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Nosocomial outbreaks due to amikacin-resistant tobramycin-sensitive Acinetobacter species: correlation with amikacin

Y Buisson1, G Tran Van Nhieu, L Ginot

  • 1Laboratoire de Biologie Clinique, Hôpital d'Instruction des Armées du Val-de-Grâce, Paris, France.

Insights

Amikacin-resistant Acinetobacter spp. emerged due to the APH(3’)-VI enzyme, spreading between patients and staff. Amikacin use correlated with increased infections, highlighting the need for antimicrobial stewardship.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Epidemiology

Background:

  • Acinetobacter spp. are opportunistic pathogens.
  • Antimicrobial resistance in Acinetobacter is a growing concern.
  • The emergence of amikacin resistance in Acinetobacter spp. was observed.

Purpose of the Study:

  • To investigate the mechanism and epidemiology of amikacin resistance in Acinetobacter spp.
  • To identify the genetic basis of this resistance phenotype.
  • To determine the correlation between amikacin consumption and infection rates.

Main Methods:

  • Phenotypic characterization of resistance.
  • Enzyme substrate profiling.
  • DNA-DNA hybridization for gene identification.
  • Retrospective epidemiological survey.
  • Analysis of amikacin consumption data.

Main Results:

  • Fifty-seven cases of infection/colonization with amikacin-resistant, tobramycin-sensitive Acinetobacter spp. were identified.
  • The resistance was linked to the 3'-O-aminoglycoside phosphotransferase (APH(3')-VI) enzyme.
  • This resistance was found in Acinetobacter baumannii and Acinetobacter johnsonii isolates.
  • A significant correlation was found between amikacin consumption and case incidence.

Conclusions:

  • The APH(3')-VI enzyme is responsible for amikacin resistance in Acinetobacter spp.
  • The gene conferring resistance has disseminated among different Acinetobacter biotypes and species.
  • Hospital amikacin consumption is a risk factor for the emergence and spread of resistant Acinetobacter infections.

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