Related Experiment Videos
tcaA inactivation increases glycopeptide resistance in Staphylococcus aureus
Hideki Maki1, Nadine McCallum, Markus Bischoff
1Department of Medical Microbiology, University of Zürich, Gloriastr. 32, CH-8028 Zürich, Switzerland.
Antimicrobial Agents and Chemotherapy
|May 25, 2004
Summary
Inactivating the tcaA gene in Staphylococcus aureus increases resistance to teicoplanin. This gene plays a significant role in glycopeptide resistance in clinical isolates.
Area of Science:
- Microbiology
- Genetics
- Molecular Biology
Background:
- The tcaRAB region deletion increases teicoplanin resistance in Staphylococcus aureus.
- Glycopeptide resistance is a growing concern in Staphylococcus aureus infections.
Purpose of the Study:
- To identify the specific gene within the tcaRAB region responsible for altered glycopeptide resistance.
- To investigate the role of tcaA in glycopeptide resistance in clinical isolates of Staphylococcus aureus.
Main Methods:
- Sequential genetic complementation of tcaRAB mutants.
- Northern blot analysis to study tcaA gene expression.
- Genetic analysis of clinical glycopeptide-intermediate-resistant Staphylococcus aureus (GISA) strains.
Main Results:
- The tcaA gene was identified as the key determinant of glycopeptide resistance within the tcaRAB region.
- tcaA expression is weakly constitutive and strongly induced by teicoplanin.
- Truncated tcaA genes were found in GISA strains Michigan and SA137/93G.
- Complementation with functional tcaA reduced teicoplanin resistance five- to eightfold and vancomycin resistance twofold in GISA strains.
Conclusions:
- Inactivation of tcaA contributes to glycopeptide resistance in Staphylococcus aureus.
- tcaA plays a relevant role in the development of resistance in clinical isolates.
- Targeting tcaA may offer a strategy to combat glycopeptide resistance in Staphylococcus aureus.