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Query: UNIPROT:Q29983 (MIC)
 21,138 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A strain of Staphylococcus aureus (no. FAR4) has been isolated at intervals, for 32 months, from the sputum of a patient with cystic fibrosis of the lung. Changes in the properties of isolates of this strain over the first 18 months have been reported previously (Lacey et al., 1973 and 1974). During the last 14 months (May 1973 to July 1974), further evolution has occurred to produce a total of 31 distinct phenotypes. Recent changes are as follows. 1. The ability of isolates to produce penicillinase in vitro was closely correlated with flucloxacillin therapy. Inactivation of flucloxacillin by penicillinase was demonstrated by diffusion testing (but not MIC determination) in vitro and may have occurred to a significant extent in vivo. 2. Lincomycin-resistant mutants slowly disappeared from the sputum after the termination of clindamycin therapy. 3. All of the recent isolates were resistant to erythromycin, possibly because of the linkage of the genes coding for erythromycin resistance with those coding for the production of delta-haemolysin; delta-haemolysin may be an important "virulence factor".
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PMID:Further evolution of a strain of Staphylococcus aureus in vivo: evidence for significant inactivation of flucloxacillin by penicillinase. 104 Jun 76

The post-antibiotic effects (PAE) of ceftazidime, ciprofloxacin, imipenem, piperacillin and tobramycin were studied for ten strains of Pseudomonas cepacia isolated from patients with cystic fibrosis. Antibiotic concentrations used for exposure were either the MIC of each agent for the sensitive isolates or the recommended sensitivity breakpoint concentrations for the resistant isolates. After 2 h of exposure, cultures were rapidly diluted 1000-fold to eliminate the antibiotic. Out of the ten isolates, there were eight sensitive to ceftazidime, six to ciprofloxacin, six to imipenem, nine to piperacillin and five to tobramycin. All antibiotics tested demonstrated PAE for some isolates of P. cepacia, however, each antibiotic failed to produce a PAE for at least one isolate. The mean PAE was 1.35 h for ceftazidime, 2.38 h for ciprofloxacin, 2.39 h for imipenem, 2.16 h for piperacillin and 1.77 h for tobramycin. Imipenem demonstrated PAE of > or = 0.5 h for all sensitive isolates tested; ceftazidime, piperacillin, ciprofloxacin and tobramycin demonstrated PAE of > or = 0.5 h for 6/8, 8/9, 5/6 and 2/5 sensitive isolates, respectively. These data indicate that several antibiotics have significant (> or = 0.5 h) PAE for isolates of P. cepacia.
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PMID:Post-antibiotic effect of ceftazidime, ciprofloxacin, imipenem, piperacillin and tobramycin for Pseudomonas cepacia. 128 6

Five serial exposures of mucoid Pseudomonas aeruginosa from patients with cystic fibrosis to subinhibitory concentrations of ciprofloxacin resulted in stepwise increases in the MIC, with a mean proportional increase of 10. MICs were significantly lower in an iron-limited chemically defined medium than in Iso-Sensitest broth. The mucoid phenotype was maintained in chemically defined medium. Acquired resistance was retained either partially or completely in 85% of the isolates following 10 transfers in drug-free media. In cases in which susceptibility was regained, an increase in the MIC was observed on one further exposure to ciprofloxacin.
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PMID:Development of resistance to ciprofloxacin in nutrient-rich and nutrient-limited growth conditions in vitro by Pseudomonas aeruginosa isolates from patients with cystic fibrosis. 181 Feb 2

The bactericidal kinetic of 60 P. aeruginosa isolates (40 from cystic fibrosis sputum and 20 from various origins) was studied. Liquid medium micromethod was performed. Bacteria were incubated with tobramycin and amikacin alone at several concentrations and combined with piperacillin, cefsulodin, ceftazidim, imipenem, and ciprofloxacin at concentrations obtained in vivo. When used alone, tobramycin showed the most rapid bactericidal activity, whatever the concentration used. The bactericidal activity (greater than or equal to 99.99% killing of the inoculum) was obtained in 5 hours, with 1 or 2 x MIC of the majority of the strains, with the 2 aminoglycosides. No difference was found between tobramycin and amikacin, when combinated with an antibiotic which provides a notable increase of the rapidity of the bactericidal activity. The combination of amikacin plus imipenem was more rapidly bactericidal: 48% of strains; 26% were synergistically inhibited by amikacin plus ciprofloxacin. When correlated with the susceptibility patterns of studied micro-organisms, the results were rather unpredictive.
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PMID:[In vitro bactericidal activity of tobramycin and amikacin alone or in combination against Pseudomonas aeruginosa isolated from patients with cystic fibrosis]. 211 6

Susceptibility in vitro of 179 staphylococcal strains from 107 cystic fibrosis patients against 31 antibiotics indicates that only teicoplanin, vancomycin and netilmicin were active against all strains. The use of betalactam antibiotics is impaired by 11.7% of methicillin-resistant strains. The bactericidal kinetics of cephalexin and flucloxacillin as determined in a pharmacodynamic model demonstrates the killing of strains resistant to cephalexin (MIC 8 mg/l to 32 mg/l) by flucloxacillin. For the rational selection of antistaphylococcal antibiotics for cystic fibrosis patients, both the MIC of the isolates and the concentration of the antibiotics in cystic fibrosis patients have to be considered.
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PMID:Selection of antibiotics for treatment and prophylaxis of staphylococcal infections in cystic fibrosis patients. 233 48

On the basis of preliminary in vitro data, we evaluated E-1040, a new cephalosporin, against 188 cystic fibrosis (CF) sputum isolates obtained from 26 CF centers in the United States. These isolates included mucoid and nonmucoid Pseudomonas aeruginosa, Pseudomonas cepacia, Staphylococcus aureus, Haemophilus influenzae, and Escherichia coli. In addition to MICs measured under standard conditions, selected isolates were tested at various pH values, inoculum sizes, and diluent (CF serum and sputum) conditions. E-1040 activities (MICs for 50 and 90% of the strains) against the isolates were as follows: P. aeruginosa (mucoid and nonmucoid), 1 and 4 micrograms/ml; P. cepacia, 4 and 16 micrograms/ml; S. aureus, 8 and 8 micrograms/ml; H. influenzae, 1 and 4 micrograms/ml; and E. coli, less than or equal to 0.12 and less than or equal to 0.12 microgram/ml. E-1040 activity against mucoid P. aeruginosa was 4-fold greater than that of aztreonam, 16-fold greater than that of ceftazidime, and 32-fold greater than that of piperacillin. E-1040 was similar to other broad-spectrum cephalosporins against S. aureus, H. influenzae, and E. coli. Bactericidal activity was less than or equal to 1 dilution of MIC for 88% of the strains, although kinetic studies with mucoid strains of P. aeruginosa demonstrated effective killing only at eight times the MIC. Variations in pH from 5 to 8, in inoculum size from 10(3) to 10(7) CFU/ml, and in diluent (CF serum or CF sputum) did not affect E-1040 activity.
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PMID:In vitro activity of E-1040, a 3-substituted cephalosporin, against pathogens from cystic fibrosis sputum. 238 68

The susceptibilities of 270 clinical isolates of Pseudomonas aeruginosa from diverse sources (82 burn patients, 76 cystic fibrosis [CF] patients, and 112 other sources) to ciprofloxacin and three other quinolones, nine extended-spectrum beta-lactams, and three aminoglycosides were determined by an agar dilution method in cation-supplemented Mueller-Hinton medium. Ciprofloxacin, ceftazidime, imipenem, and aztreonam were the most active. MICs for burn isolates were consistently higher than those for other isolates for most antibiotics, whereas those for CF strains were consistently lower. Multidrug resistance to aminoglycosides and beta-lactams occurred in 21% of the burn isolates, 2.6% of the CF isolates, and 8.9% of the other isolates. Ninety percent of these strains remained susceptible to ciprofloxacin. Seven percent of the isolates were resistant to ciprofloxacin (MIC, greater than or equal to 2 micrograms/ml). Concurrent resistance to ciprofloxacin and beta-lactams or aminoglycosides was rare (1.8 to 4%). Analysis by Spearman rank correlation revealed a high degree of correlation of MICs among antibiotics within the same class, except for imipenem. An inoculum effect was observed for all antibiotics between 10(6) and 10(4) CFU (P less than 0.05), with those for piperacillin and cefoperazone being the most pronounced (16-fold and 8-fold differences, respectively), and was least apparent for the quinolones, aminoglycosides, imipenem, and aztreonam (twofold differences). Selected strains for which there were high MICs of ciprofloxacin (greater than or equal to 1 micrograms/ml) were tested against ciprofloxacin in combination with other agents in a checkerboard agar dilution assay. Synergistic (summated fractional inhibitory concentration, </=0.5) interactions at clinically achievable concentrations were most frequent with mezlocillin (33%), piperacillin (21%), and (7.6%), aztreonam (3.7%), and the aminoglycosides (3.7%). Antagonism (summated fractional inhibitory concentration, >/= 4) was observed in only one instance (with gentamicin).
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PMID:Cross-resistance of Pseudomonas aeruginosa to ciprofloxacin, extended-spectrum beta-lactams, and aminoglycosides and susceptibility to antibiotic combinations. 250 46

The in vitro activity of enoxacin was tested in 14 German microbiological centers shortly after the introduction of the drug in Germany. 2748 unselected clinical isolates including 15 bacterial species were analysed using microtiter plates. The MIC90-values were as follows: Staphylococcus aureus 4 mg/l, Enterococcus faecalis 16 mg/l, Enterobacteriaceae 0.5 mg/l, Pseudomonas aeruginosa 8 mg/l. There is good correlation between these results and those of former investigations. It is known that quinolones are only moderately active against enterococci. 8.5% of S. aureus, and 1.4% of Enterobacteriaceae were found to be resistant (MIC greater than 4 mg/l). As to P. aeruginosa, the study revealed that despite a generally low rate of resistance in specific clinical settings, specific problems can arise: in one institution, the MIC90 of P. aeruginosa was 32 mg/l, with a resistance rate of 56.1% (n = 57). In the other centers the MIC90 was 2 mg/l and the resistance rate 5.0% (n = 302). In the first center, many of the isolates were from paraplegic patients or patients with cystic fibrosis pretreated with quinolones. This study will be repeated in two years' time in order to determine an eventual change in resistance.
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PMID:[In-vitro activity of enoxacin: a multicenter study]. 250 73

The antibacterial activity in vitro of meropenem was compared with another carbapenem, imipenem, the penem HRE 664, and ceftazidime. MICs were not influenced by pH nor by inoculum size below 5 X 10(5) cfu/ml: higher inocula caused a modest increase in MIC. Cation supplementation of Mueller-Hinton broth was without effect. Meropenem was more active than imipenem and the other comparative agents against the majority of Gram-negative species (in particular proteus, providencia, morganella, haemophilus, neisseria and Pseudomonas aeruginosa, including isolates from patients with cystic fibrosis). Against Gram-positive organisms, the activity of meropenem was equal to or slightly less that of imipenem. Neither meropenem nor imipenem were influenced by the extended spectrum beta-lactamases that confer resistance to third generation cephalosporins produced by Escherichia coli, Klebsiella pneumoniae, K. oxytoca or Serratia marcescens.
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PMID:In-vitro activity of meropenem imipenem, the penem HRE 664 and ceftazidine against clinical isolates from West Germany. 250 18

The mechanism of chloramphenicol resistance was examined in a high-level-resistant isolate of Pseudomonas cepacia from a patient with cystic fibrosis. We investigated potential resistance mechanisms, including production of chloramphenicol acetyltransferase, ribosomal resistance, and decreased permeability. This strain (MIC, 200 micrograms/ml) had no detectable chloramphenicol acetyltransferase activity. In in vitro translation experiments in which we compared the resistant isolate with a susceptible strain of P. cepacia, inhibition of amino acid incorporation was equivalent even in organisms that were preincubated with sub-MICs of chloramphenicol. A 21.9-kilobase (kb) fragment of DNA was cloned which coded for chloramphenicol resistance; this fragment was expressed in P. cepacia but not in Escherichia coli. Quantitation of chloramphenicol uptake in the isogenic pair of susceptible and resistant organisms revealed a nearly 10-fold decrease of drug entry into the resistant strain. Comparison of isolated outer membrane proteins and lipopolysaccharide patterns identified no significant differences between the isogenic pair of organisms. We concluded that the mechanism of chloramphenicol resistance in this strain is decreased permeability.
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PMID:Chloramphenicol resistance in Pseudomonas cepacia because of decreased permeability. 271 57


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