Aminoglycoside Resistance Mechanisms in Clinical Isolates of Pseudomonas aeruginosa from the Canary Islands
Strains of Pseudomonas aeruginosa resistant to aminoglycoside antibiotics were selected from 152 clinical isolates. We identified two patterns of resistance correlating with the resistance mechanism characterized by changes in permeability, enzymatic modification due to the acetylating enzyme, AAC(6...
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| Veröffentlicht in: | Zentralblatt für Bakteriologie 2000, Vol.289 (8), p.817-826 |
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| container_title | Zentralblatt für Bakteriologie |
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| creator | Rodríguez Esparragón, Francisco González Martín, Margarita González Lama, Zoilo Sabatelli, Frank J. Tejedor Junco, María Teresa |
| description | Strains of
Pseudomonas aeruginosa resistant to aminoglycoside antibiotics were selected from 152 clinical isolates. We identified two patterns of resistance correlating with the resistance mechanism characterized by changes in permeability, enzymatic modification due to the acetylating enzyme, AAC(6′)-II, or a combination of both. We detected enzymatic activity of the phosphorylase enzyme, APH(3′), in all the isolates. We compared the mechanisms of resistance detected by three methods i. e., radioenzymatic assay, phenotype of resistance and DNA probes. The phenotype of resistance was tested using a kit developed by Schering-Plough Corp. Hybridization was made with 18 DNA probes for the most frequent genes encoding for aminoglycoside-modifying enzymes. All isolates with AAC(6′) activity hybridized with the
aac(6′)-Ib probes and to a minor degree, with the
aac(6′)-IIb probe. None of the isolates showed hybridization with
aph(3′)-I,
aph(3′)-II, or
aph(3′)-III DNA probes. Serotyping of the strains showed that the O:11 serotype was the most frequent one in strains whose resistance was due to the AAC(6′) enzyme. The O:6 serotype was associated with changes in permeability. Encoding of the resistance mechanism seemed to be chromosomal in all the strains. |
| doi_str_mv | 10.1016/S0934-8840(00)80008-0 |
| format | Article |
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Pseudomonas aeruginosa resistant to aminoglycoside antibiotics were selected from 152 clinical isolates. We identified two patterns of resistance correlating with the resistance mechanism characterized by changes in permeability, enzymatic modification due to the acetylating enzyme, AAC(6′)-II, or a combination of both. We detected enzymatic activity of the phosphorylase enzyme, APH(3′), in all the isolates. We compared the mechanisms of resistance detected by three methods i. e., radioenzymatic assay, phenotype of resistance and DNA probes. The phenotype of resistance was tested using a kit developed by Schering-Plough Corp. Hybridization was made with 18 DNA probes for the most frequent genes encoding for aminoglycoside-modifying enzymes. All isolates with AAC(6′) activity hybridized with the
aac(6′)-Ib probes and to a minor degree, with the
aac(6′)-IIb probe. None of the isolates showed hybridization with
aph(3′)-I,
aph(3′)-II, or
aph(3′)-III DNA probes. Serotyping of the strains showed that the O:11 serotype was the most frequent one in strains whose resistance was due to the AAC(6′) enzyme. The O:6 serotype was associated with changes in permeability. Encoding of the resistance mechanism seemed to be chromosomal in all the strains.</description><identifier>ISSN: 0934-8840</identifier><identifier>DOI: 10.1016/S0934-8840(00)80008-0</identifier><identifier>PMID: 10705613</identifier><language>eng</language><publisher>Germany</publisher><subject>Aminoglycosides ; Anti-Bacterial Agents - metabolism ; Anti-Bacterial Agents - pharmacology ; Atlantic Islands ; Drug Resistance, Microbial ; Humans ; Microbial Sensitivity Tests ; Nucleic Acid Hybridization ; Plasmids - genetics ; Pseudomonas aeruginosa ; Pseudomonas aeruginosa - classification ; Pseudomonas aeruginosa - drug effects ; Pseudomonas aeruginosa - isolation & purification ; Pseudomonas Infections - microbiology ; Serotyping ; Spain, Canary Is</subject><ispartof>Zentralblatt für Bakteriologie, 2000, Vol.289 (8), p.817-826</ispartof><rights>1999 Urban & Fischer Verlag</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c392t-b9d3240eb987672f6484db09804ed1ec9252ca993f71f0bc766e1f93e6cc94f53</citedby><cites>FETCH-LOGICAL-c392t-b9d3240eb987672f6484db09804ed1ec9252ca993f71f0bc766e1f93e6cc94f53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10705613$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rodríguez Esparragón, Francisco</creatorcontrib><creatorcontrib>González Martín, Margarita</creatorcontrib><creatorcontrib>González Lama, Zoilo</creatorcontrib><creatorcontrib>Sabatelli, Frank J.</creatorcontrib><creatorcontrib>Tejedor Junco, María Teresa</creatorcontrib><title>Aminoglycoside Resistance Mechanisms in Clinical Isolates of Pseudomonas aeruginosa from the Canary Islands</title><title>Zentralblatt für Bakteriologie</title><addtitle>Zentralbl Bakteriol</addtitle><description>Strains of
Pseudomonas aeruginosa resistant to aminoglycoside antibiotics were selected from 152 clinical isolates. We identified two patterns of resistance correlating with the resistance mechanism characterized by changes in permeability, enzymatic modification due to the acetylating enzyme, AAC(6′)-II, or a combination of both. We detected enzymatic activity of the phosphorylase enzyme, APH(3′), in all the isolates. We compared the mechanisms of resistance detected by three methods i. e., radioenzymatic assay, phenotype of resistance and DNA probes. The phenotype of resistance was tested using a kit developed by Schering-Plough Corp. Hybridization was made with 18 DNA probes for the most frequent genes encoding for aminoglycoside-modifying enzymes. All isolates with AAC(6′) activity hybridized with the
aac(6′)-Ib probes and to a minor degree, with the
aac(6′)-IIb probe. None of the isolates showed hybridization with
aph(3′)-I,
aph(3′)-II, or
aph(3′)-III DNA probes. Serotyping of the strains showed that the O:11 serotype was the most frequent one in strains whose resistance was due to the AAC(6′) enzyme. The O:6 serotype was associated with changes in permeability. Encoding of the resistance mechanism seemed to be chromosomal in all the strains.</description><subject>Aminoglycosides</subject><subject>Anti-Bacterial Agents - metabolism</subject><subject>Anti-Bacterial Agents - pharmacology</subject><subject>Atlantic Islands</subject><subject>Drug Resistance, Microbial</subject><subject>Humans</subject><subject>Microbial Sensitivity Tests</subject><subject>Nucleic Acid Hybridization</subject><subject>Plasmids - genetics</subject><subject>Pseudomonas aeruginosa</subject><subject>Pseudomonas aeruginosa - classification</subject><subject>Pseudomonas aeruginosa - drug effects</subject><subject>Pseudomonas aeruginosa - isolation & purification</subject><subject>Pseudomonas Infections - microbiology</subject><subject>Serotyping</subject><subject>Spain, Canary Is</subject><issn>0934-8840</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1O3TAQRr2gAkp5BJBXqF2kHceJE68qdNUfJCoQtGvLscdgSGLqSSrx9jVcVHXHypJ1vhn7fIwdCfgoQKhP16BlU_V9A-8BPvQA0Feww_b_Xe-xt0R3AG0NqtllewI6aJWQ--z-dIpzuhkfXaLokV8hRVrs7JD_QHdr50gT8TjzzRjn6OzIzyiNdkHiKfBLwtWnKc2WuMW83pRZZHnIaeLLLfKNnW1-LJHRzp7esTfBjoSHL-cB-_X1y8_N9-r84tvZ5vS8clLXSzVoL-sGcNB9p7o6qKZv_AC6hwa9QKfrtnZWaxk6EWBwnVIogpaonNNNaOUBO9nOfcjp94q0mCmSw7E8AtNKpiteOinkq6DoWpCq1gVst6DLiShjMA85TuVrRoB5qsA8V2CeXBsA81yBgZI7flmwDhP6_1Jb_wX4vAWw-PgTMRtyEYt9HzO6xfgUX1nxF4kVmQQ</recordid><startdate>2000</startdate><enddate>2000</enddate><creator>Rodríguez Esparragón, Francisco</creator><creator>González Martín, Margarita</creator><creator>González Lama, Zoilo</creator><creator>Sabatelli, Frank J.</creator><creator>Tejedor Junco, María Teresa</creator><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>7QL</scope><scope>7T7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>2000</creationdate><title>Aminoglycoside Resistance Mechanisms in Clinical Isolates of Pseudomonas aeruginosa from the Canary Islands</title><author>Rodríguez Esparragón, Francisco ; González Martín, Margarita ; González Lama, Zoilo ; Sabatelli, Frank J. ; Tejedor Junco, María Teresa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c392t-b9d3240eb987672f6484db09804ed1ec9252ca993f71f0bc766e1f93e6cc94f53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Aminoglycosides</topic><topic>Anti-Bacterial Agents - metabolism</topic><topic>Anti-Bacterial Agents - pharmacology</topic><topic>Atlantic Islands</topic><topic>Drug Resistance, Microbial</topic><topic>Humans</topic><topic>Microbial Sensitivity Tests</topic><topic>Nucleic Acid Hybridization</topic><topic>Plasmids - genetics</topic><topic>Pseudomonas aeruginosa</topic><topic>Pseudomonas aeruginosa - classification</topic><topic>Pseudomonas aeruginosa - drug effects</topic><topic>Pseudomonas aeruginosa - isolation & purification</topic><topic>Pseudomonas Infections - microbiology</topic><topic>Serotyping</topic><topic>Spain, Canary Is</topic><toplevel>online_resources</toplevel><creatorcontrib>Rodríguez Esparragón, Francisco</creatorcontrib><creatorcontrib>González Martín, Margarita</creatorcontrib><creatorcontrib>González Lama, Zoilo</creatorcontrib><creatorcontrib>Sabatelli, Frank J.</creatorcontrib><creatorcontrib>Tejedor Junco, María Teresa</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Zentralblatt für Bakteriologie</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rodríguez Esparragón, Francisco</au><au>González Martín, Margarita</au><au>González Lama, Zoilo</au><au>Sabatelli, Frank J.</au><au>Tejedor Junco, María Teresa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aminoglycoside Resistance Mechanisms in Clinical Isolates of Pseudomonas aeruginosa from the Canary Islands</atitle><jtitle>Zentralblatt für Bakteriologie</jtitle><addtitle>Zentralbl Bakteriol</addtitle><date>2000</date><risdate>2000</risdate><volume>289</volume><issue>8</issue><spage>817</spage><epage>826</epage><pages>817-826</pages><issn>0934-8840</issn><abstract>Strains of
Pseudomonas aeruginosa resistant to aminoglycoside antibiotics were selected from 152 clinical isolates. We identified two patterns of resistance correlating with the resistance mechanism characterized by changes in permeability, enzymatic modification due to the acetylating enzyme, AAC(6′)-II, or a combination of both. We detected enzymatic activity of the phosphorylase enzyme, APH(3′), in all the isolates. We compared the mechanisms of resistance detected by three methods i. e., radioenzymatic assay, phenotype of resistance and DNA probes. The phenotype of resistance was tested using a kit developed by Schering-Plough Corp. Hybridization was made with 18 DNA probes for the most frequent genes encoding for aminoglycoside-modifying enzymes. All isolates with AAC(6′) activity hybridized with the
aac(6′)-Ib probes and to a minor degree, with the
aac(6′)-IIb probe. None of the isolates showed hybridization with
aph(3′)-I,
aph(3′)-II, or
aph(3′)-III DNA probes. Serotyping of the strains showed that the O:11 serotype was the most frequent one in strains whose resistance was due to the AAC(6′) enzyme. The O:6 serotype was associated with changes in permeability. Encoding of the resistance mechanism seemed to be chromosomal in all the strains.</abstract><cop>Germany</cop><pmid>10705613</pmid><doi>10.1016/S0934-8840(00)80008-0</doi><tpages>10</tpages></addata></record> |
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| source | MEDLINE; Alma/SFX Local Collection |
| subjects | Aminoglycosides Anti-Bacterial Agents - metabolism Anti-Bacterial Agents - pharmacology Atlantic Islands Drug Resistance, Microbial Humans Microbial Sensitivity Tests Nucleic Acid Hybridization Plasmids - genetics Pseudomonas aeruginosa Pseudomonas aeruginosa - classification Pseudomonas aeruginosa - drug effects Pseudomonas aeruginosa - isolation & purification Pseudomonas Infections - microbiology Serotyping Spain, Canary Is |
| title | Aminoglycoside Resistance Mechanisms in Clinical Isolates of Pseudomonas aeruginosa from the Canary Islands |
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