OXA-23 β-Lactamase Overexpression in Acinetobacter baumannii Drives Physiological Changes Resulting in New Genetic Vulnerabilities

Author:

Colquhoun Jennifer M.12,Farokhyfar Marjan3,Hutcheson Anna R.3,Anderson Alexander4ORCID,Bethel Christopher R.5,Bonomo Robert A.56789ORCID,Clarke Anthony J.410,Rather Philip N.123

Affiliation:

1. Department of Microbiology and Immunology, Emory University, Atlanta, Georgia, USA

2. Emory Antibiotic Resistance Center, Emory University, Atlanta, Georgia, USA

3. Research Service, Atlanta VA Medical Center, Decatur, Georgia, USA

4. Department of Molecular and Cellular Biology, University of Guelph, Guelph, Ontario, Canada

5. Research Service, Louis Stokes Cleveland Department of Veterans Affairs, Cleveland, Ohio, USA

6. Department of Biochemistry, Case Western Reserve University, Cleveland, Ohio, USA

7. Department of Medicine, Case Western Reserve University, Cleveland, Ohio, USA

8. Department of Molecular Biology and Microbiology, Case Western Reserve University, Cleveland, Ohio, USA

9. Department of Pharmacology, Case Western Reserve University, Cleveland, Ohio, USA

10. Department of Chemistry & Biochemistry, Wilfrid Laurier University, Waterloo, Ontario, Canada

Abstract

Acinetobacter baumannii has become a serious pathogen in both hospital and community settings. The β-lactam class of antibiotics is a primary treatment option for A. baumannii infections, and expression of β-lactamases is the most frequent mechanism of resistance in this bacterium.

Funder

HHS | National Institutes of Health

U.S. Department of Veterans Affairs

Gouvernement du Canada | Natural Sciences and Engineering Research Council of Canada

Publisher

American Society for Microbiology

Subject

Virology,Microbiology

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