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Ann Pharmacother. 2011 Feb;45(2):218-28. doi: 10.1345/aph.1P084.

Genetic Mechanisms of Antimicrobial Resistance of Acinetobacter baumannii.

Author information

1
John S Esterly PharmD BCPS, at time of writing, Infectious Diseases Pharmacotherapy Fellow, Department of Pharmacy Practice, College of Pharmacy, Midwestern University Chicago, Downers Grove, IL; now, Assistant Professor of Pharmacy Practice, College of Pharmacy, Chicago State University, Chicago, IL; Infectious Diseases Pharmacist, Northwestern Memorial Hospital, Chicago.
2
Chad L Richardson PharmD, at time of writing, Infectious Diseases Pharmacotherapy Resident, Department of Pharmacy Practice, College of Pharmacy, Midwestern University Chicago; now, Solid Organ Transplant Pharmacist, Northwestern Memorial Hospital.
3
Noha S Eltoukhy PharmD BCPS, at time of writing, Infectious Diseases Pharmacy Resident, Department of Pharmacy Practice, College of Pharmacy, Midwestern University Chicago; Rush University Medical Center, Chicago; now, Infectious DIseases Clinical Pharmacy Specialist, St. Mary Medical Center, Langhorne, PA.
4
Chao Qi PhD, Assistant Professor of Pathology, Feinberg School of Medicine, Northwestern University; Assistant Director, Clinical Microbiology Laboratory, Northwestern Memorial Hospital, Chicago.
5
Marc H Scheetz PharmD MSc BCPS, Assistant Professor of Pharmacy Practice, College of Pharmacy, Midwestern University Chicago; Infectious Diseases Pharmacist, Northwestern Memorial Hospital mscheetz@nmh.org.

Abstract

OBJECTIVE:

To summarize published data identifying known genetic mechanisms of antibiotic resistance in Acinetobacter baumannii and the correlating phenotypic expression of antibiotic resistance.

DATA SOURCES:

MEDLINE databases (1966-July 15, 2010) were searched to identify original reports of genetic mechanisms of antibiotic resistance in A. baumannii.

DATA SYNTHESIS:

Numerous genetic mechanisms of resistance to multiple classes of antibiotics are known to exist in A. baumannii, a gram-negative bacterium increasingly implicated in nosocomial infections. Mechanisms may be constitutive or acquired via plasmids, integrons, and transposons. Methods of resistance include enzymatic modification of antibiotic molecules, modification of antibiotic target sites, expression of efflux pumps, and downregulation of cell membrane porin channel expression. Resistance to β-lactams appears to be primarily caused by β-lactamase production, including extended spectrum β-lactamases (b/aTEM, blaSHV, b/aTX-M,b/aKPC), metallo-β-lactamases (blaMP, blaVIM, bla, SIM), and most commonly, oxacillinases (blaOXA). Antibiotic target site alterations confer resistance to fluoroquinolones (gyrA, parC) and aminoglycosides (arm, rmt), and to a much lesser extent, β-lactams. Efflux pumps (tet, ade, abe) contribute to resistance against β-lactams, tetracyclines, fluoroquinolones, and aminoglycosides. Finally, porin channel deletion (carO, oprD) appears to contribute to β-lactam resistance and may contribute to rarely seen polymyxin resistance. Of note, efflux pumps and porin deletions as solitary mechanisms may not render clinical resistance to A. baumannii.

CONCLUSIONS:

A. baumannii possesses copious genetic resistance mechanisms. Knowledge of local genotypes and expressed phenotypes for A. baumannii may aid clinicians more than phenotypic susceptibilities reported in large epidemiologic studies.

KEYWORDS:

Acinetobacter baumannii; antibiotics; genetic mechanisms; resistance; β-lactamases

PMID:
21304033
DOI:
10.1345/aph.1P084
[Indexed for MEDLINE]

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