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Biomedical subjects

F W Goldstein

Publications and source records attributed to F W Goldstein.

101 records · Page 6Linked to original sources
PubMedDate not supplied

[beta-Lactamases of Branhamella catarrhalis and their phenotypic implications].

Of the 50 strains of beta-lactamase-producing Branhamella catarrhalis isolated at Saint Joseph's Hospital (Paris) that were studied, 94% produced BRO-1 type beta-lactamase and 6% produced the BRO-2 type. We examined the transfer of BRO-1 and BRO-2 genes and found that, among 7 donor strains producing BRO-1, all were able to transfer the gene for BRO-1 production by conjugation. Of the 4 donor strains producing BRO-2, 2 were able to transfer the gene for BRO-2 production by conjugation. Three BRO-1 beta-lactamase-producing transformants were obtained from total DNA extracted from 3 strains producing BRO-1. Plasmid bands were demonstrated in strains of B. catarrhalis, but no change in plasmid profiles was seen in beta-lactamase-positive recombinants, supporting previous studies that suggested the beta-lactamases are chromosomal. In vitro activity of oral beta-lactams was tested for 67 strains of B. catarrhalis (56 beta-lactamase-producing strains). Cefixime, cefpodoxime and the combination ampicillin-clavulanic acid were very active against the beta-lactamase-producing strains. BRO-1 beta-lactamase appears to affect the activity of cefaclor, cefuroxime and loracarbef. BRO-2 beta-lactamases have no effect on the activity of these cephalosporins. Cefixime and cefpodoxime seemed the least affected by beta-lactamase production.

Anti-Bacterial Agents↗
PubMedDate not supplied

Molecular epidemiology of resistance to trimethoprim in enterobacteria isolated in a Parisian hospital.

Between January, 1981 and December, 1984, 419 strains of enterobacteria isolated from patients at the Hôpital Saint-Joseph were studied for (1) the level of resistance to trimethoprim (Tp) by determination of minimal inhibitory concentration (MIC), (2) transferability of this resistance by conjugation into Escherichia coli, (3) plasmid content of wild-type strains and transconjugants by agarose gel electrophoresis of crude bacterial lysates and by incompatibility grouping, and (4) type of dihydrofolate reductase (DHFR) by colony hybridization with probes specific for DHFR types I and II. Tp resistance was defined as MIC greater than or equal to 4 micrograms/ml and high-level resistance by MIC greater than or equal to 1000 micrograms/ml. Amongst the strains studied, 90% were resistant to high levels of Tp, while 10% had low-level resistance to Tp was detected in 180 strains corresponding to 185 plasmids. In the vast majority of the plasmids, resistance to Tp was associated with resistance to sulphonamide (94%), streptomycin (75-90%), ampicillin (75-90%) and chloramphenicol (65-80%). Plasmids conferring resistance to Tp were often large, most (84%) ranging in size from 90 to 175 Kb. They belonged to six different incompatibility groups and Inc6-C was the most prevalent (34 to 75%). The study of the distribution of the dfr genes by colony hybridization in 183 transconjugants and 89 strains with non-transferable Tp resistance revealed the presence of dfrI genes in most of these strains (48 and 53%, respectively). DHFR of types I and II were found in only 3% of the transconjugants, but in 15% of the strains with non-transferable resistance. DHFR of other types were found equally (15%) in strains with transferable and non-transferable resistance. The high incidence of the type I enzyme among the Tp-resistant strains probably results from the integration of transposon Tn7 into the chromosome or into a non-transferable plasmid.

Ampicillin↗
PubMedDate not supplied

Genetic aspects and epidemiologic implications of resistance to trimethoprim.

Trimethoprim-resistant gram-negative bacilli have been isolated since shortly after the combination of a sulfonamide with trimethoprim available for clinical use 10 years ago. Factors not yet fully understood are responsible for the high or low percentage of resistant strains isolated in different countries at different times. Despite the widespread use of this combination, the percentage of trimethoprim-resistant bacteria has not exceeded 25% in a general hospital in Paris. Resistance to trimethoprim can be mediated by mutations within the bacterial chromosome or can be plasmid-mediated.

Bacteria↗
PubMedDate not supplied

Use of rifampin for the treatment of serious staphylococcal and gram-negative bacillary infections.

The use of rifampin combined with other antimicrobial agents for the treatment of 40 serious bacterial infections against which other treatment regimens had failed was reviewed. Seven of 17 staphylococcal infections (16 due to Staphylococcus aureus and one due to Staphylococcus epidermidis) were cured, as were 16 of 23 infections caused by gram-negative bacilli. In vitro tests of interaction between rifampin and other antibiotics produced variable results. However, eight rifampin-resistant strains (six of S. aureus, one of Pseudomonas aeruginosa, and one of Proteus mirabilis) emerged during combination therapy in seven patients; the drugs involved were rifampin plus vancomycin in three instances, rifampin plus gentamicin in two, rifampin plus colistin in one, and rifampin plus pristinamycin in one. Thus, while rifampin produced a dramatic beneficial effect in some patients with serious bacterial infections, the emergence of resistant strains, even with dual drug therapy, was identified as a potential problem.

Bacterial Infections↗
PubMedDate not supplied

The changing pattern of trimethoprim resistance in Paris, with a review of worldwide experience.

From 1972 to 1984, all Enterobacteriaceae isolated from clinical specimens at St. Joseph Hospital in Paris were tested for susceptibility to trimethoprim. During this period, resistance to trimethoprim increased from 17.9% to 25.5%; the increase was due mainly to strains with high-level resistance. Genetic studies, including transferability, incompatibility grouping, determination of the molecular mass of plasmids, and hybridization with dihydrofolate reductase I and II genes, were performed with randomly selected strains, and the results were compared with those of similar studies in other countries. The most striking phenomenon in trimethoprim-resistant strains was the presence of various resistance mechanisms and of different plasmids, transposons, and genetic determinants.

DNA Transposable Elements↗
PubMedDate not supplied

[Plasmidic resistance of "Haemophilus sp." to aminoglycoside antibiotics: isolation and study of a new phosphotransferase (author's transl)].

Plasmid mediated phosphorylating activities have been found in Haemophilus sp. strains resistant to some aminoglycoside antibiotics. The enzymes responsible for this phenomenon have been purified and studied. They belong to the group of aminoglycoside phosphotransferases which are able to phosphorylate these antibiotics on the 3'- or 5"-hydroxyl group. The first enzyme studied is closely related to APH(3')I whereas the second one is different from the former on the basis of substrate specificities and physicochemical properties. We propose to call this second enzyme APH(3')Ib as compared to APH(3')I which will be called APH(3')Ia.

Aminoglycosides↗
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[Increased resistance of streptococcus pneumoniae to antibiotics and prevalence of their capsular serotypes (author's transl)].

From January 1970 to December 1976, 867 strains of Streptococcus pneumoniae isolated from clinical specimens were routinely typed and tested for sensitivity to 12 antibiotics. The prevalent serotypes were 19, 23, 6, 3, 7 and 14. Twenty seven p. cent of the strains were found resistant to tetracycline, and 4,2% were resistant to tetracycline and chloramphenicol. Two strains were resistant to erythromycin. The minimal inhibitory concentrations of penicillin G, cephalotin, chloramphenicol, tetracycline, minocycline and erythromycin were determined by the agar dilution method on 80 strains. The incidence of tetracycline resistant strains increased from 10% to 40%. These strains were less susceptible to minocycline when tested in vitro and they were clinically resistant. Chloramphenicol resistant strains are isolated since 1972 and represented in 1976 more than 6% of the isolates. They belong to 14 different serotypes. We have previously reported that resistance to chloramphenicol is due to a chloramphenicol-acetyl-transferase which is probably plasmid mediated. The epidemiological and clinical implications of these results are discussed.

Animals↗
PubMedDate not supplied

[Activity of sulbactam and clavulanic acid, alone and combined, on Acinetobacter calcoaceticus].

Sulbactam and clavulanic acid, both beta-lactamase inhibitors, were studied alone or associated on 85 isolates of Acinetobacter calcoaceticus. When sulbactam was tested alone the minimal inhibitory concentration (MIC) was less than 2 micrograms/ml with the carbenicillin-sensitive strains of A. Calcoaceticus and between 8 to 16 micrograms/ml with the carbenicillin-resistant strains. In the presence of clavulanic acid (5 or 10 micrograms/ml) the MIC of sulbactam on all the carbenicillin-resistant strains decreased to less than 4 micrograms/ml.

Acinetobacter↗
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In vivo and in vitro emergence of simultaneous resistance to both beta-lactam and aminoglycoside antibiotics in a strain of Serratia marcescens.

In a patient with Serratia marcescens bacteraemia, a variant resistant to cefotaxime and amikacin was isolated in a blood culture under combined treatment with cefotaxime and amikacin. In addition, in vitro selection on cefotaxime and/or amikacin yielded resistant mutants from the sensitive parent strain. These mutants displayed the same type of cross-resistance as the clinical strain to all beta-lactam and aminoglycoside antibiotics. The mechanism for this resistance was a decrease in the permeability of the cell. To our knowledge, the isolation of such strains from blood cultures and the mechanism responsible for this "broad-spectrum resistance" have not been previously described.

Aminoglycosides↗
PubMedDate not supplied

["Pseudomonas aeruginosa" beta-lactamases and sensitivity to carbenicillin (author's transl)].

This report discusses the differences in enzymes of two populations of P. aeruginosa, one sensitive and the other resistant to carbenicillin, which were strains isolated from four patients with chronic urinary infections. These sensitive and resistant strains biosynthetize only one beta-lactamase which appears to be a cephalosporinase of the class Id of Richmond and Sykes (1973). In the four cases the bacterial resistance to carbenicillin does not involve a new beta-lactamase and is due to other factors.

Amidohydrolases↗