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Updated: Jul 3, 2026

Characterizing Multidrug Efflux Systems in Acinetobacter baumannii Using an Efflux-Deficient Bacterial Strain and a Single-Copy Gene Expression System
05:06

Characterizing Multidrug Efflux Systems in Acinetobacter baumannii Using an Efflux-Deficient Bacterial Strain and a Single-Copy Gene Expression System

Published on: January 5, 2024

ARI 1: beta-lactamase-mediated imipenem resistance in Acinetobacter baumannii

R Paton1, R S Miles, J Hood

  • 1Department of Medical Microbiology, University of Edinburgh Medical School, Edinburgh, UK.

International Journal of Antimicrobial Agents
|February 1, 1993
PubMed

Insights

Acinetobacter baumannii strain 6B92 exhibited resistance to multiple antibiotics, including imipenem. Researchers identified a novel beta-lactamase, ARI 1, responsible for this resistance, which was lost when the bacteria were treated with ethidium bromide.

Area of Science:

  • Microbiology
  • Biochemistry
  • Molecular Biology

Background:

  • Acinetobacter baumannii is an opportunistic pathogen frequently associated with hospital-acquired infections.
  • Antibiotic resistance in A. baumannii, particularly to carbapenems like imipenem, poses a significant clinical challenge.
  • Beta-lactamases are enzymes that confer resistance to beta-lactam antibiotics by hydrolyzing their core structure.

Purpose of the Study:

  • To characterize the beta-lactamase enzymes responsible for imipenem and broad-spectrum cephalosporin resistance in a clinical isolate of Acinetobacter baumannii.
  • To investigate the genetic basis of this antibiotic resistance, including the potential role of plasmids.

Main Methods:

  • Isolation and characterization of a resistant Acinetobacter baumannii strain (6B92).
  • Protein extraction, isoelectric focusing, and enzyme assays to identify and characterize beta-lactamases.
  • Treatment with ethidium bromide to assess the stability of resistance and the role of plasmids.
  • Determination of enzyme molecular size and inhibition profiles.

Main Results:

  • The resistant strain possessed two beta-lactamases: a high pI chromosomal cephalosporinase and a novel beta-lactamase, ARI 1 (pI 6.65).
  • Treatment with ethidium bromide cured the imipenem and penicillin resistance, coinciding with the loss of ARI 1, but no resistance plasmid was detected.
  • ARI 1 slowly hydrolyzed penicillin, ampicillin, and cephaloridine, and inactivated imipenem via a mechanism demonstrable only microbiologically.
  • ARI 1 has a molecular size of 23 kDa and is not inhibited by common inhibitors like EDTA, p-CMB, or clavulanate.

Conclusions:

  • A novel beta-lactamase, ARI 1, contributes significantly to imipenem resistance in Acinetobacter baumannii.
  • The resistance mechanism associated with ARI 1 may be chromosomally encoded or involve a non-visualized/non-transferable plasmid.
  • Further investigation is needed to elucidate the precise genetic basis and mechanism of imipenem inactivation by ARI 1.

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