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A liaF codon deletion abolishes daptomycin bactericidal activity against vancomycin-resistant Enterococcus faecalis.

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A specific genetic mutation in LiaF, a cell envelope regulator, causes daptomycin (DAP) tolerance in enterococci. This finding may impact future DAP therapy effectiveness.

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Area of Science:

  • Microbiology
  • Genetics
  • Antimicrobial Resistance

Background:

  • Antibiotic tolerance poses a significant challenge in treating bacterial infections.
  • Daptomycin (DAP) is a crucial lipopeptide antibiotic effective against enterococci.
  • The genetic underpinnings of antibiotic tolerance remain largely uncharacterized.

Purpose of the Study:

  • To investigate the genetic basis of daptomycin tolerance in enterococci.
  • To identify specific genetic alterations contributing to reduced susceptibility to DAP.
  • To elucidate the role of the LiaFSR system in DAP tolerance.

Main Methods:

  • Utilized time-kill assays to evaluate bacterial killing kinetics.
  • Employed genetic analysis to identify mutations associated with DAP tolerance.
  • Focused on the LiaF protein, a component of the LiaFSR regulatory system.

Main Results:

  • Identified a specific deletion of isoleucine at position 177 in the LiaF protein.
  • Demonstrated that this LiaF mutation directly confers a daptomycin-tolerant phenotype in enterococci.
  • The identified mutation is linked to the LiaFSR cell envelope stress response system.

Conclusions:

  • A deletion in LiaF (Ile177) is a direct genetic cause of daptomycin tolerance in enterococci.
  • This genetic defect may impair the efficacy of daptomycin treatment.
  • Understanding these genetic mechanisms is vital for optimizing antibiotic therapy.