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Biomedical subjects

B E Murray

Publications and source records attributed to B E Murray.

177 records · Page 10Linked to original sources
PubMed1982

In-vivo acquisition of two different types of aminoglycoside resistance by a single strain of Klebsiella pneumoniae causing severe infection.

Multiple isolates of Klebsiella pneumoniae obtained from a patient were of the same biotype and capsular type and had three common plasmids. Initially, three isolates (from blood) were susceptible to aminoglycosides. Three other isolates, obtained after gentamicin treatment was begun, were susceptible to amikacin but resistant to gentamicin and tobramycin, produced 2"-aminoglycoside adenylytransferase, and had acquired an R-factor. A later isolate, obtained after amikacin therapy was begun, was susceptible to gentamicin and tobramycin, resistant to amikacin, was a small-colony variant, produced no aminoglycoside-modifying enzymes, and no longer contained the R-factor. In-vitro protein synthesis by ribosomes from this isolate was inhibited by amikacin whereas uptake of amikacin was markedly less than with previous isolates. Thus, this case illustrates the apparent in-vivo acquisition of plasmid-mediated resistance to gentamicin and tobramycin followed by loss of the plasmid and development of amikacin resistance due to decreased aminoglycoside uptake.

Amikacin↗
PubMed1981

Toxin detection after storage or cultivation of enterotoxigenic with colicinogenic Escherichia coli: a possible mechanism for toxin-negative pools.

Of 100 non-enterotoxigenic Escherichia coli isolated from children with diarrhea in Bangkok, Thailand, 24 were found to produce colicin(s). Of these, 87% were active against one or more enterotoxigenic E. coli isolated from the same population. Storage of nine enterotoxigenic E. coli with known inhibitory colicin-producing E. coli in different proportions caused 51 of 96 pools to become negative in the suckling mouse assay (heat-stable toxin) and 17 of 52 to become negative in the Y-1 adrenal cell assay (heat-labile toxin). Cocultivation of the same strains, without prior storage, caused 12 of 96 pools to become negative for heat-stable toxin and 1 of 52 pools to become negative for heat-labile toxin. Storage or cultivation of E. coli in pools may cause negative results in the suckling mouse and Y-1 adrenal cell assays if any of the isolates in the pool produces colicin(s).

Bacteriological Techniques↗
PubMed1981

Cephalosporins.

Explore the source record for details and available documents.

Administration, Oral↗
PubMed1980

Diphtheroid prosthetic valve endocarditis. A study of clinical features and infecting organisms.

The clinical features of 19 patients with prosthetic valve endocarditis due to diphtheroids were studied. Infection was noted within 60 days of cardiac surgery in 12 (63 percent) patients. Prosthetic dysfunction and infection of the valve annulus was common (74 percent). Agar dilution minimal inhibitory concentrations for 18 diphtheroids isolated from patients with prosthetic valve endocarditis indicated that 88 percent were susceptible to gentamicin, amikacin, streptomycin, erythromycin and tetracycline; all strains were susceptible to vancomycin. In time-kill studies vancomycin was highly bactericidal as was gentamicin for susceptible strains. For gentamicin-susceptible strains, penicillin-gentamicin combinations were synergistic regardless of the susceptibility of the strains to penicillin. Bactericidal synergy of penicillin-gentamicin combinations was not seen with gentamicin-resistant strains. The biochemical and physiologic features of 20 strains were studied; with the exception of colonial morphology, 18 strains were found to be similar. Four strains were classified as belonging to the group JK by the Center for Disease Control (CDC) and 14 other strains fulfilled CDC criteria for group JK diphtheroids. A technique and criteria for single disc diffusion susceptibility testing are suggested.

Anti-Bacterial Agents↗
PubMed1980

A novel mechanism of resistance to penicillin-gentamicin synergism in Streptococcus faecalis.

A patient with enterococcal endocarditis, who relapsed after repeated courses of apparently adequate treatment with ampicillin plus gentamicin, was subsequently cured with ampicillin-tobramycin therapy. The organisms isolated from this patient were strains of Streptococcus faecalis that were resistant to penicillin (or ampicillin)-gentamicin synergism but not to penicillin (or ampicillin)-tobramycin synergism. The mechanism of resistance in these strains appears to be related to a specific defect in the intracellular uptake of gentamicin (but not tobramycin) in the presence of penicillin.

Dose-Response Relationship, Drug↗
PubMed1980

Evidence of plasmid-mediated production of aminoglycoside-modifying enzymes not previously described in Acinetobacter.

Two blood culture isolates of Acinetobacter calcoaceticus subsp. anitratus (Herellea vaginicola) were recently observed to be unusually resistant to aminoglycosides. Each strain was found to contain aminoglycoside-modifying enzymes which have not been described previously in this species, including 2"-adenylyltransferase, 3"-adenylyltransferase, 3'-phosphotransferase-III, and 3-acetyltransferase. Treatment of one strain (H-S) with novobiocin led to a loss of resistance to multiple antimicrobial agents and a loss of two aminoglycoside-modifying enzymes; agarose gel electrophoresis of lysates of this strain revealed that the loss of resistance markers was associated with the loss of a large-molecular-weight plasmid. Treatment of the second strain (H-D) with novobiocin produced derivative strains with three different resistance patterns. Agarose gel electrophoresis of deoxyribonucleic acid from crude lysates and from cesium chloride-ethidium bromide gradients of this strain showed only a small plasmid (molecular weight, 5 X 10(6)) common to all variants and failed to explain the loss of resistance markers.

Acinetobacter↗
PubMed1979

Aminoglycoside-modifying enzymes among clinical isolates of Acinetobacter calcoaceticus subsp. anitratus (Herellea vaginicola): explanation for high-level aminoglycoside resistance.

Acinetobacter calcoaceticus subsp. anitratus (Herellea vaginicola) is an important cause of nosocomial infection in our hospital where A. calcoaceticus subsp. anitratus is the most frequently isolated gram-negative species resistant to one or more of the aminoglycoside antibiotics. Of 167 strains tested for susceptibility to aminoglycosides, only 6 strains were found that were resistant to >/=128 mug of kanamycin per ml; all others were susceptible to </=32 mug/ml. Five of these six strains were found to produce aminoglycoside-modifying enzymes. Two strains produced a phosphotransferase which mediates resistance to kanamycin and neomycin; three strains produced an acetyltransferase which mediates resistance to kanamycin, tobramycin, and amikacin (minimal inhibitory concentration >/= 128 mug/ml for each drug). No strain with lower level resistance to kanamycin, tobramycin, or amikacin had enzyme activity. Fourteen strains resistant to gentamicin failed to show significant enzymatic modification of that antibiotic. Although agarose gel electrophoresis of deoxyribonucleic acid preparations from the enzyme-producing strains showed plasmid bands in all, no transfer of aminoglycoside resistance could be achieved, nor was it cured by exposure to novobiocin, ethidium bromide, acridine orange, heat, or prolonged storage. Resistance to mercuric chloride, present in 2 of 60 strains, was lost by 1 strain after exposure to novobiocin, and the loss of resistance was associated with an apparent deletion of plasmid deoxyribonucleic acid.

Acinetobacter↗
PubMedDate not supplied

Enterococci: new aspects of an old organism.

Enterococci are a long-known cause of bacterial endocarditis and a more recently recognized cause of nosocomial infection and superinfection. While much is known about the many antibiotic resistances of enterococci, less is known about the organism itself and how it causes disease. This article presents a brief overview of enterococci and its possible virulence factors and summarizes the authors' efforts to understand the features of this organism that may contribute to its disease potential.

Animals↗
PubMedDate not supplied

Impact of fluoroquinolones on the gastrointestinal flora.

A number of studies have evaluated the effect of fluoroquinolones on fecal flora. The results of these studies have consistently shown marked suppression or elimination of gram-negative facultative bacteria. The effect on gram-positive bacteria is more variable, with slight to moderate suppression reported most frequently. Total fecal anaerobes have generally been unchanged, although some anaerobic species have been moderately suppressed. The effect on facultative gram-negative bacteria can be explained by high fecal levels of quinolones and very low MICs for most of the organisms. The general lack of effect of anaerobes may be due to the higher MICs and an inoculum effect on the MBCs that is caused by the large number of organisms (10(9)-10(11) colony-forming units/g) characteristically found in feces.

4-Quinolones↗
PubMedDate not supplied

Resistance of Shigella, Salmonella, and other selected enteric pathogens to antimicrobial agents.

Antimicrobial agents are commonly used therapeutically and prophylactically for travelers' diarrhea. Resistance of enteric pathogens to these agents may prevent the success of such therapy, with the result depending upon the level of resistance and the drug concentrations achieved in the gastrointestinal tract. Data from a number of geographic locations were collected in order to determine whether consistent trends exist and whether predictions can be made regarding the susceptibility of various enteric pathogens worldwide. These data showed marked variability in the prevalence of resistance. Among Shigella, the percentage of strains resistant to commonly used agents varied within the following ranges: ampicillin, 7% (Dacca) to 87% (Thailand); tetracycline, 11% (Sri Lanka) to 91% (Mexico); and trimethoprim-sulfamethoxazole, 0 (Dacca, 1980) to 55% (Dacca, 1984). Resistance in Salmonella strains showed a similar marked variability. Few strains of enteroxigenic Escherichia coli (less than or equal to 10%) were resistant to trimethoprim-sulfamethoxazole. Relatively recent isolates of all pathogens examined tended to be more resistant than earlier isolates to trimethoprim-sulfamethoxazole as well as to other agents.

Anti-Bacterial Agents↗
PubMedDate not supplied

Diversity among multidrug-resistant enterococci.

Enterococci are associated with both community- and hospital-acquired infections. Even though they do not cause severe systemic inflammatory responses, such as septic shock, enterococci present a therapeutic challenge because of their resistance to a vast array of antimicrobial drugs, including cell-wall active agents, all commercially available aminoglycosides, penicillin and ampicillin, and vancomycin. The combination of the latter two occurs disproportionately in strains resistant to many other antimicrobial drugs. The propensity of enterococci to acquire resistance may relate to their ability to participate in various forms of conjugation, which can result in the spread of genes as part of conjugative transposons, pheromone-responsive plasmids, or broad host-range plasmids. Enterococcal hardiness likely adds to resistance by facilitating survival in the environment (and thus enhancing potential spread from person to person) of a multidrug-resistant clone. The combination of these attributes within the genus Enterococcus suggests that these bacteria and their resistance to antimicrobial drugs will continue to pose a challenge.

Animals↗