Lack of efflux mechanism in a clinical isolate of Pseudomonas aeruginosa highly resistant to beta-lactams and imipenem
Language English Country United States Media print
Document type Journal Article
PubMed
14533486
DOI
10.1007/bf02931336
Knihovny.cz E-resources
- MeSH
- Biological Transport, Active MeSH
- Anti-Bacterial Agents metabolism pharmacology MeSH
- Genes, Bacterial MeSH
- Cephalosporins metabolism MeSH
- Cefepime MeSH
- Ceftazidime metabolism pharmacology MeSH
- Ceftriaxone metabolism pharmacology MeSH
- Cystic Fibrosis microbiology MeSH
- Electrophoresis, Polyacrylamide Gel MeSH
- Imipenem metabolism pharmacology MeSH
- Conjugation, Genetic MeSH
- Humans MeSH
- Membrane Transport Proteins metabolism MeSH
- Microbial Sensitivity Tests MeSH
- Drug Resistance, Multiple, Bacterial genetics MeSH
- Cell Membrane Permeability MeSH
- Porins metabolism MeSH
- Bacterial Outer Membrane Proteins metabolism MeSH
- Pseudomonas aeruginosa drug effects genetics metabolism MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Anti-Bacterial Agents MeSH
- Cephalosporins MeSH
- Cefepime MeSH
- Ceftazidime MeSH
- Ceftriaxone MeSH
- Imipenem MeSH
- Membrane Transport Proteins MeSH
- OprD protein, Pseudomonas aeruginosa MeSH Browser
- OprM protein, Pseudomonas aeruginosa MeSH Browser
- Porins MeSH
- Bacterial Outer Membrane Proteins MeSH
An isolate of Pseudomonas aeruginosa from cystic fibrosis was highly resistant to beta-lactams and beta-lactamase inhibitors. The resistant determinants of clinical isolate to imipenem, ceftazidim, cefriaxone and cefepime were conjugally nontransferable. The slow or nonenzymically mediated breakdown of imipenem and other broad-spectrum beta-lactams suggested the resistance of P. aeruginosa isolate to these drugs which may be attributed to both permeability and efflux. Impaired penetration of imipenem and other beta-lactams through the membrane was detected by a diminished expression of outer-membrane proteins of approximate molar mass of 46 and 39 kDa, matched to OprD and OprF, respectively. Efflux resistance mechanism for meropenem and beta-lactams has been ruled out since the isolate failed to express outer-membrane protein of approximately 50 kDa which is matched to the OprM protein channel. Thus, reduced permeability in the clinical isolate is the main mechanism conferring resistance against beta-lactams including imipenem.
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