Abstract
Antimicrobial-resistant pathogenic members of the Enterobacteriaceae are a well-defined global problem. We hypothesized that one of the main reservoirs of dissemination of antimicrobial resistance genes in Vietnam is non-pathogenic intestinal flora, and sought to isolate antimicrobial-resistant organisms from hospitalized patients and non-hospitalized healthy individuals in Ho Chi Minh City. The results identified substantial faecal carriage of gentamicin-, ceftazidime- and nalidixic acid-resistant members of the Enterobacteriaceae in both hospitalized patients and non-hospitalized healthy individuals. A high prevalence of quinolone resistance determinants was identified, particularly the qnrS gene, in both community- and hospital-associated strains. Furthermore, the results demonstrated that a combination of quinolone resistance determinants can confer resistance to nalidixic acid and ciprofloxacin, even in the apparent absence of additional chromosomal resistance mutations in wild-type strains and laboratory strains with transferred plasmids. These data suggest that intestinal commensal organisms are a significant reservoir for the dissemination of plasmid-mediated quinolone resistance in Ho Chi Minh City.
Highlights
Pathogenic enteric bacteria that exhibit antimicrobial resistance are a widespread phenomenon and arguably constitute a global epidemic
Quinolones and fluoroquinolones are groups of antimicrobial compounds that are commonly used for the treatment of many bacterial infections
The more recent discovery and rapid dissemination of plasmid-mediated quinolone resistance (PMQR) genes has further highlighted the problem of quinolone and Downloaded from www.microbiologyresearch.org by
Summary
Pathogenic enteric bacteria that exhibit antimicrobial resistance are a widespread phenomenon and arguably constitute a global epidemic. Amplicons produced from all strains specific for the gyrA, parC, qnrS, qepA and aac(69)-Ib genes were sequenced with the same primers used for amplification. All hospital strains and all of the qnr- or aac(69)-Ib-cr-positive community strains were typed by random amplified polymorphic DNA (RAPD) PCR using three different primers (Table 1)
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