Joint tolerance to beta-lactam and fluoroquinolone antibiotics in Escherichia coli results from overexpression of hipA.
The basis of joint tolerance to beta-lactam and fluoroquinolone antibiotics in Escherichia coli mediated by hipA was examined. An antibiotic tolerance phenotype was produced by overexpression of hipA under conditions that did not affect the growth rate of the organism. Overexpressing hipA probably decreases the period in which bacteria are susceptible to the antibiotics by temporarily affecting some aspect of chromosome replication or cell division.
Falla
T J
TJ
Department of Microbiology and Antimicrobial Research Centre, University of Leeds, Leeds LS2 9JT, United Kingdom.
Chopra
I
I
D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D000890:Anti-Infective Agents / Q000494:pharmacology*; D001426:Bacterial Proteins / Q000096:biosynthesis*; D002876:Chromosomes, Bacterial / Q000235:genetics; D004352:Drug Resistance, Microbial; D018432:Drug Resistance, Multiple; D004926:Escherichia coli / Q000187:drug effects* / Q000235:genetics / Q000254:growth & development; D029968:Escherichia coli Proteins; D024841:Fluoroquinolones; D015964:Gene Expression Regulation, Bacterial / Q000187:drug effects*; D008826:Microbial Sensitivity Tests; D010957:Plasmids; D047090:beta-Lactams
D000900:Anti-Bacterial Agents; D000890:Anti-Infective Agents; D001426:Bacterial Proteins; D029968:Escherichia coli Proteins; D024841:Fluoroquinolones; D047090:beta-Lactams; C070741:hipA protein, E coli