Lack of efflux mechanism in a clinical isolate of Pseudomonas aeruginosa highly resistant to beta-lactams and imipenem
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články
PubMed
14533486
DOI
10.1007/bf02931336
Knihovny.cz E-zdroje
- MeSH
- aktivní transport MeSH
- antibakteriální látky metabolismus farmakologie MeSH
- bakteriální geny MeSH
- cefalosporiny metabolismus MeSH
- cefepim MeSH
- ceftazidim metabolismus farmakologie MeSH
- ceftriaxon metabolismus farmakologie MeSH
- cystická fibróza mikrobiologie MeSH
- elektroforéza v polyakrylamidovém gelu MeSH
- imipenem metabolismus farmakologie MeSH
- konjugace genetická MeSH
- lidé MeSH
- membránové transportní proteiny metabolismus MeSH
- mikrobiální testy citlivosti MeSH
- mnohočetná bakteriální léková rezistence genetika MeSH
- permeabilita buněčné membrány MeSH
- poriny metabolismus MeSH
- proteiny vnější bakteriální membrány metabolismus MeSH
- Pseudomonas aeruginosa účinky léků genetika metabolismus MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- antibakteriální látky MeSH
- cefalosporiny MeSH
- cefepim MeSH
- ceftazidim MeSH
- ceftriaxon MeSH
- imipenem MeSH
- membránové transportní proteiny MeSH
- OprD protein, Pseudomonas aeruginosa MeSH Prohlížeč
- OprM protein, Pseudomonas aeruginosa MeSH Prohlížeč
- poriny MeSH
- proteiny vnější bakteriální membrány 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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