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mecA-blaZ corepressors in clinical Staphylococcus aureus isolates
Adriana E Rosato1, Barry N Kreiswirth, William A Craig
1Department of Medicine, Medical College of Virginia Campus of Virginia Commonwealth University, Richmond, Virginia 23298, USA.
Antimicrobial Agents and Chemotherapy
|March 26, 2003
Summary
Oxacillin-resistant Staphylococcus aureus requires functional mecA regulators. Studies show that mutations in mecI or the presence of blaI are crucial for this resistance, indicating at least one regulator must be active.
Area of Science:
- Microbiology
- Molecular Biology
- Antimicrobial Resistance
Background:
- The mecA gene in Staphylococcus aureus confers resistance to oxacillin and other beta-lactam antibiotics.
- Two key regulators, mecI and blaI, control the expression of the mecA gene.
- Understanding the interplay between mecI and blaI is crucial for comprehending oxacillin resistance mechanisms.
Purpose of the Study:
- To investigate the presence and nucleotide sequences of mecI and blaI in clinical Staphylococcus aureus isolates.
- To determine the correlation between mecI mutations or deletions and the presence of blaI.
- To elucidate the necessity of functional mecA regulators for oxacillin resistance.
Main Methods:
- Analysis of 73 clinical Staphylococcus aureus isolates.
- Assessment of mecI and blaI presence and nucleotide sequences.
- Clonal typing based on spa nucleotide repeat patterns for isolates with mecI mutations.
Main Results:
- 96% of isolates with mutant or deleted mecI possessed blaI.
- 78% of isolates with wild-type mecI also contained blaI (P < 0.05).
- All isolates lacking blaI exhibited wild-type mecI sequences.
Conclusions:
- Oxacillin resistance in Staphylococcus aureus necessitates at least one functional mecA regulator (mecI or blaI).
- The presence of blaI is significantly associated with mecI status.
- Disruptions in mecI appear to be compensated by blaI presence, maintaining oxacillin resistance.