Occurrence and mechanisms of amikacin resistance and its association with β-lactamases in Pseudomonas aeruginosa: a Korean nationwide study
Objectives We investigated the occurrence and mechanism of amikacin resistance and its association with various β-lactamase genes in Pseudomonas aeruginosa isolates. Methods Of the total 250 consecutive, non-duplicated isolates of P. aeruginosa, 55 isolates showed amikacin resistance. PCR amplificat...
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Veröffentlicht in: | Journal of antimicrobial chemotherapy 2008-09, Vol.62 (3), p.479-483 |
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description | Objectives We investigated the occurrence and mechanism of amikacin resistance and its association with various β-lactamase genes in Pseudomonas aeruginosa isolates. Methods Of the total 250 consecutive, non-duplicated isolates of P. aeruginosa, 55 isolates showed amikacin resistance. PCR amplification of genes for aminoglycoside (AG)-modifying enzymes [aac(3)-I, aac(3)-II/VI, aac(3)-III/IV, aac(6′)-I, aac(6′)-II, ant(2″)-I, ant(4′)-II and aph(3′)-VI], 16S rRNA methylases (rmtA, rmtB, rmtC and armA) and class 1 integrons was performed. In addition, we analysed the association of AG resistance genes with various β-lactamase genes. Results and conclusions In Korea, the amikacin resistance rate in P. aeruginosa was high (22%), and it varied among provinces (3.8% to 40%). Four types of AG-modifying enzyme genes [aph(3′)-VI, ant(2″)-I, aac(6′)-I and aac(3)-II/VI] were found in 48 isolates. Thirty-six strains harboured two or more types of enzymes, of which a combination of aph(3′)-VI and ant(2″)-I was the most frequent (24/36 isolates, 66.7%). None harboured aac(3)-I, aac(3)-III/IV, aac(6′)-II, ant(4′)-II, rmtA, rmtB, rmtC or armA. Forty-two isolates co-harboured β-lactamase genes (mostly blaOXA-10). A class 1 integron was detected in all but one, and all the ant(2″)-I and 26/29 blaOXA-10 were found in it. In contrast, aph(3′)-VI was not found to be associated with the class 1 integron. Considering the possibility of co-selection and dissemination, constant monitoring of resistance evolution is necessary. |
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Methods Of the total 250 consecutive, non-duplicated isolates of P. aeruginosa, 55 isolates showed amikacin resistance. PCR amplification of genes for aminoglycoside (AG)-modifying enzymes [aac(3)-I, aac(3)-II/VI, aac(3)-III/IV, aac(6′)-I, aac(6′)-II, ant(2″)-I, ant(4′)-II and aph(3′)-VI], 16S rRNA methylases (rmtA, rmtB, rmtC and armA) and class 1 integrons was performed. In addition, we analysed the association of AG resistance genes with various β-lactamase genes. Results and conclusions In Korea, the amikacin resistance rate in P. aeruginosa was high (22%), and it varied among provinces (3.8% to 40%). Four types of AG-modifying enzyme genes [aph(3′)-VI, ant(2″)-I, aac(6′)-I and aac(3)-II/VI] were found in 48 isolates. Thirty-six strains harboured two or more types of enzymes, of which a combination of aph(3′)-VI and ant(2″)-I was the most frequent (24/36 isolates, 66.7%). None harboured aac(3)-I, aac(3)-III/IV, aac(6′)-II, ant(4′)-II, rmtA, rmtB, rmtC or armA. Forty-two isolates co-harboured β-lactamase genes (mostly blaOXA-10). A class 1 integron was detected in all but one, and all the ant(2″)-I and 26/29 blaOXA-10 were found in it. In contrast, aph(3′)-VI was not found to be associated with the class 1 integron. Considering the possibility of co-selection and dissemination, constant monitoring of resistance evolution is necessary.</description><identifier>ISSN: 0305-7453</identifier><identifier>EISSN: 1460-2091</identifier><identifier>DOI: 10.1093/jac/dkn244</identifier><identifier>PMID: 18606785</identifier><identifier>CODEN: JACHDX</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Amikacin - pharmacology ; aminoglycoside-modifying enzymes ; Anti-Bacterial Agents - pharmacology ; Antibiotics. Antiinfectious agents. Antiparasitic agents ; aph(3′)-VI ; beta-Lactam Resistance ; beta-Lactamases - biosynthesis ; beta-Lactamases - genetics ; Biological and medical sciences ; DNA, Bacterial - genetics ; Genes, Bacterial ; Humans ; integrons ; Korea ; Medical sciences ; Microbial Sensitivity Tests ; Pharmacology. Drug treatments ; Polymerase Chain Reaction - methods ; Pseudomonas aeruginosa - drug effects ; Pseudomonas aeruginosa - enzymology ; Pseudomonas aeruginosa - genetics ; Pseudomonas Infections - microbiology ; β-lactamases</subject><ispartof>Journal of antimicrobial chemotherapy, 2008-09, Vol.62 (3), p.479-483</ispartof><rights>The Author 2008. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org 2008</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c419t-43e84ee2247eacbdda11ccda0ff31567d9af1e020319bc4baa886121f99c9e0b3</citedby><cites>FETCH-LOGICAL-c419t-43e84ee2247eacbdda11ccda0ff31567d9af1e020319bc4baa886121f99c9e0b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1578,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20635281$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18606785$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Ja-Young</creatorcontrib><creatorcontrib>Park, Yeon-Joon</creatorcontrib><creatorcontrib>Kwon, Hi Jeong</creatorcontrib><creatorcontrib>Han, Kyungja</creatorcontrib><creatorcontrib>Kang, Moon Won</creatorcontrib><creatorcontrib>Woo, Gun-Jo</creatorcontrib><title>Occurrence and mechanisms of amikacin resistance and its association with β-lactamases in Pseudomonas aeruginosa: a Korean nationwide study</title><title>Journal of antimicrobial chemotherapy</title><addtitle>J Antimicrob Chemother</addtitle><description>Objectives We investigated the occurrence and mechanism of amikacin resistance and its association with various β-lactamase genes in Pseudomonas aeruginosa isolates. Methods Of the total 250 consecutive, non-duplicated isolates of P. aeruginosa, 55 isolates showed amikacin resistance. PCR amplification of genes for aminoglycoside (AG)-modifying enzymes [aac(3)-I, aac(3)-II/VI, aac(3)-III/IV, aac(6′)-I, aac(6′)-II, ant(2″)-I, ant(4′)-II and aph(3′)-VI], 16S rRNA methylases (rmtA, rmtB, rmtC and armA) and class 1 integrons was performed. In addition, we analysed the association of AG resistance genes with various β-lactamase genes. Results and conclusions In Korea, the amikacin resistance rate in P. aeruginosa was high (22%), and it varied among provinces (3.8% to 40%). Four types of AG-modifying enzyme genes [aph(3′)-VI, ant(2″)-I, aac(6′)-I and aac(3)-II/VI] were found in 48 isolates. Thirty-six strains harboured two or more types of enzymes, of which a combination of aph(3′)-VI and ant(2″)-I was the most frequent (24/36 isolates, 66.7%). None harboured aac(3)-I, aac(3)-III/IV, aac(6′)-II, ant(4′)-II, rmtA, rmtB, rmtC or armA. Forty-two isolates co-harboured β-lactamase genes (mostly blaOXA-10). A class 1 integron was detected in all but one, and all the ant(2″)-I and 26/29 blaOXA-10 were found in it. In contrast, aph(3′)-VI was not found to be associated with the class 1 integron. Considering the possibility of co-selection and dissemination, constant monitoring of resistance evolution is necessary.</description><subject>Amikacin - pharmacology</subject><subject>aminoglycoside-modifying enzymes</subject><subject>Anti-Bacterial Agents - pharmacology</subject><subject>Antibiotics. Antiinfectious agents. Antiparasitic agents</subject><subject>aph(3′)-VI</subject><subject>beta-Lactam Resistance</subject><subject>beta-Lactamases - biosynthesis</subject><subject>beta-Lactamases - genetics</subject><subject>Biological and medical sciences</subject><subject>DNA, Bacterial - genetics</subject><subject>Genes, Bacterial</subject><subject>Humans</subject><subject>integrons</subject><subject>Korea</subject><subject>Medical sciences</subject><subject>Microbial Sensitivity Tests</subject><subject>Pharmacology. Drug treatments</subject><subject>Polymerase Chain Reaction - methods</subject><subject>Pseudomonas aeruginosa - drug effects</subject><subject>Pseudomonas aeruginosa - enzymology</subject><subject>Pseudomonas aeruginosa - genetics</subject><subject>Pseudomonas Infections - microbiology</subject><subject>β-lactamases</subject><issn>0305-7453</issn><issn>1460-2091</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90c1u1DAQwHELgehSuPAAyBc4IIXaseMk3GAFFFGpSHyKizWxJ9TdxF48iUrfgafhQXgmAru0N06-_GZG-pux-1I8kaJVR-fgjvwmllrfYCupjShK0cqbbCWUqIpaV-qA3SE6F0KYyjS32YFsjDB1U63Yj1Pn5pwxOuQQPR_RnUEMNBJPPYcxbMCFyDNSoAn-qTARB6LkAkwhRX4RpjP-62cxgJtgBELiy9BbwtmnMUVYNOb5a4iJ4CkH_iZlhMjj3-mL4JHTNPvLu-xWDwPhvf17yD68fPF-fVycnL56vX52Ujgt26nQChuNWJa6RnCd9yClcx5E3ytZmdq30EsUpVCy7ZzuAJrGyFL2betaFJ06ZI92e7c5fZuRJjsGcjgMEDHNZE2rVaNEs8DHO-hyIsrY220OI-RLK4X9094u7e2u_YIf7LfO3Yj-mu5jL-DhHgA5GPq89Ax05UphVFU28tqlefv_g8XOLV-D368k5I01taore_z5i3333Kw_GVnbj-o3ACutSA</recordid><startdate>20080901</startdate><enddate>20080901</enddate><creator>Kim, Ja-Young</creator><creator>Park, Yeon-Joon</creator><creator>Kwon, Hi Jeong</creator><creator>Han, Kyungja</creator><creator>Kang, Moon Won</creator><creator>Woo, Gun-Jo</creator><general>Oxford University Press</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20080901</creationdate><title>Occurrence and mechanisms of amikacin resistance and its association with β-lactamases in Pseudomonas aeruginosa: a Korean nationwide study</title><author>Kim, Ja-Young ; Park, Yeon-Joon ; Kwon, Hi Jeong ; Han, Kyungja ; Kang, Moon Won ; Woo, Gun-Jo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c419t-43e84ee2247eacbdda11ccda0ff31567d9af1e020319bc4baa886121f99c9e0b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Amikacin - pharmacology</topic><topic>aminoglycoside-modifying enzymes</topic><topic>Anti-Bacterial Agents - pharmacology</topic><topic>Antibiotics. Antiinfectious agents. Antiparasitic agents</topic><topic>aph(3′)-VI</topic><topic>beta-Lactam Resistance</topic><topic>beta-Lactamases - biosynthesis</topic><topic>beta-Lactamases - genetics</topic><topic>Biological and medical sciences</topic><topic>DNA, Bacterial - genetics</topic><topic>Genes, Bacterial</topic><topic>Humans</topic><topic>integrons</topic><topic>Korea</topic><topic>Medical sciences</topic><topic>Microbial Sensitivity Tests</topic><topic>Pharmacology. Drug treatments</topic><topic>Polymerase Chain Reaction - methods</topic><topic>Pseudomonas aeruginosa - drug effects</topic><topic>Pseudomonas aeruginosa - enzymology</topic><topic>Pseudomonas aeruginosa - genetics</topic><topic>Pseudomonas Infections - microbiology</topic><topic>β-lactamases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Ja-Young</creatorcontrib><creatorcontrib>Park, Yeon-Joon</creatorcontrib><creatorcontrib>Kwon, Hi Jeong</creatorcontrib><creatorcontrib>Han, Kyungja</creatorcontrib><creatorcontrib>Kang, Moon Won</creatorcontrib><creatorcontrib>Woo, Gun-Jo</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of antimicrobial chemotherapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Ja-Young</au><au>Park, Yeon-Joon</au><au>Kwon, Hi Jeong</au><au>Han, Kyungja</au><au>Kang, Moon Won</au><au>Woo, Gun-Jo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Occurrence and mechanisms of amikacin resistance and its association with β-lactamases in Pseudomonas aeruginosa: a Korean nationwide study</atitle><jtitle>Journal of antimicrobial chemotherapy</jtitle><addtitle>J Antimicrob Chemother</addtitle><date>2008-09-01</date><risdate>2008</risdate><volume>62</volume><issue>3</issue><spage>479</spage><epage>483</epage><pages>479-483</pages><issn>0305-7453</issn><eissn>1460-2091</eissn><coden>JACHDX</coden><abstract>Objectives We investigated the occurrence and mechanism of amikacin resistance and its association with various β-lactamase genes in Pseudomonas aeruginosa isolates. Methods Of the total 250 consecutive, non-duplicated isolates of P. aeruginosa, 55 isolates showed amikacin resistance. PCR amplification of genes for aminoglycoside (AG)-modifying enzymes [aac(3)-I, aac(3)-II/VI, aac(3)-III/IV, aac(6′)-I, aac(6′)-II, ant(2″)-I, ant(4′)-II and aph(3′)-VI], 16S rRNA methylases (rmtA, rmtB, rmtC and armA) and class 1 integrons was performed. In addition, we analysed the association of AG resistance genes with various β-lactamase genes. Results and conclusions In Korea, the amikacin resistance rate in P. aeruginosa was high (22%), and it varied among provinces (3.8% to 40%). Four types of AG-modifying enzyme genes [aph(3′)-VI, ant(2″)-I, aac(6′)-I and aac(3)-II/VI] were found in 48 isolates. Thirty-six strains harboured two or more types of enzymes, of which a combination of aph(3′)-VI and ant(2″)-I was the most frequent (24/36 isolates, 66.7%). None harboured aac(3)-I, aac(3)-III/IV, aac(6′)-II, ant(4′)-II, rmtA, rmtB, rmtC or armA. Forty-two isolates co-harboured β-lactamase genes (mostly blaOXA-10). A class 1 integron was detected in all but one, and all the ant(2″)-I and 26/29 blaOXA-10 were found in it. In contrast, aph(3′)-VI was not found to be associated with the class 1 integron. Considering the possibility of co-selection and dissemination, constant monitoring of resistance evolution is necessary.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>18606785</pmid><doi>10.1093/jac/dkn244</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Amikacin - pharmacology aminoglycoside-modifying enzymes Anti-Bacterial Agents - pharmacology Antibiotics. Antiinfectious agents. Antiparasitic agents aph(3′)-VI beta-Lactam Resistance beta-Lactamases - biosynthesis beta-Lactamases - genetics Biological and medical sciences DNA, Bacterial - genetics Genes, Bacterial Humans integrons Korea Medical sciences Microbial Sensitivity Tests Pharmacology. Drug treatments Polymerase Chain Reaction - methods Pseudomonas aeruginosa - drug effects Pseudomonas aeruginosa - enzymology Pseudomonas aeruginosa - genetics Pseudomonas Infections - microbiology β-lactamases |
title | Occurrence and mechanisms of amikacin resistance and its association with β-lactamases in Pseudomonas aeruginosa: a Korean nationwide study |
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