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Involvement of multiple genetic loci in Staphylococcus aureus teicoplanin resistance

Bischoff, Markus ; Roos, Martin ; Putnik, Jasmina ; Wada, Akihito ; Glanzmann, Philipp ; Giachino, Philipp ; Vaudaux, Pierre ; Berger-Bächi, B.

In: FEMS Microbiology Letters, 2001, vol. 194, no. 1, p. 77-82

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    Titre
    • Involvement of multiple genetic loci in Staphylococcus aureus teicoplanin resistance
    Auteur
    • Bischoff, Markus. Institute of Medical Microbiology, University of Zürich, Gloriastr. 32, Postfach, CH-8028 Zürich, Switzerland
    • Roos, Martin. Robert Koch Institut, Nordufer 20, D-13353 Berlin, Germany
    • Putnik, Jasmina. Institute of Medical Microbiology, University of Zürich, Gloriastr. 32, Postfach, CH-8028 Zürich, Switzerland
    • Wada, Akihito. Institute of Medical Microbiology, University of Zürich, Gloriastr. 32, Postfach, CH-8028 Zürich, Switzerland
    • Glanzmann, Philipp. Institute of Medical Microbiology, University of Zürich, Gloriastr. 32, Postfach, CH-8028 Zürich, Switzerland
    • Giachino, Philipp. Institute of Medical Microbiology, University of Zürich, Gloriastr. 32, Postfach, CH-8028 Zürich, Switzerland
    • Vaudaux, Pierre. Division of Infectious Diseases, University Hospital Geneva, CH-1211 Geneva, Switzerland
    • Berger-Bächi, B.. Institute of Medical Microbiology, University of Zürich, Gloriastr. 32, Postfach, CH-8028 Zürich, Switzerland
    Type de document
    • Postprint
    Identifiant OAI-PMH
    • oai:doc.rero.ch:298028
    Summary
    Teicoplanin resistance was transformed from a teicoplanin-resistant Staphylococcus aureus into the susceptible strain BB255 to give strain BB938. The cell wall composition, amidation of the iD-glutamate, and peptide crosslinking were identical in BB938 as in BB255 except for a 60% increased length of the glycan chain. Transductional crosses revealed that at least two distinct loci contributed in a cumulative fashion to teicoplanin resistance. One of these loci correlated with a mutation inactivating the anti-sigma factor RsbW. This mutation must have occurred during transformation and selection for teicoplanin resistance in BB938. Genetic manipulations involving the sigB operon showed that transcription factor SigB contributed to decreased teicoplanin susceptibility