Quinolone resistance from a transferable plasmid
Bacteria can mutate to acquire quinolone resistance by target alterations or diminished drug accumulation. Plasmid-mediated resistance to quinolones in clinical isolates has been claimed but not confirmed. We investigated whether a multiresistance plasmid could transfer resistance to quinolones betw...
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| Veröffentlicht in: | The Lancet (British edition) 1998-03, Vol.351 (9105), p.797-799 |
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| creator | Martínez-Martínez, Luis Pascual, Alvaro Jacoby, George A |
| description | Bacteria can mutate to acquire quinolone resistance by target alterations or diminished drug accumulation. Plasmid-mediated resistance to quinolones in clinical isolates has been claimed but not confirmed. We investigated whether a multiresistance plasmid could transfer resistance to quinolones between bacteria.
We transferred resistance between strains by conjugation. The resistance plasmid was visualised in different hosts by agarose-gel electrophoresis. We determined the frequency of spontaneous mutations to ciprofloxacin or nalidixic-acid resistance in
Escherichia coli strains, with or without the quinolone resistance plasmid.
A multiresistance plasmid (pMG252) from a clinical isolate of
Klebsiella pneumoniae was found to increase quinolone resistance to minimum inhibitory concentrations (MICs) as high as 32 μg/mL for ciprofloxacin when transferred to strains of
K pneumoniae deficient in outer-membrane porins. Much lower resistance was seen when pMG252 was introduced into
K pneumoniae or
E coli strains with normal porins. The plasmid had a wide host range and expressed quinolone resistance in other enterobacteriaceae and in
Pseudomonas aeruginosa. From a plasmid-containing
E coli strain with ciprofloxacin MIC of 0·25 μg/mL and nalidixic-acid MIC of 32 μg/mL, quinolone-resistant mutants could be obtained at more than 100 times the frequency of a plasmid-free strain, reaching MICs for ciprofloxacin of 4 μg/mL and for nalidixic acid of 256 μg/mL.
Transferable resistance to fluoroquinines and nalidixic acid has been found in a clinical isolate of
K pneumoniae on a broad host range plasmid. Although resistance was low in wild-type strains, higher levels of quinolone resistance arose readily by mutation. Such a plasmid can speed the development and spread of resistance to these valuable antimicrobial agents. |
| doi_str_mv | 10.1016/S0140-6736(97)07322-4 |
| format | Article |
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We transferred resistance between strains by conjugation. The resistance plasmid was visualised in different hosts by agarose-gel electrophoresis. We determined the frequency of spontaneous mutations to ciprofloxacin or nalidixic-acid resistance in
Escherichia coli strains, with or without the quinolone resistance plasmid.
A multiresistance plasmid (pMG252) from a clinical isolate of
Klebsiella pneumoniae was found to increase quinolone resistance to minimum inhibitory concentrations (MICs) as high as 32 μg/mL for ciprofloxacin when transferred to strains of
K pneumoniae deficient in outer-membrane porins. Much lower resistance was seen when pMG252 was introduced into
K pneumoniae or
E coli strains with normal porins. The plasmid had a wide host range and expressed quinolone resistance in other enterobacteriaceae and in
Pseudomonas aeruginosa. From a plasmid-containing
E coli strain with ciprofloxacin MIC of 0·25 μg/mL and nalidixic-acid MIC of 32 μg/mL, quinolone-resistant mutants could be obtained at more than 100 times the frequency of a plasmid-free strain, reaching MICs for ciprofloxacin of 4 μg/mL and for nalidixic acid of 256 μg/mL.
Transferable resistance to fluoroquinines and nalidixic acid has been found in a clinical isolate of
K pneumoniae on a broad host range plasmid. Although resistance was low in wild-type strains, higher levels of quinolone resistance arose readily by mutation. Such a plasmid can speed the development and spread of resistance to these valuable antimicrobial agents.</description><identifier>ISSN: 0140-6736</identifier><identifier>EISSN: 1474-547X</identifier><identifier>DOI: 10.1016/S0140-6736(97)07322-4</identifier><identifier>PMID: 9519952</identifier><identifier>CODEN: LANCAO</identifier><language>eng</language><publisher>London: Elsevier Ltd</publisher><subject>Anti-Infective Agents - pharmacology ; Antibiotics ; Antibiotics. Antiinfectious agents. Antiparasitic agents ; Antimicrobial agents ; Bacteria ; Biological and medical sciences ; Ciprofloxacin - pharmacology ; Conjugation, Genetic ; Drug resistance ; Drug Resistance, Microbial - genetics ; Drug Resistance, Multiple - genetics ; E coli ; Escherichia coli - drug effects ; Escherichia coli - genetics ; Humans ; Klebsiella pneumoniae - drug effects ; Klebsiella pneumoniae - genetics ; Medical sciences ; Miscellaneous. Antibiotics with multiple activities ; Mutation ; Nalidixic Acid - pharmacology ; Pharmacology. Drug treatments ; Plasmids - genetics</subject><ispartof>The Lancet (British edition), 1998-03, Vol.351 (9105), p.797-799</ispartof><rights>1998 Elsevier Ltd</rights><rights>1998 INIST-CNRS</rights><rights>Copyright Lancet Ltd. Mar 14, 1998</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c468t-8226bfb1e83ea0bdfb89cc4d74e4e04e16ca46f3436628258b40e032a5628783</citedby><cites>FETCH-LOGICAL-c468t-8226bfb1e83ea0bdfb89cc4d74e4e04e16ca46f3436628258b40e032a5628783</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0140673697073224$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2171410$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9519952$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Martínez-Martínez, Luis</creatorcontrib><creatorcontrib>Pascual, Alvaro</creatorcontrib><creatorcontrib>Jacoby, George A</creatorcontrib><title>Quinolone resistance from a transferable plasmid</title><title>The Lancet (British edition)</title><addtitle>Lancet</addtitle><description>Bacteria can mutate to acquire quinolone resistance by target alterations or diminished drug accumulation. Plasmid-mediated resistance to quinolones in clinical isolates has been claimed but not confirmed. We investigated whether a multiresistance plasmid could transfer resistance to quinolones between bacteria.
We transferred resistance between strains by conjugation. The resistance plasmid was visualised in different hosts by agarose-gel electrophoresis. We determined the frequency of spontaneous mutations to ciprofloxacin or nalidixic-acid resistance in
Escherichia coli strains, with or without the quinolone resistance plasmid.
A multiresistance plasmid (pMG252) from a clinical isolate of
Klebsiella pneumoniae was found to increase quinolone resistance to minimum inhibitory concentrations (MICs) as high as 32 μg/mL for ciprofloxacin when transferred to strains of
K pneumoniae deficient in outer-membrane porins. Much lower resistance was seen when pMG252 was introduced into
K pneumoniae or
E coli strains with normal porins. The plasmid had a wide host range and expressed quinolone resistance in other enterobacteriaceae and in
Pseudomonas aeruginosa. From a plasmid-containing
E coli strain with ciprofloxacin MIC of 0·25 μg/mL and nalidixic-acid MIC of 32 μg/mL, quinolone-resistant mutants could be obtained at more than 100 times the frequency of a plasmid-free strain, reaching MICs for ciprofloxacin of 4 μg/mL and for nalidixic acid of 256 μg/mL.
Transferable resistance to fluoroquinines and nalidixic acid has been found in a clinical isolate of
K pneumoniae on a broad host range plasmid. Although resistance was low in wild-type strains, higher levels of quinolone resistance arose readily by mutation. Such a plasmid can speed the development and spread of resistance to these valuable antimicrobial agents.</description><subject>Anti-Infective Agents - pharmacology</subject><subject>Antibiotics</subject><subject>Antibiotics. Antiinfectious agents. Antiparasitic agents</subject><subject>Antimicrobial agents</subject><subject>Bacteria</subject><subject>Biological and medical sciences</subject><subject>Ciprofloxacin - pharmacology</subject><subject>Conjugation, Genetic</subject><subject>Drug resistance</subject><subject>Drug Resistance, Microbial - genetics</subject><subject>Drug Resistance, Multiple - genetics</subject><subject>E coli</subject><subject>Escherichia coli - drug effects</subject><subject>Escherichia coli - genetics</subject><subject>Humans</subject><subject>Klebsiella pneumoniae - drug effects</subject><subject>Klebsiella pneumoniae - genetics</subject><subject>Medical sciences</subject><subject>Miscellaneous. Antibiotics with multiple activities</subject><subject>Mutation</subject><subject>Nalidixic Acid - pharmacology</subject><subject>Pharmacology. 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Antiinfectious agents. Antiparasitic agents</topic><topic>Antimicrobial agents</topic><topic>Bacteria</topic><topic>Biological and medical sciences</topic><topic>Ciprofloxacin - pharmacology</topic><topic>Conjugation, Genetic</topic><topic>Drug resistance</topic><topic>Drug Resistance, Microbial - genetics</topic><topic>Drug Resistance, Multiple - genetics</topic><topic>E coli</topic><topic>Escherichia coli - drug effects</topic><topic>Escherichia coli - genetics</topic><topic>Humans</topic><topic>Klebsiella pneumoniae - drug effects</topic><topic>Klebsiella pneumoniae - genetics</topic><topic>Medical sciences</topic><topic>Miscellaneous. Antibiotics with multiple activities</topic><topic>Mutation</topic><topic>Nalidixic Acid - pharmacology</topic><topic>Pharmacology. 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Academic</collection><jtitle>The Lancet (British edition)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Martínez-Martínez, Luis</au><au>Pascual, Alvaro</au><au>Jacoby, George A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Quinolone resistance from a transferable plasmid</atitle><jtitle>The Lancet (British edition)</jtitle><addtitle>Lancet</addtitle><date>1998-03-14</date><risdate>1998</risdate><volume>351</volume><issue>9105</issue><spage>797</spage><epage>799</epage><pages>797-799</pages><issn>0140-6736</issn><eissn>1474-547X</eissn><coden>LANCAO</coden><abstract>Bacteria can mutate to acquire quinolone resistance by target alterations or diminished drug accumulation. Plasmid-mediated resistance to quinolones in clinical isolates has been claimed but not confirmed. We investigated whether a multiresistance plasmid could transfer resistance to quinolones between bacteria.
We transferred resistance between strains by conjugation. The resistance plasmid was visualised in different hosts by agarose-gel electrophoresis. We determined the frequency of spontaneous mutations to ciprofloxacin or nalidixic-acid resistance in
Escherichia coli strains, with or without the quinolone resistance plasmid.
A multiresistance plasmid (pMG252) from a clinical isolate of
Klebsiella pneumoniae was found to increase quinolone resistance to minimum inhibitory concentrations (MICs) as high as 32 μg/mL for ciprofloxacin when transferred to strains of
K pneumoniae deficient in outer-membrane porins. Much lower resistance was seen when pMG252 was introduced into
K pneumoniae or
E coli strains with normal porins. The plasmid had a wide host range and expressed quinolone resistance in other enterobacteriaceae and in
Pseudomonas aeruginosa. From a plasmid-containing
E coli strain with ciprofloxacin MIC of 0·25 μg/mL and nalidixic-acid MIC of 32 μg/mL, quinolone-resistant mutants could be obtained at more than 100 times the frequency of a plasmid-free strain, reaching MICs for ciprofloxacin of 4 μg/mL and for nalidixic acid of 256 μg/mL.
Transferable resistance to fluoroquinines and nalidixic acid has been found in a clinical isolate of
K pneumoniae on a broad host range plasmid. Although resistance was low in wild-type strains, higher levels of quinolone resistance arose readily by mutation. Such a plasmid can speed the development and spread of resistance to these valuable antimicrobial agents.</abstract><cop>London</cop><pub>Elsevier Ltd</pub><pmid>9519952</pmid><doi>10.1016/S0140-6736(97)07322-4</doi><tpages>3</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0140-6736 |
| ispartof | The Lancet (British edition), 1998-03, Vol.351 (9105), p.797-799 |
| issn | 0140-6736 1474-547X |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals; Business Source Complete |
| subjects | Anti-Infective Agents - pharmacology Antibiotics Antibiotics. Antiinfectious agents. Antiparasitic agents Antimicrobial agents Bacteria Biological and medical sciences Ciprofloxacin - pharmacology Conjugation, Genetic Drug resistance Drug Resistance, Microbial - genetics Drug Resistance, Multiple - genetics E coli Escherichia coli - drug effects Escherichia coli - genetics Humans Klebsiella pneumoniae - drug effects Klebsiella pneumoniae - genetics Medical sciences Miscellaneous. Antibiotics with multiple activities Mutation Nalidixic Acid - pharmacology Pharmacology. Drug treatments Plasmids - genetics |
| title | Quinolone resistance from a transferable plasmid |
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