Mechanisms of antibiotic resistance in Burkholderia pseudomallei: implications for treatment of melioidosis.
Identifieur interne : 001995 ( Main/Exploration ); précédent : 001994; suivant : 001996Mechanisms of antibiotic resistance in Burkholderia pseudomallei: implications for treatment of melioidosis.
Auteurs : Herbert P. Schweizer [États-Unis]Source :
- Future microbiology [ 1746-0921 ] ; 2012.
Descripteurs français
- KwdFr :
- Antibactériens (pharmacologie), Antibactériens (usage thérapeutique), Burkholderia pseudomallei (effets des médicaments et des substances chimiques), Gènes bactériens (MeSH), Humains (MeSH), Mélioïdose (traitement médicamenteux), Résistance bactérienne aux médicaments (MeSH), Voies et réseaux métaboliques (génétique).
- MESH :
- effets des médicaments et des substances chimiques : Burkholderia pseudomallei.
- génétique : Voies et réseaux métaboliques.
- pharmacologie : Antibactériens.
- traitement médicamenteux : Mélioïdose.
- usage thérapeutique : Antibactériens.
- Gènes bactériens, Humains, Résistance bactérienne aux médicaments.
English descriptors
- KwdEn :
- MESH :
- chemical , pharmacology : Anti-Bacterial Agents.
- chemical , therapeutic use : Anti-Bacterial Agents.
- drug effects : Burkholderia pseudomallei.
- drug therapy : Melioidosis.
- genetics : Metabolic Networks and Pathways.
- Drug Resistance, Bacterial, Genes, Bacterial, Humans.
Abstract
Burkholderia pseudomallei is the etiologic agent of melioidosis. This multifaceted disease is difficult to treat, resulting in high morbidity and mortality. Treatment of B. pseudomallei infections is lengthy and necessitates an intensive phase (parenteral ceftazidime, amoxicillin-clavulanic acid or meropenem) and an eradication phase (oral trimethoprim-sulfamethoxazole). The main resistance mechanisms affecting these antibiotics include enzymatic inactivation, target deletion and efflux from the cell, and are mediated by chromosomally encoded genes. Overproduction and mutations in the class A PenA β-lactamase cause ceftazidime and amoxicillin-clavulanic acid resistance. Deletion of the penicillin binding protein 3 results in ceftazidime resistance. BpeEF-OprC efflux pump expression causes trimethoprim and trimethoprim-sulfamethoxazole resistance. Although resistance is still relatively rare, therapeutic efficacies may be compromised by resistance emergence due to increased use of antibiotics in endemic regions. Novel agents and therapeutic strategies are being tested and, in some instances, show promise as anti-B. pseudomallei infectives.
DOI: 10.2217/fmb.12.116
PubMed: 23231488
PubMed Central: PMC3568953
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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This multifaceted disease is difficult to treat, resulting in high morbidity and mortality. Treatment of B. pseudomallei infections is lengthy and necessitates an intensive phase (parenteral ceftazidime, amoxicillin-clavulanic acid or meropenem) and an eradication phase (oral trimethoprim-sulfamethoxazole). The main resistance mechanisms affecting these antibiotics include enzymatic inactivation, target deletion and efflux from the cell, and are mediated by chromosomally encoded genes. Overproduction and mutations in the class A PenA β-lactamase cause ceftazidime and amoxicillin-clavulanic acid resistance. Deletion of the penicillin binding protein 3 results in ceftazidime resistance. BpeEF-OprC efflux pump expression causes trimethoprim and trimethoprim-sulfamethoxazole resistance. Although resistance is still relatively rare, therapeutic efficacies may be compromised by resistance emergence due to increased use of antibiotics in endemic regions. Novel agents and therapeutic strategies are being tested and, in some instances, show promise as anti-B. pseudomallei infectives.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23231488</PMID><DateCompleted><Year>2013</Year><Month>05</Month><Day>23</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1746-0921</ISSN><JournalIssue CitedMedium="Internet"><Volume>7</Volume><Issue>12</Issue><PubDate><Year>2012</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Future microbiology</Title><ISOAbbreviation>Future Microbiol</ISOAbbreviation></Journal><ArticleTitle>Mechanisms of antibiotic resistance in Burkholderia pseudomallei: implications for treatment of melioidosis.</ArticleTitle><Pagination><MedlinePgn>1389-99</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.2217/fmb.12.116</ELocationID><Abstract><AbstractText>Burkholderia pseudomallei is the etiologic agent of melioidosis. This multifaceted disease is difficult to treat, resulting in high morbidity and mortality. Treatment of B. pseudomallei infections is lengthy and necessitates an intensive phase (parenteral ceftazidime, amoxicillin-clavulanic acid or meropenem) and an eradication phase (oral trimethoprim-sulfamethoxazole). The main resistance mechanisms affecting these antibiotics include enzymatic inactivation, target deletion and efflux from the cell, and are mediated by chromosomally encoded genes. Overproduction and mutations in the class A PenA β-lactamase cause ceftazidime and amoxicillin-clavulanic acid resistance. Deletion of the penicillin binding protein 3 results in ceftazidime resistance. BpeEF-OprC efflux pump expression causes trimethoprim and trimethoprim-sulfamethoxazole resistance. Although resistance is still relatively rare, therapeutic efficacies may be compromised by resistance emergence due to increased use of antibiotics in endemic regions. 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name="Colorado"><name sortKey="Schweizer, Herbert P" sort="Schweizer, Herbert P" uniqKey="Schweizer H" first="Herbert P" last="Schweizer">Herbert P. 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