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Global spread of three multidrug-resistant lineages of Staphylococcus epidermidis.
Lee, Jean Y H; Monk, Ian R; Gonçalves da Silva, Anders; Seemann, Torsten; Chua, Kyra Y L; Kearns, Angela; Hill, Robert; Woodford, Neil; Bartels, Mette D; Strommenger, Birgit; Laurent, Frederic; Dodémont, Magali; Deplano, Ariane; Patel, Robin; Larsen, Anders R; Korman, Tony M; Stinear, Timothy P; Howden, Benjamin P.
Afiliação
  • Lee JYH; Department of Microbiology and Immunology, The University of Melbourne at The Doherty Institute for Infection and Immunity, Melbourne, Australia.
  • Monk IR; Department of Microbiology and Immunology, The University of Melbourne at The Doherty Institute for Infection and Immunity, Melbourne, Australia.
  • Gonçalves da Silva A; Microbiological Diagnostic Unit Public Health Laboratory, Department of Microbiology and Immunology, The University of Melbourne at The Doherty Institute for Infection and Immunity, Melbourne, Australia.
  • Seemann T; Doherty Applied Microbial Genomics, Department of Microbiology and Immunology, The University of Melbourne at The Doherty Institute for Infection and Immunity, Melbourne, Australia.
  • Chua KYL; Doherty Applied Microbial Genomics, Department of Microbiology and Immunology, The University of Melbourne at The Doherty Institute for Infection and Immunity, Melbourne, Australia.
  • Kearns A; Melbourne Bioinformatics, The University of Melbourne, Melbourne, Australia.
  • Hill R; Department of Microbiology, Austin Health, Melbourne, Australia.
  • Woodford N; AMRHAI Reference Unit, National Infection Service, Public Health England, London, UK.
  • Bartels MD; AMRHAI Reference Unit, National Infection Service, Public Health England, London, UK.
  • Strommenger B; AMRHAI Reference Unit, National Infection Service, Public Health England, London, UK.
  • Laurent F; Department of Clinical Microbiology, Hvidovre University Hospital, Hvidovre, Denmark.
  • Dodémont M; National Reference Centre for Staphylococci and Enterococci, Division Nosocomial Pathogens and Antibiotic Resistances, Department of Infectious Diseases, Robert Koch Institute, Wernigerode Branch, Wernigerode, Germany.
  • Deplano A; Department of Bacteriology, Institute for Infectious Agents, French National Reference Centre for Staphylococci, International Centre for Infectiology Research, Institute for Pharmaceutical and Biological Sciences Of Lyon, University of Lyon, Lyon, France.
  • Patel R; National Reference Centre for Staphylococci, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium.
  • Larsen AR; National Reference Centre for Staphylococci, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium.
  • Korman TM; Division of Clinical Microbiology, Department of Laboratory Medicine and Pathology, and Division of Infectious Diseases, Department of Medicine, Mayo Clinic, Rochester, USA.
  • Stinear TP; Reference Laboratory for Antimicrobial Resistance and Staphylococci, Statens Serum Institut, Copenhagen, Denmark.
  • Howden BP; Monash Infectious Diseases, Centre for Inflammatory Diseases, Monash University, Melbourne, Australia.
Nat Microbiol ; 3(10): 1175-1185, 2018 10.
Article em En | MEDLINE | ID: mdl-30177740
Staphylococcus epidermidis is a conspicuous member of the human microbiome, widely present on healthy skin. Here we show that S. epidermidis has also evolved to become a formidable nosocomial pathogen. Using genomics, we reveal that three multidrug-resistant, hospital-adapted lineages of S. epidermidis (two ST2 and one ST23) have emerged in recent decades and spread globally. These lineages are resistant to rifampicin through acquisition of specific rpoB mutations that have become fixed in the populations. Analysis of isolates from 96 institutions in 24 countries identified dual D471E and I527M RpoB substitutions to be the most common cause of rifampicin resistance in S. epidermidis, accounting for 86.6% of mutations. Furthermore, we reveal that the D471E and I527M combination occurs almost exclusively in isolates from the ST2 and ST23 lineages. By breaching lineage-specific DNA methylation restriction modification barriers and then performing site-specific mutagenesis, we show that these rpoB mutations not only confer rifampicin resistance, but also reduce susceptibility to the last-line glycopeptide antibiotics, vancomycin and teicoplanin. Our study has uncovered the previously unrecognized international spread of a near pan-drug-resistant opportunistic pathogen, identifiable by a rifampicin-resistant phenotype. It is possible that hospital practices, such as antibiotic monotherapy utilizing rifampicin-impregnated medical devices, have driven the evolution of this organism, once trivialized as a contaminant, towards potentially incurable infections.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Rifampina / Infecções Estafilocócicas / Staphylococcus epidermidis / Farmacorresistência Bacteriana Múltipla / Antibacterianos Idioma: En Ano de publicação: 2018 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Rifampina / Infecções Estafilocócicas / Staphylococcus epidermidis / Farmacorresistência Bacteriana Múltipla / Antibacterianos Idioma: En Ano de publicação: 2018 Tipo de documento: Article