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Biomedical subjects

F W Goldstein

Publications and source records attributed to F W Goldstein.

At least 73 records · Page 4Linked to original sources
PubMed1991

Evidence for clonal spread of a single strain of beta-lactamase-producing Enterococcus (Streptococcus) faecalis to six hospitals in five states.

Beta-lactamase-producing (Bla+) enterococci have been reported in three state and two countries. Pulsed-field gel electrophoresis was used to compare 14 Bla+ Enterococcus (Streptococcus) faecalis isolated from hospitalized patients in seven states and three continents. The restriction endonuclease digestion patterns of isolates from Connecticut, Massachusetts, Lebanon, and Argentina were all markedly different, indicating that these were different strains. However, isolates from Delaware, Texas, Pennsylvania (Philadelphia and Pittsburgh), Florida, and Virginia were similar, indicating that these isolates were derivatives of a single strain. This conclusion was supported by hybridization using individual fragments as probes. Spread of Bla+ enterococci within the hospital setting was also demonstrated. These findings illustrate the value of pulsed-field gel electrophoresis for epidemiologic analyses and support the importance of identifying and containing organisms with new resistance properties in an effort to decrease their transmission to and from, as well as within, hospitals.

Argentina↗
PubMed1991

Activities of two new teicoplanin amide derivatives (MDL 62211 and MDL 62873) compared with activities of teicoplanin and vancomycin against 800 recent staphylococcal isolates from France and the United States.

MDL 62211 is the amide derivative of the teicoplanin complex and MDL 62873 is a more focused amide derivative of the teicoplanin A2-2 peak. Each investigational compound had nearly identical activity and was 2- to 16-fold more active than teicoplanin or vancomycin. The MDL 62873 MICs for 90% of the strains tested were as follows: Staphylococcus aureus, oxacillin susceptible, 0.12 micrograms/ml; S. aureus, oxacillin resistant, 0.25 micrograms/ml; coagulase-negative staphylococci (CNS), oxacillin susceptible, 0.25 micrograms/ml; and CNS, oxacillin resistant, 2 micrograms/ml. CNS isolates from France were generally more susceptible than those tested in the United States. Teicoplanin-resistant U.S. isolates were usually Staphylococcus haemolyticus (1.8% of all tested strains), for which MICs ranged from 32 to greater than 128 micrograms/ml. MDL 62873 was not active against the Bacteroides fragilis group but was generally effective against gram-positive anaerobic strains.

Anti-Bacterial Agents↗
PubMed1990

In-vitro activity of azithromycin against various Gram-negative bacilli and anaerobic bacteria.

The MICs of azithromycin, erythromycin and roxithromycin were determined (by an agar dilution method) for 65 strains of Gram-negative bacteria responsible for endocarditis and gastrointestinal infections, for 20 strains of non-fermenting Gram-negative bacteria and for 16 strains of anaerobic bacteria. The MICs of azithromycin were up to eight times lower than those of erythromycin and (except in the case of Flavobacterium spp.) up to 16 times lower than those of roxithromycin. Azithromycin was ineffective against strains showing a high degree of erythromycin resistance.

Azithromycin↗
PubMed1990

Bacteriostatic and bactericidal activity of azithromycin against Haemophilus influenzae.

Macrolide antibiotics, commonly used in upper and lower respiratory tract infections, are inconsistently active against Haemophilus influenzae. The new azalide, azithromycin, was compared with erythromycin and roxithromycin against this pathogen. Azithromycin (MIC range 0.06-1 mg/l) was four to eight times more potent than erythromycin (MIC range 0.5-8 mg/l) and roxithromycin (MIC range 0.5-16 mg/l). At 1 mg/l, 100% of the strains of H. influenzae were inhibited by azithromycin compared with 16% with erythromycin and 5% with roxithromycin. Azithromycin exhibited a rapid bactericidal effect, with a 99.9% kill at 4 h. The MBC was equal to or up to four-times greater than the MIC.

Azithromycin↗
PubMed1990

Percentages and distributions of teicoplanin- and vancomycin-resistant strains among coagulase-negative staphylococci.

The activities of teicoplanin and vancomycin against 362 coagulase-negative staphylococci were determined by an agar dilution method. At the 4- and 32-micrograms/ml breakpoint levels of the National Committee for Clinical Laboratory Standards, 23.2% of the strains were intermediate and 1.7% were resistant to teicoplanin, in contrast to less than 0.3% intermediate to vancomycin. Resistant strains belonged to the species Staphylococcus epidermidis (74%) and S. haemolyticus (19%).

Coagulase↗
PubMed1989

Inducible resistance to vancomycin in Enterococcus faecium D366.

Strain D366, a clinical isolate of Enterococcus faecium, is resistant (minimum inhibitory concentration [MIC] 32 mg/L) to vancomycin. When exponential-phase cultures were exposed to half the MIC of vancomycin, a lag of 3-4 h occurred before growth resumed. Cells preexposed to 1/2 MICs of vancomycin did not show any lag. Pregrowth of D366 with vancomycin caused resistance to all glycopeptides tested. Pregrowth in vancomycin resulted in synthesis of a 3.95-kDa cytoplasmic-membrane-associated protein. This protein was correlated with resistance in mutants with high-level resistance, in the presence of NaCl, which inhibited the activity of vancomycin, and when several glycopeptides with varying activities were tested. Vancomycin-grown cells appeared abnormal and lysed at a much slower rate than did normal cells. We conclude that (1) vancomycin resistance in D366 is inducible; (2) resistance is correlated with the synthesis of 39.5-kDa cytoplasmic membrane protein; and (3) this protein play an additional role in the inhibition of normal lytic functions.

Aged↗
PubMed1989

SHV-5, a novel SHV-type beta-lactamase that hydrolyzes broad-spectrum cephalosporins and monobactams.

SHV-5 (pI 8.2), a novel broad-spectrum beta-lactamase encoded by a ca. 150-kilobase plasmid, was found in Klebsiella pneumoniae 160. SHV-5 beta-lactamase caused decreased susceptibility to most penicillins, cephalosporins, and monobactams, except imipenem and compounds which have a C6 or C7 alpha-methoxy substituent. beta-Lactamase inhibitors (clavulanic acid, sulbactam, and tazobactam) inhibited its activity and showed a synergistic effect when associated with different hydrolyzable beta-lactam compounds. Hybridization studies suggested that this enzyme may be related to, or derived from, the SHV enzyme. Increased MICs of cephamycins and temocillin associated with a decreased synergistic effect of the inhibitors on K. pneumoniae 160 might be linked to a decrease in two outer membrane proteins.

Anti-Bacterial Agents↗
PubMed1988

A seventeen-year epidemiological survey of antimicrobial resistance in pneumococci in two hospitals.

During a 17 year period (1970-1986), 2753 clinical isolates of Streptococcus pneumoniae isolated in two hospitals were serotyped and tested for antibiotic susceptibility. In the last ten years the number of multiply resistant strains has increased to 60% of the resistant isolates. Resistance to tetracycline was already present in 14% of the isolates in 1970, and was the most frequent resistance encountered during this study (30% of the strains). Resistance to chloramphenicol was first detected in 1972, but this resistance has remained infrequent (3%). Resistance to penicillin is extremely rare and since 1978, only six strains with relative penicillin resistance (MIC 0.1-1.0 mg/l) have been isolated. Resistance to macrolides, lincosamides and streptogramin B (MLSB resistant phenotype) was first detected in 1976. From 1983 to 1986, 131 isolates were MLSB resistant strains. These strains belonged to 20 different serotypes but 75% of the MLSB resistant pneumococci belonged to serotypes 6, 23, 19 and 14 which were among the most frequently isolated serotypes. In contrast serotypes 3 and 9 were epidemic but not resistant during the same period. Resistance markers in S. pneumoniae are often related to particular serotypes. The large monthly fluctuation in the isolation of resistant strains might explain the variable clinical results of empirical treatment of respiratory infections with macrolides.

Cross Infection↗
PubMed1988

Dissemination of the novel plasmid-mediated beta-lactamase CTX-1, which confers resistance to broad-spectrum cephalosporins, and its inhibition by beta-lactamase inhibitors.

The novel beta-lactamase CTX-1 (pI 6.3) encoded on a transferable 84-kilobase plasmid was found in six different bacterial species. It was responsible for a significant decrease in susceptibility towards most penicillins and cephalosporins, except imipenem, temocillin, and cephalosporins which have a 7-alpha-methoxy substituent. Synergy between either ampicillin, piperacillin, cefotaxime, ceftazidime, or aztreonam and three beta-lactamase inhibitors (clavulanic acid, sulbactam, and YTR 830) was generally found for different strains harboring CTX-1. This enzyme may be related to or derived from the TEM enzyme, since an intragenic probe of the TEM-1 gene hybridized with a fragment of the plasmid carrying CTX-1.

Cephalosporins↗
PubMed1988

Mutation of Salmonella paratyphi A conferring cross-resistance to several groups of antibiotics by decreased permeability and loss of invasiveness.

A spontaneous one-step mutant of Salmonella paratyphi A selected on ampicillin showed cross-resistance to all beta-lactam antibiotics except imipenem and to aminoglycosides, chloramphenicol, tetracycline, trimethoprim, and quinolones. It also grew as small colonies. Examination of the cell envelope of the mutant showed a quantitative decrease in three major outer membrane proteins of 40.6, 39.6 (presumably porins), and 24 kilodaltons and quantitative as well as qualitative modifications in the ladder pattern of lipopolysaccharide. Direct evidence for decreased permeability in the mutant included reduced uptake of [3H]glucose and norfloxacin, reduced accessibility of aztreonam and benzylpenicillin to penicillin-binding proteins in whole cells, and decreased diffusion of lactose and cephaloridine into proteoliposomes that were reconstituted with outer membrane proteins from the mutant. There was also loss of invasiveness of the mutant into HeLa cells. We assume that a pleiotropic mutation was responsible for multiple alterations in the outer membrane components of the resistant mutant of S. paratyphi A.

Aminoglycosides↗
PubMed1986

Strategies in aminoglycoside use and impact upon resistance.

Assessment of amikacin resistance over a 10-year period at our institution revealed that the number of resistant strains remained stable. Qualitatively, amikacin-resistant Enterobacteriaceae and Pseudomonas were fairly stable. There was a slight increase in amikacin-resistant Acinetobacter and staphylococci. Different factors influencing the emergence and spread of resistant hospital bacteria have been studied at different periods and compared with similar data on gentamicin-resistant strains. Transmissible plasmids, multiple mechanisms of resistance, and high levels of resistance were more frequent in gentamicin-resistant strains. In the amikacin-resistant strains, the level of resistance was 16 to 32 mg/liter with few autotransferable plasmids. A synergistic or additive effect with cephalosporins, which may be a factor in decreasing the risk of selection of the resistant strains since there is no plasmid-mediated resistance to cephalosporins, was demonstrated in Enterobacteriaceae. To control the development of aminoglycoside resistance in hospitals, it may be necessary to restrict the use of more than the one drug to which resistance is developing; to use the antibiotic at the right dosage and, when necessary, in a combination that may prevent the emergence of resistant organisms and plasmids; and to develop measures to control bacterial and R factor transmission.

Acinetobacter↗
PubMed1986

Plasmid-mediated resistance to multiple antibiotics in Salmonella typhi.

Two hundred forty-one strains of Salmonella typhii isolated in Lima, Peru, from October 1981 through February 1983 were tested for susceptibility to antimicrobial agents. Seventy-two strains (29.9%) were resistant to chloramphenicol and other antibiotics, including ampicillin, sulfonamides, and trimethoprim. The minimal inhibitory concentrations of 17 antimicrobial agents were determined for all of these chloramphenicol-resistant strains. Sch 25393, new beta-lactams, new quinolones, and the formulation clavulanic acid-amoxicillin were effective against all the strains. Four different resistance patterns distributed among eight phage types were observed. The 72 resistant S. typhi could transfer the resistance marker into Escherichia coli C1, and all the plasmids belonged to the incompatibility group H1.

Adolescent↗
PubMed1986

Timentin in the antimicrobial treatment of nosocomial and polymicrobial infections.

The combination of ticarcillin and clavulanic acid (Timentin) was used in a nonrandomized open study in 28 patients with severe nosocomial infections. The infections were polymicrobial in 19 cases. Ten patients were bacteraemic and all were severely ill, receiving mechanical ventilation and with at least one organ system failure. Seventeen patients were treated with Timentin alone, 11 with a combination of Timentin and aminoglycosides. Timentin was used empirically, before identification of the bacteria in 14 patients (group I) and after identification of all the micro-organisms in 14 patients (group II). In group I, the empirical choice of Timentin was wrong in four cases, because at least one micro-organism was resistant to this drug. In the remaining 24 evaluable patients 12 patients were definitively cured. A relapse of the infection occurred in two cases. Five patients were initially improved but a secondary failure occurred due to a residual abscess in one case and to the underlying disease in four cases. Five initial failures due to the underlying disease in three cases were noted. The antimicrobial spectrum of Timentin is valuable in the management of nosocomial and polymicrobial infection, especially intra-abdominal infections and this study confirms a good clinical efficacy. However, combination with aminoglycosides seems mandatory, at least until the identification of all the micro-organisms involved in the infection.

Aminoglycosides↗
PubMed1986

Transfer of amikacin resistance by closely related plasmids in members of the family Enterobacteriaceae isolated in Chile.

During a 9-month period when amikacin was the sole aminoglycoside used clinically in a hospital in Santiago, Chile, resistance to amikacin and other antibiotics was encountered in 42 strains of the family Enterobacteriaceae, including Escherichia coli, Klebsiella pneumoniae, Citrobacter freundii, Enterobacter cloacae, Serratia marcescens, and Serratia liquefaciens. Amikacin resistance was transferable by conjugation and carried by IncM plasmids ranging in size from ca. 48.4 to 58.1 kilobase pairs. The plasmids had ca. 70 to 80% of their structure in common, as judged after digestion with restriction endonucleases. The resistance was mediated by a 6' aminoglycoside acetyltransferase. We conclude that selective pressure has favored the dissemination of a wide-host-range amikacin resistance plasmid and its derivatives.

Amikacin↗
PubMed1986

R-factors in gram-positive and gram-negative aerobic bacteria selected by antimicrobial therapy.

Populations of resistant bacteria emerge by the operation of selective pressure on resistant bacteria. The acquisition of resistance by sensitive bacteria is dependent upon the genetic determinant of the resistance, and its ability to move between different bacterial cells and within cells between different replicons. In contrast to chromosomal mediated resistance, plasmids and transposable elements coding for resistance to antibiotics have been the major factors in the spread of resistance and the prevalence of resistant bacteria in humans, farm animals and poultry. Different types of R-factors can be described. Resistance to ampicillin, tetracycline, chloramphenicol, gentamicin, trimethoprim, erythromycin may exemplify epidemiological aspects of resistance genes in Gram-negative and Gram-positive bacteria. The ecological destiny of resistant bacterial populations suggests the role of other factors than antibiotic resistance: characters of a particular host, host-plasmid relationship and properties which may lead to survival and adaptation in a given niche.

Animals↗