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Induction of ermAMR from a clinical strain of Enterococcus faecalis by 16-membered-ring macrolide antibiotics

T G Oh1, A R Kwon, E C Choi

  • 1College of Pharmacy, Seoul National University, Seoul 151-742, Korea.

Journal of Bacteriology
|October 29, 1998
PubMed

Insights

We identified the MLSB resistance gene in Enterococcus faecalis. A specific mutation in the leader peptide and a duplication in the control region were found to increase resistance to tylosin and other macrolides.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Enterococcus faecalis is a common cause of hospital-acquired infections.
  • Macrolide resistance in bacteria is a growing public health concern.
  • The MLSB resistance determinant confers resistance to macrolides, lincosamides, and streptogramin B antibiotics.

Purpose of the Study:

  • To elucidate the molecular basis of MLSB resistance in a clinical isolate of Enterococcus faecalis.
  • To identify the specific genetic elements responsible for resistance induction by tylosin.

Main Methods:

  • Polymerase chain reaction (PCR) was used to clone the MLSB resistance determinant.
  • Site-directed mutagenesis was employed to analyze the cloned gene (ermAMR).
  • Reporter gene assays were performed to assess gene expression levels.

Main Results:

  • The cloned gene, ermAMR, was successfully isolated from Enterococcus faecalis 373.
  • An arginine-to-cysteine substitution in the seventh codon of the putative leader peptide was crucial for tylosin resistance inducibility.
  • A TAAA duplication in the control region led to a significant increase in the expression of the downstream methylase gene.

Conclusions:

  • The study identified key genetic alterations conferring macrolide resistance in Enterococcus faecalis.
  • The findings provide insights into the mechanisms of antibiotic resistance and can inform strategies to combat resistant infections.

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