Plasmid-Borne erm(T) from invasive, macrolide-resistant Streptococcus pyogenes strains.
Robyn L Woodbury1, Kathryn A Klammer, Yang Xiong
1Division of Bacterial Diseases, Respiratory Diseases Branch, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA.
Antimicrobial Agents and Chemotherapy
|January 9, 2008
Summary
Group A Streptococcus (GAS) isolates show new resistance to erythromycin and clindamycin. This resistance is linked to a novel plasmid carrying the erm(T) gene, previously undetected in GAS.
Area of Science:
- Microbiology
- Molecular Biology
- Infectious Diseases
Background:
- Group A Streptococcus (GAS) is a significant human pathogen.
- Antibiotic resistance in GAS is a growing public health concern.
- Macrolide resistance mechanisms in GAS are typically well-characterized.
Purpose of the Study:
- To investigate the genetic basis of erythromycin and clindamycin resistance in specific GAS isolates.
- To identify novel resistance determinants in invasive GAS strains.
Main Methods:
- Analysis of 23 invasive GAS isolates from US surveillance.
- Phenotypic testing for erythromycin and clindamycin resistance.
- Molecular detection of known and novel macrolide resistance genes.
- Plasmid analysis and sequencing.
Main Results:
- All 23 GAS isolates exhibited erythromycin resistance and inducible clindamycin resistance.
- These isolates lacked previously identified macrolide resistance determinants.
- A novel broad-host-range plasmid carrying the erm(T) methylase gene was identified in all resistant isolates.
- The erm(T) gene has not been previously reported in GAS.
- The resistant isolates belonged to four distinct GAS clones.
Conclusions:
- The erm(T) gene on a novel plasmid is responsible for the observed macrolide resistance in these GAS isolates.
- This finding highlights a new mechanism of antibiotic resistance emergence in GAS.
- Continued surveillance for novel resistance determinants in GAS is crucial.
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