Prevalence of aminoglycoside-modifying enzymes genes among isolates of Enterococcus faecalis and Enterococcus faecium

Mohammad Mehdi Feizabadi1, Parviz Maleknejad, Ahmad Asgharzadeh

  • 1Department of Microbiology, Faculty of Medicine, Tehran University of Medical Science, Tehran, Iran. mfeizabadi@tums.ac.ir

Microbial Drug Resistance (Larchmont, N.Y.)
|January 18, 2007
PubMed

Insights

High-level gentamicin resistance (HLGR) in Enterococcus is often linked to the aac(6')-aph(2") gene. This study found aac(6')-aph(2") and aph(3')-IIIa genes were common in resistant Enterococcus faecalis and E. faecium isolates.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Antimicrobial Resistance

Background:

  • High-level gentamicin resistance (HLGR) in Enterococcus species is a significant clinical concern, impacting treatment options.
  • Enterococcus faecalis and Enterococcus faecium are common causes of hospital-acquired infections.

Purpose of the Study:

  • To investigate the prevalence of HLGR phenotype in Enterococcus isolates from Tehran hospitals.
  • To identify the aminoglycoside modifying enzyme (AME) genes responsible for gentamicin resistance in these isolates.

Main Methods:

  • Disk diffusion and macrobroth dilution assays were used to determine gentamicin resistance and minimum inhibitory concentrations (MICs).
  • Polymerase chain reaction (PCR) was employed to detect specific AME genes, including aac(6 rifluoromethyl)-aph(2 rifluoromethyl), aph(3 rifluoromethyl)-IIIa, and others.
  • Susceptibility to other aminoglycosides (amikacin, netilmicin, tobramycin, kanamycin) was also assessed.

Main Results:

  • 52% of Enterococcus isolates exhibited the HLGR phenotype.
  • The aac(6 rifluoromethyl)-aph(2 rifluoromethyl) gene was present in all HLGR isolates and those with high gentamicin MICs.
  • The aph(3 rifluoromethyl)-IIIa gene was frequently found in HLGR isolates and those with MICs < 500 µg/mL.
  • Co-occurrence of aac(6 rifluoromethyl)-aph(2 rifluoromethyl) and aph(3 rifluoromethyl)-IIIa was observed in a majority of HLGR isolates.

Conclusions:

  • The aac(6 rifluoromethyl)-aph(2 rifluoromethyl) gene is the predominant mechanism for high-level gentamicin resistance in Enterococcus faecalis and E. faecium in this region.
  • The aph(3 rifluoromethyl)-IIIa gene also contributes significantly to aminoglycoside resistance.
  • Molecular detection of these AME genes is crucial for understanding and managing gentamicin resistance in Enterococcus infections.

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