
- Staphylococcus haemolyticus účinky léků genetika izolace a purifikace MeSH
- teikoplanin farmakologie MeSH
- vankomycin farmakologie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- Geografické názvy
- Polsko MeSH
We investigated the genetic basis of glycopeptide resistance in laboratory-derived strains of S. haemolyticus with emphasis on differences between vancomycin and teicoplanin. The genomes of two stable teicoplanin-resistant laboratory mutants selected on vancomycin or teicoplanin were sequenced and compared to parental S. haemolyticus strain W2/124. Only the two non-synonymous mutations, VraS Q289K and WalK V550L were identified. No other mutations or genome rearrangements were detected. Increased cell wall thickness, resistance to lysostaphin-induced lysis and adaptation of cell growth rates specifically to teicoplanin were phenotypes observed in a sequenced strain with the VraS Q289K mutation. Neither of the VraS Q289K and WalK V550L mutations was present in the genomes of 121S. haemolyticus clinical isolates. However, all but two of the teicoplanin resistant strains carried non-synonymous SNPs in vraSRTU and walKR-YycHIJ operons pointing to their importance for the glycopeptide resistance.
Department of Clinical Medicine UiT The Arctic University of Norway Tromsø 9037 Norway
Department of Pediatrics University Hospital of North Norway Sykehusvegen 38 Tromsø 9019 Norway
Citace poskytuje Crossref.org
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- $a Vimberg, Vladimir $u Institute of Microbiology v. v. i., The Czech Academy of Sciences, Průmyslová 595, Vestec 252 50, Czech Republic.
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- $a We investigated the genetic basis of glycopeptide resistance in laboratory-derived strains of S. haemolyticus with emphasis on differences between vancomycin and teicoplanin. The genomes of two stable teicoplanin-resistant laboratory mutants selected on vancomycin or teicoplanin were sequenced and compared to parental S. haemolyticus strain W2/124. Only the two non-synonymous mutations, VraS Q289K and WalK V550L were identified. No other mutations or genome rearrangements were detected. Increased cell wall thickness, resistance to lysostaphin-induced lysis and adaptation of cell growth rates specifically to teicoplanin were phenotypes observed in a sequenced strain with the VraS Q289K mutation. Neither of the VraS Q289K and WalK V550L mutations was present in the genomes of 121S. haemolyticus clinical isolates. However, all but two of the teicoplanin resistant strains carried non-synonymous SNPs in vraSRTU and walKR-YycHIJ operons pointing to their importance for the glycopeptide resistance.
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