title: Molecular mechanisms of antimicrobial resistance in fecal Escherichia coli of healthy dogs after enrofloxacin or amoxicillin administration.
abstract: Escherichia coli respond to selective pressure of antimicrobial therapy by developing resistance through a variety of mechanisms. The purpose of this study was to characterize the genetic mechanisms of antimicrobial resistance in fecal E. coli after the routine use of 2 popular antimicrobials. Fourteen resistant E. coli isolates, representing predominant clones that emerged in healthy dogs' feces after treatment with either amoxicillin (11 E. coli isolates) or enrofloxacin (3 E. coli isolates), were tested for mutations in DNA gyrase (gyrA and gyrB) and in topoisomerase IV (parC) and for the presence of β-lactamases (bla(TEM), bla(SHV), bla(PSE-1) and bla(CTX-M)) and plasmid-mediated quinolone resistance (qnrA, qnrB, qnrS, aac(6')-Ib, and qepA), by polymerase chain reaction. Escherichia coli isolates cultured following amoxicillin therapy only expressed single-drug resistance to β-lactams, while the isolates cultured from dogs receiving enrofloxacin therapy expressed multidrug resistance (MDR). The use of RND efflux pump inhibitors increased the susceptibility of the 3 MDR E. coli isolates to doxycycline, chloramphenicol, enrofloxacin, and ciprofloxacin, which indicates a role of the efflux pump in the acquisition of the MDR phenotype. Amplification and sequencing of AcrAB efflux pump regulators (soxR, soxS, marR, and acrR) revealed only the presence of a single mutation in soxS in the 3 MDR isolates.
authors.affiliation: Department of Medical Microbiology and Immunology, Faculty of Medicine, Assiut University, Assiut, Egypt.
authors.forename: Sherine A
authors.initials: SA
authors.lastname: Aly
authors.forename: Nipattra
authors.initials: N
authors.lastname: Debavalya
authors.forename: Sang-Jin
authors.initials: SJ
authors.lastname: Suh
authors.forename: Omar A
authors.initials: OA
authors.lastname: Oryazabal
authors.forename: Dawn M
authors.initials: DM
authors.lastname: Boothe
mesh_terms: D000658:Amoxicillin / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D027081:DNA Gyrase / Q000235:genetics; D027101:DNA Topoisomerase IV / Q000235:genetics; D004285:Dogs; D004352:Drug Resistance, Microbial / Q000187:drug effects / Q000235:genetics*; D000077422:Enrofloxacin; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics / Q000302:isolation & purification; D029968:Escherichia coli Proteins / Q000235:genetics; D005243:Feces / Q000382:microbiology*; D024841:Fluoroquinolones / Q000008:administration & dosage / Q000494:pharmacology*; D022761:Gene Transfer, Horizontal; D009154:Mutation; D010957:Plasmids / Q000235:genetics; D016133:Polymerase Chain Reaction; D001618:beta-Lactamases / Q000235:genetics; D047090:beta-Lactams / Q000494:pharmacology
chemical_list: D000900:Anti-Bacterial Agents; D029968:Escherichia coli Proteins; D024841:Fluoroquinolones; D047090:beta-Lactams; D000077422:Enrofloxacin; D000658:Amoxicillin; D001618:beta-Lactamases; D027101:DNA Topoisomerase IV; D027081:DNA Gyrase