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      Antimicrobial Resistance, Class 1 Integrons, and Genomic Island 1 in Salmonella Isolates from Vietnam

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          Abstract

          Background

          The objective was to investigate the phenotypic and genotypic resistance and the horizontal transfer of resistance determinants from Salmonella isolates from humans and animals in Vietnam.

          Methodology/Principal Findings

          The susceptibility of 297 epidemiologically unrelated non-typhoid Salmonella isolates was investigated by disk diffusion assay. The isolates were screened for the presence of class 1 integrons and Salmonella genomic island 1 by PCR. The potential for the transfer of resistance determinants was investigated by conjugation experiments. Resistance to gentamicin, kanamycin, chloramphenicol, streptomycin, trimethoprim, ampicillin, nalidixic acid, sulphonamides, and tetracycline was found in 13 to 50% of the isolates. Nine distinct integron types were detected in 28% of the isolates belonging to 11 Salmonella serovars including S. Tallahassee. Gene cassettes identified were aadA1, aadA2, aadA5, bla PSE-1, bla OXA-30, dfrA1, dfrA12, dfrA17, and sat, as well as open reading frames with unknown functions. Most integrons were located on conjugative plasmids, which can transfer their antimicrobial resistance determinants to Escherichia coli or Salmonella Enteritidis, or with Salmonella Genomic Island 1 or its variants. The resistance gene cluster in serovar Emek identified by PCR mapping and nucleotide sequencing contained SGI1-J3 which is integrated in SGI1 at another position than the majority of SGI1. This is the second report on the insertion of SGI1 at this position. High-level resistance to fluoroquinolones was found in 3 multiresistant S. Typhimurium isolates and was associated with mutations in the gyrA gene leading to the amino acid changes Ser83Phe and Asp87Asn.

          Conclusions

          Resistance was common among Vietnamese Salmonella isolates from different sources. Legislation to enforce a more prudent use of antibiotics in both human and veterinary medicine should be implemented by the authorities in Vietnam.

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          Most cited references 38

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          Mechanisms of quinolone resistance in Escherichia coli and Salmonella: recent developments.

          Fluoroquinolones are broad-spectrum antimicrobials highly effective for treatment of a variety of clinical and veterinary infections. Their antibacterial activity is due to inhibition of DNA replication. Usually resistance arises spontaneously due to point mutations that result in amino acid substitutions within the topoisomerase subunits GyrA, GyrB, ParC or ParE, decreased expression of outer membrane porins, or overexpression of multidrug efflux pumps. In addition, the recent discovery of plasmid-mediated quinolone resistance could result in horizontal transfer of fluoroquinolone resistance between strains. Acquisition of high-level resistance appears to be a multifactorial process. Care needs to taken to avoid overuse of this important class of antimicrobial in both human and veterinary medicine to prevent an increase in the occurrence of resistant zoonotic and non-zoonotic bacterial pathogens that could subsequently cause human or animal infections.
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            PCR mapping of integrons reveals several novel combinations of resistance genes.

            The integron is a new type of mobile element which has evolved by a site-specific recombinational mechanism. Integrons consist of two conserved segments of DNA separated by a variable region containing one or more genes integrated as cassettes. Oligonucleotide probes specific for the conserved segments have revealed that integrons are widespread in recently isolated clinical bacteria. Also, by using oligonucleotide probes for several antibiotic resistance genes, we have found novel combinations of resistance genes in these strains. By using PCR, we have determined the content and order of the resistance genes inserted between the conserved segments in the integrons of these clinical isolates. PCR mapping of integrons can be a useful epidemiological tool to study the evolution of multiresistance plasmids and transposons and dissemination of antibiotic resistance genes.
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              Mechanisms of fluoroquinolone resistance.

               David Hooper (1999)
              Mechanisms of bacterial resistance to fluoroquinolones fall into two principal categories, alterations in drug target enzymes and alterations that limit permeation of drug to the target, both resulting from chromosomal mutations. No specific resistance mechanisms of quinolone degradation or modification have been found. The target enzymes, DNA gyrase and topoisomerase IV are most commonly altered in domains near the enzyme active sites and in some cases reduced drug binding affinity has been demonstrated. Drug permeation is altered by mutations that increase expression of endogenous multidrug efflux pumps, alter outer membrane diffusion channels, or both. Recently a new plasmid-mediated resistance of an as yet undefined mechanism was found in clinical isolates of Klebsiella pneumoniae. Copyright 1999 Harcourt Publishers Ltd.
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                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS One
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, USA )
                1932-6203
                2010
                26 February 2010
                : 5
                : 2
                Affiliations
                [1 ]Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands
                [2 ]Department of Medical Microbiology, University Medical Centre Utrecht, Utrecht, The Netherlands
                [3 ]Faculty of Animal Husbandry and Veterinary Medicine, Nong Lam University, Ho Chi Min City, Vietnam
                Charité-Universitätsmedizin Berlin, Germany
                Author notes

                Conceived and designed the experiments: EvD WG. Performed the experiments: AV ACF. Analyzed the data: AV WG ACF. Contributed reagents/materials/analysis tools: AV. Wrote the paper: AV EvD WG ACF.

                Article
                09-PONE-RA-14646
                10.1371/journal.pone.0009440
                2829082
                20195474
                Vo et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
                Page count
                Pages: 8
                Categories
                Research Article
                Microbiology
                Microbiology/Medical Microbiology
                Infectious Diseases/Antimicrobials and Drug Resistance
                Infectious Diseases/Epidemiology and Control of Infectious Diseases

                Uncategorized

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