| pubmed-article:1591950 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1591950 | lifeskim:mentions | umls-concept:C1273518 | lld:lifeskim |
| pubmed-article:1591950 | lifeskim:mentions | umls-concept:C0033809 | lld:lifeskim |
| pubmed-article:1591950 | lifeskim:mentions | umls-concept:C0023810 | lld:lifeskim |
| pubmed-article:1591950 | lifeskim:mentions | umls-concept:C1533693 | lld:lifeskim |
| pubmed-article:1591950 | lifeskim:mentions | umls-concept:C0242646 | lld:lifeskim |
| pubmed-article:1591950 | lifeskim:mentions | umls-concept:C0205195 | lld:lifeskim |
| pubmed-article:1591950 | lifeskim:mentions | umls-concept:C1515926 | lld:lifeskim |
| pubmed-article:1591950 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:1591950 | pubmed:dateCreated | 1992-6-30 | lld:pubmed |
| pubmed-article:1591950 | pubmed:abstractText | Resistant variants of three clinical Pseudomonas aeruginosa isolates were obtained in the presence of aztreonam. The variants exhibited a four- to eightfold increase in the minimal inhibitory concentrations to beta-lactam antibiotics (except imipenem) to quinolones, such as norfloxacin and fleroxacin, chloramphenicol and tetracycline, but not to gentamicin and polymyxin B. beta-Lactamase production was barely detectable in both wild-type strains and the resistant clones. Only ampicillin, cefoxitin and imipenem increased the production of beta-lactamase, whereas various other beta-lactams did not. Penicillin-binding proteins remained unchanged in the aztreonam-resistant clones. The analysis of the outer membrane proteins did not reveal differences in the outer membrane proteins between the wild-type strains and the aztreonam-resistant clones. Two of the three antibiotic-resistant isogenic clones contained less lipopolysaccharides (LPSs) than their corresponding wild-type strains. Moreover, it could be demonstrated that the ratio of 2-keto-3-deoxy octonate to carbohydrate of the LPS changed in any case between the wild-type strains and the aztreonam-resistant clones. These alterations were accompanied by a decrease in surface hydrophobicity of the resistant clones as compared to the wild-type strains. Therefore, quantitative as well as qualitative alterations in the LPS may provide an explanation for the resistant phenotype observed. | lld:pubmed |
| pubmed-article:1591950 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1591950 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1591950 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1591950 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1591950 | pubmed:issn | 0009-3157 | lld:pubmed |
| pubmed-article:1591950 | pubmed:author | pubmed-author:RothRR | lld:pubmed |
| pubmed-article:1591950 | pubmed:author | pubmed-author:CullmannWW | lld:pubmed |
| pubmed-article:1591950 | pubmed:author | pubmed-author:BüscherK HKH | lld:pubmed |
| pubmed-article:1591950 | pubmed:author | pubmed-author:LeyingH JHJ | lld:pubmed |
| pubmed-article:1591950 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1591950 | pubmed:volume | 38 | lld:pubmed |
| pubmed-article:1591950 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1591950 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1591950 | pubmed:pagination | 82-91 | lld:pubmed |
| pubmed-article:1591950 | pubmed:dateRevised | 2009-11-11 | lld:pubmed |
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| pubmed-article:1591950 | pubmed:meshHeading | pubmed-meshheading:1591950-... | lld:pubmed |
| pubmed-article:1591950 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1591950 | pubmed:articleTitle | Lipopolysaccharide alterations responsible for combined quinolone and beta-lactam resistance in Pseudomonas aeruginosa. | lld:pubmed |
| pubmed-article:1591950 | pubmed:affiliation | Department of Medical Microbiology, Ruhr University, Bochum, FRG. | lld:pubmed |
| pubmed-article:1591950 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1591950 | pubmed:publicationType | Comparative Study | lld:pubmed |
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