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At least 19 recordsLinked to original sources
PubMed1976

Emergence of gentamicin-resistant bacteria: experience with tobramycin therapy of infections due to gentamicin-resistant organisms.

A computerized system for testing and surveillance of bacterial susceptibility to antibiotics was used in monitoring the emergence of gentamicin-resistant strains of aerobic and facultative gram-negative bacilli at Massachusetts General Hospital since the release of gentamicin for clinical use in 1971. During the period studied, there was a significant increase in the prevalence of gentamicin-resistant bacteria, particularly among Pseudomonas, Acinetobacter (Herellea), and Proteus and, more recently, among Enterobacter and Klebsiella. Most gentamicin-resistant strains of Pseudomonas aeruginosa and Acinetobacter calcoaceticus var. anitratum (Herellea varginicola) retained susceptibility to tobramycin. Of the other gentamicin-resistant organisms, most were also resistant to tobramycin. Twelve patients with infections caused by gentamicin-resistant organisms were treated with tobramycin. All 12 patients were seriously ill, and all but one had failed to respond to previous therapy with gentamicin. Nine patients responded favorably to tobramycin, and six were cured. P. aeruginosa and A. calcoaceticus var. anitratum were most frequently the infecting organisms in these patients. Patients received tobramycin for three to 42 days; no significant drug-related toxicity was noted. These results emphasize the increasing clinical importance of gentamicin-resistant bacteria and suggest that tobramycin may be effective for treatment of some, but not all, infections caused by gentamicin-resistant bacteria.

Acinetobacter↗
PubMed1992

Antimicrobial gentamicin activity in the presence of exogenous protease inhibitor (Bowman-Birk inhibitor) in gentamicin-induced nephrotoxicity in rats.

In our previous studies, we found increased levels of urinary trypsin inhibitory activity in gentamicin-induced nephrotoxicity in rats. Following administration of the Bowman-Birk trypsin and chymotrypsin inhibitor (BBI), no proteinuria was detected in gentamicin-treated rats, and a decrease in creatinine clearance was noted in only 50% of the injected rats. In the present study, we examined the antimicrobial activity of gentamicin against Escherichia coli in the presence of BBI in gentamicin-induced nephrotoxicity in rats. We found that 50% of rats with E. coli-positive blood cultures died of septicemia. All the rats injected with E. coli plus gentamicin or E. coli plus gentamicin plus BBI survived, the latter showing no proteinuria or deterioration in creatinine clearance. In conclusion, BBI, which is an effective inhibitor of gentamicin-induced nephrotoxicity, does not affect the antimicrobial activity of gentamicin sulfate.

Animals↗
PubMed1975

Gentamicin sulfate pharmacokinetics: lower levels of gentamicin in blood during fever.

The effect of fever on serum concentrations and urinary excretion of gentamicin sulfate was studied in humans and dogs. Endotoxin-induced fever in dogs resulted in a decrease of approximately 25% in levels of gentamicin in serum 30 and 60 min after intravenous injection of the antibiotic (1.5 mg/kg) when compared with corresponding afebrile values. In six volunteers with etiocholanolone-stimulated fever, serum concentrations of gentamicin was reduced by an average of 40% in all measurements made 1.2, and 3 hr after intramuscular injection (1.5 mg/kg) as compared with afebrile control values in the same subject. Fever was thought to be the principal factor associated with lower levels of gentamicin, although the half-life of gentamicin in serum and renal clearance of the antibiotic were not significantly affected. These findings emphasize the need for frequent measurements of gentamicin in serum as a guide to adjustment of gentamicin treatment in febrile subjects, and perhaps in all patients receiving the antibiotic.

Adult↗
PubMed1976

Gentamicin resistance in clinical-isolates of Pseudomonas aeruginosa associated with diminished gentamicin accumulation and no detectable enzymatic modification.

Three strains of Pseudomonas aeruginosa resistant to gentamicin obtained as representative gentamicin-resistant clinical isolates from the University of Alberta Hospital (UAH) in Edmonton, Canada were characterized to determine their mechanism of resistance. All strains showed wide aminoglycoside resistance (tobramycin, sisomicin, amikacin, streptomycin, kanamycin, SCH 20569) but contained no evidence of gentamicin-acetylating, adenylating or phosphorylating activity. Gentamicin inhibited amino-acid incorporation in cell-free systems equally well with either ribosomes or soluble cell fractions obtained from either resistant or sensitive strains. Plasmid DNA was detected in two strains but resistance could not be transferred by conjugation to either P. aeruginosa or Escherichia coli recipients. The resistant strains showed a marked reduction in energy-dependent accumulation of gentamicin compared to a sensitive strain. These strains which are common at UAH are most likely resistant due to a failure of gentamicin to be transported across the cytoplasmic membrane to ribosomal sites until relatively high external gentamicin concentrations.

Amino Acids↗
PubMed1975

The gentamicin antibiotics. 6. Gentamicin C2b, an aminoglycoside antibiotic produced by Micromonospora purpurea mutant JI-33.

A mutant strain of Micromonospora purpurea, designated var. JI-33, produced an antibiotic complex consisting primarily of gentamicin C1a. A further product of this fermentation was identical to a very minor component isolated from the fermentation of the parent organism and named gentamicin C2b. Physical measurements indicated its structure to be 6'-N-methylgentamicin C1a and this was confirmed by synthesis from gentamicin C1a. The in vitro antibacterial activity of gentamicin C2b was very similar to that of the gentamicin C complex. Antibiotic XK-62-2, produced by Micromonospora sagamiensis, appears to be identical to gentamicin C1b.

Chemical Phenomena↗
PubMed1975

Gentamicin and gentamicin C1 in the treatment of complicated urinary tract infections: comparative study of efficacy, tolerance, and pharmacokinetics.

The clinical efficacy, patient tolerance, and pharmacokinetics of gentamicin and the single component gentamicin C(1) were studied after single and multiple doses in elderly male patients. Patient tolerance was extremely good at the dose levels used. There was some evidence of renal function impairment due to repeated intramuscular doses of gentamicin, but not gentamicin C(1). The antibiotics were equally effective against the organisms present in the urine of these patients. The pharmacokinetics of the two antibiotic forms were similar, although gentamicin C(1) appeared to have a larger distribution space.

Aged↗
PubMed1979

Investigations on the potential nephrotoxicity of cefazedone and gentamicin and of their combination, in comparison with the combination of cefazolin and cephalothin with gentamicin.

The nephrotoxicity of (6R,7R)-7-(2-[3,5-Dichloro-4-oxo-1(4H)-pyridyl]-acetamido)-3-([(5-methyl-1,3,4-thiadiazol-2-yl)-thio]methyl)-8-oxo-5-thia-1-azabicyclo[4,2,0]oct-2-ene-2-carboxylic acid (cefazedone, Refosporen), cephalothin, cefazolin and gentamicin was investigated by the determination of alanine-amino-peptidase (AAP) in urine of healthy volunteers. The results were compared with those obtained by application of the respective combination. The beta-lactam antibiotics showed no effect on the elimination of the characteristic tubule enzyme, while gentamicin, as is known, induced a marked increase of the enzyme elimination. The results with cefazedone + gentamicin show that the determining component on the extent of AAP elimination is the aminoglycoside exclusively, where high and low responders can be observed. When the experiments with gentamicin and with the combination gentamicin and cefazedone were carried out with the same volunteers, no additive effects could be observed.

Adolescent↗
PubMed1977

Effects of membrane-energy mutations and cations on streptomycin and gentamicin accumulation by bacteria: a model for entry of streptomycin and gentamicin in susceptible and resistant bacteria.

Several mutants of Escherichia coli affecting aerobic energy generation and energization of the bacterial membrane have been examined for their effect on streptomycin and gentamicin accumulation and susceptibility. A heme-deficient mutant (K207) and two mutants (CJ-8 [colicin K insensitive] and NR-70) associated with defective aerobic active transport were associated with decreased transport of streptomycin and gentamicin and increased resistance to those antibiotics. These mutants also exhibited increased resistance to several other aminoglycoside antibiotics, but not the aminocyclitol spectinomycin. The same observations were made with a ubiquinone-deficient mutant, but a strA derivative of this mutant was shown additionally to be saturable for streptomycin accumulation at a concentration four or more times lower than that required for saturation of the parent. A mutant uncoupled for adenosine 5'-triphosphate synthesis from electron transport and membrane Mg-adenosine 5'-triphosphatase deficient was hypersensitive to those aminoglycosides tested and spectinomycin, and showed enhanced transport of streptomycin and gentamicin. A variety of compounds structurally related to streptomycin were examined at high concentrations for inhibition of streptomycin uptake in a strA mutant of E. coli K-12 SA 1306, but no evidence for competition was detected, suggesting the absence of a common transport carrier. Four different divalent cations were shown to inhibit streptomycin and gentamicin accumulation in E. coli K-12 SA 1306. Divalent cations were shown to inhibit uptake of these two drugs in two bacterial species with distinct cell wall structures, Pseudomonas aeruginosa and Staphylococcus aureus, and to inhibit streptomycin uptake in spheroplasts of streptomycin-susceptible and -resistant E. coli. However, calcium had almost no inhibitory effect on streptomycin uptake by the ubiquinone-deficient mutant E. coli AN66. These and previous findings have been used to formulate a model for aminoglycoside entry into bacteria using a low-affinity membranous complex involved in membrane energization that includes respiratory quinones, which probably act to bind and transport aminoglycosides across the cell membrane. This phase of transport is associated with the lowest accumulation rate (termed energy-dependent phase I) that is rate limiting for susceptibility. It is further proposed that subsequent association of the membrane-bound aminoglycoside with higher-affinity binding sites on membrane-associated ribosomes carrying out a normal ribosomal cycle and protein synthesis results in a more rapid transport rate (termed energy-dependent phase II). The increased rate could result from a state of membrane energization analogous to that causing enhanced aminoglycoside transport rates seen in the uncoupled mutant, AN120. How this model explains the mechanism by which enzymatically modified aminoglycosides render cells resistant to unmodified aminoglycosides is also discussed.

Adenosine Triphosphatases↗
PubMed1976

Intraventricular treatment of Serratia marcescens meningitis with gentamicin. Pharmacokinetic studies of gentamicin concentration in one case.

A neurosurgical patient with postoperative meningitis caused by Serratia marcescens was treated with intraventricular as well as intramuscular gentamicin. Gentamicin concentration in serum and CSF was determined at different times after the administration. Serratia marcescens could not be isolated from CSF after 3 days of therapy. Determination of gentamicin concentrations in CSF showed that gentamicin should not be given intraventricularly more than once a day to avoid accumulation of the drug. No adverse effect was noticed although the CSF concentration reached 450 mug/ml.

Bacterial Infections↗
PubMed1979

A comparison of clindamycin-gentamicin and penicillin-gentamicin in the treatment of post-cesarean section endomyometritis.

A random comparison of clindamycin-gentamicin (C-G) and penicillin-gentamicin was made in 200 women who developed endomyometritis following cesarean section. All pretreatment profiles indicated similar populations. The clinical response was more favorable in the women receiving clindamycin-gentamicin. The implications of these results upon clinical practice is discussed.

Adult↗
PubMed1979

Changing phage typing patterns of epidemic gentamicin-resistant Staphylococcus aureus. Evidence for transmission of gentamicin resistance.

In a 10-week period, infection with gentamicin resistant Staphylococcus aureus appeared in 24 adults and infants in one hospital. Medical staff were affected first, and subsequently 16 infants in the neonatal intensive-care unit. The gentamicin-resistant staphyloccal isolates showed three distinct phage susceptibility patterns in two distinct phage groups during the early, middle, and late phases of the outbreak. Although not confirmed with in-vitro or in-vivo laboratory data, this outbreak suggests that gentamicin resistance may be transferred between different strains of Staph. aureus in vivo.

Adult↗
PubMed1992

Comparison of LY264826-gentamicin with vancomycin-gentamicin against enterococci from blood cultures.

The combination of the new glycopeptide LY264826 and gentamicin was compared with the combination of vancomycin and gentamicin against 30 strains of enterococci, comprising 20 strains of Enterococcus faecalis, five strains of Enterococcus faecium and five strains of Enterococcus avium, isolated from blood cultures. LY264826 plus gentamicin was synergic against E. faecalis and E. faecium, but not against E. avium.

Anti-Bacterial Agents↗
PubMedDate not supplied

An improved radioimmunoassay for serum gentamicin levels using 125I-labelled gentamicin.

1. A radioimmunoassay is described for the measurement of gentamicin in serum or plasma. 2. The assay technique uses a tracer labelled with iodine-125 rather than tritium, and has advantages over previously reported radioimmunoassay methods (Longmore et al., 1976; Lewis, Nelson & Elder, 1972) with regard to rapidity, precision and simplicity of preparation of labelled gentamicin. 3. The iodination technique is simple and gives tracer in high yield, at high specific activity, and with complete immunological identity to unlabelled gentamicin. 4. There is a significant correlation between results obtained by this technique and by a microbial assay method but the radioimmunoassay is more rapid, specific and accurate.

Acylation↗
PubMed1978

1-N HAPA gentamicin B, a new aminoglycoside active against gentamicin resistant isolates--activity compared to other aminoglycosides.

1-N HAPA gentamicin B is a new aminoglycoside active against most Enterobacteriaceae, Pseudomonas aeruginosa and Staphylococcus aureus. Among 504 clinical isolates at a concentration of 12.5 microgram/ml all Staph. aureus, Escherichia coli, Klebsiella, Enterobacter, Proteus rettgeri, Providencia and 78% of Pseudomonas, 86% of Proteus morganii were inhibited. Like other aminoglycosides, the activity was greatest at an alkaline ph and reduced by high cations concentrations. 1-N HAPA gentamicin B was equal in activity to amikacin against both gentamicin-sensitive and resistant isolates. It inhibited bacteria containing many of the aminoglycoside inactivating enzymes. When combined with carbenicillin it inhibited in a synergistic manner many Gram-negative bacteria, particularly Pseudomonas and Serratia.

Aminoglycosides↗
PubMed1978

The syntheses and biological properties of 1-N-(S-4-amino-2-hydroxybutyryl)-gentamicin B and 1-N-(S-3-amino-2-hydroxypropionyl)-gentamicin B.

The syntheses of 1-N-(S-4-amino-2-hydroxybutyryl)-gentamicin B and 1-N-(S-3-amino-2-hydroxypropionyl)-gentamicin B, designated sch 20287 and Sch 21420, respectively, by procedures similar to those developed by KAWAGUCHI and co-workers for the transformation of kanamycin A to amikacin are described. The in vitro microbiological properties of Sch 20287 and Sch 21420 are compared with amikacin, gentamicin and tobramycin.

Bacteria↗
PubMed1992

[Immunochemical determination of gentamicin in serum. II. Preparation of polyclonal gentamicin antibodies].

The author describes the preparation of polyclonal rabbit antibodies against gentamicin. As immunogens gentamicin conjugates with bovine serum albumin were used, or else with thyroglobulin and haemocyanin. The immunization pattern involved combined administration of immunogens by the intravenous route, or by the intramuscular or intradermal route, using liposomes and complete Freund adjuvant. The highest antibody titres against gentamicin found by the ELISA method were obtained when procedures were used where the carrier was serum albumin and thyroglobulin and as adjuvant complete Freund adjuvant was used.

Animals↗
PubMed1977

Gentamicin assay by enzymatic adenylylation and the application of a double osmotic shock procedure to prepare gentamicin adenine mono-nucleotide transferase.

The release of gentamicin adenine mono-nucleotide transferase (GAdT) during single cold osmotic shock treatment of E. coli K12 W677/HJR66 is not always maximal. The yield of GAdT could not be improved by using E. coli harvested at different stages of growth, by prolonging the exposure to the different steps of the shock procedure, by changing the sucrose concentration, or the magnesium chloride volume. The quantity of GAdT in osmotic extracts could be increased when a double shock procedure was performed. Using an aliquot (30 microliter) of the extract, an accurate and quick assay for gentamicin, sisomicin and tobramycin in microvolumes of serum (30 microliter) can be accomplished. To avoid high background activity in the assay, the extracts should be prepared from E. coli grown in gentamicin-free medium.

Adenosine Triphosphate↗