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Resistance to Colistin in Acinetobacter baumannii Associated with Mutations in the PmrAB Two-Component System
Author(s) -
Mark D. Adams,
Gabrielle Nickel,
Saralee Bajaksouzian,
Heather Lavender,
A. Rekha Murthy,
Michael R. Jacobs,
Robert A. Bonomo
Publication year - 2009
Publication title -
antimicrobial agents and chemotherapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.07
H-Index - 259
eISSN - 1070-6283
pISSN - 0066-4804
DOI - 10.1128/aac.00284-09
Subject(s) - colistin , acinetobacter baumannii , microbiology and biotechnology , mutant , biology , acinetobacter , strain (injury) , antibiotics , drug resistance , bacteria , gene , genetics , pseudomonas aeruginosa , anatomy
The mechanism of colistin resistance (Col(r)) in Acinetobacter baumannii was studied by selecting in vitro Col(r) derivatives of the multidrug-resistant A. baumannii isolate AB0057 and the drug-susceptible strain ATCC 17978, using escalating concentrations of colistin in liquid culture. DNA sequencing identified mutations in genes encoding the two-component system proteins PmrA and/or PmrB in each strain and in a Col(r) clinical isolate. A colistin-susceptible revertant of one Col(r) mutant strain, obtained following serial passage in the absence of colistin selection, carried a partial deletion of pmrB. Growth of AB0057 and ATCC 17978 at pH 5.5 increased the colistin MIC and conferred protection from killing by colistin in a 1-hour survival assay. Growth in ferric chloride [Fe(III)] conferred a small protective effect. Expression of pmrA was increased in Col(r) mutants, but not at a low pH, suggesting that additional regulatory factors remain to be discovered.

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