The comparison of a clinical Acinetobacter baumanii isolate (strain No. 4852/88) and its selected imipenem-resistant (IMR) clone exhibited a complex reorganization of the penicillin-binding proteins (PBPs) with diminished labelling of all PBPs except the 24-kD PBP which showed an increased binding of 14C-penicillin. This protein could not be saturated by preincubation of membranes with imipenem at 8-fold the MIC of imipenem, thus indicating PBP alterations responsible for imipenem resistance. In A. baumanii 4852/88 seven PBPs with the apparent molecular weights of 94, 84, 65, 61, 48, 40 and 24 kD could be detected. β-Lactamase production was barely detectable in any case and could not be enhanced in the presence of various β-lactams as the inducer. The outer membrane proteins were found identical in both the wild-type strain and the ImR clone. So far, imipenem-resistant A. baumanii isolates have been isolated twice in our diagnostic laboratory; hovewer, no implications on the future relevance of the above findings can be made.
The mechanism of Pseudomonas aeruginosa resistance to imipenem in five imipenem-susceptible clinical isolates and in their resistant counterparts was investigated. The frequency for selecting imipenem-resistant variants ranged from 2.7 x 10-5 to 2.1 x 10-8 and was comparable to those for other ,-lactams.Cross-resistance between imipenem and other 13-lactam compounds was not observed. In all imipenemresistant variants, induction of chromosomal j3-lactamase by imipenem was markedly diminished compared with that in the susceptible parent strain. This was not the case for other inducers such as ampicillin or cefoxitin, suggesting an impaired uptake of imipenem as an explanation for resistance. Analysis of the outer membrane proteins revealed a marked decrease of either a 46-or a 45-kilodalton protein. The lipopolysaccharide of the outer membrane in the imipenem-resistant variants was not altered.Within the last 2 years, several reports have emphasized the development of resistance to imipenem in clinical Pseudomonas aeruginosa isolates (1,8,10,19,22,24). Emergence of resistance was observed especially in patients suffering from either cystic fibrosis or nosocomial lower respiratory tract infections (1,19,22). Consequently, development of cross-resistance between imipenem and other ,B-lactam compounds must be evaluated.Enzymatic inactivation of imipenem has been reported thus far only for Pseudomonas maltophilia (21). Since resistance to newer cephalosporins and broad-spectrum penicillins is often chromosomally mediated, we studied five imipenem-susceptible clinical isolates of P. aeruginosa and their derived imipenem-resistant counterparts for the production of imipenem-inactivating enzymes and for outer membrane alterations. As it was not clear whether mutation or selection of a resistant subpopulation occurred, the term "variants" will be used for the resistant counterparts.MATERIALS AND METHODS Strains. The P. aeruginosa strains used were recent clinical isolates from our laboratory and were identified by standard procedures (12). Strain FRA was kindly supplied by G. Seibert, Frankfurt, Federal Republic of Germany. None of the strains exhibited resistance to antipseudomonal P-lactam compounds.MICs. MICs were determined in Mueller-Hinton broth (E. Merck AG, Darmstadt, Federal Republic of Germany) by twofold serial dilutions representing a final inoculum of 5 x 105 CFU/ml (microdilution procedure).Selection of resistant variants. Resistant variants were selected by plating 0.05 ml of an overnight culture in Trypticase soy broth (BBL Microbiology Systems, Cockeysville, Md.) onto Mueller-Hinton agar plates (Merck) containing the antibiotic in twofold serial dilution steps above the MIC. The frequency of resistant variants was expressed as the ratio of CFU grown in the presence of the antibiotic to the CFU of the control (grown without an antibiotic). All assays were carried out in triplicate. * Corresponding author.Kinetics of j3-lactamase production. ,B-Lactamase production was studied during exponential growth. Ove...
Summary. Helicobacter pylori flagellar sheaths were isolated by sucrose density-gradient centrifugation and analysed by electronmicroscopy, SDS-PAGE and gas-liquid chromatography. Electronmicroscopy of thin sections of flagella showed an internal electron-dense filament and a surrounding flagellar sheath with the typical bilayer structure of a membrane.
The value of modified triple therapy with amoxicillin and metronidazole is significantly limited by metronidazole resistance. However, metronidazole resistance does not negatively influence treatment outcome in modified triple therapy including clarithromycin. H. pylori resistance to amoxicillin still is not present.
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