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PubMed1986

Prediction of pharmacokinetic profiles of ampicillin sodium, gentamicin sulfate, and combination ampicillin sodium-gentamicin sulfate in serum and synovia of healthy horses.

Pharmacokinetics of ampicillin sodium (11 mg/kg), gentamicin sulfate (2.2 mg/kg), and combination ampicillin sodium-gentamicin sulfate were determined for serum and synovia of healthy horses given single-dose IV injection and were not found to be different from those from other reports; however, a prolonged terminal gamma-phase for gentamicin (8,498 +/- 1,842 minutes) in serum of horses was found to exist. Pharmacokinetic interaction between combination ampicillin sodium-gentamicin sulfate was not observed int he serum or synovia. Prediction of ampicillin sodium or gentamicin sulfate concentrations in synovia, based on serum-based pharmacokinetics, cannot be accomplished solely upon analysis of peripheral-compartment pharmacokinetics. However, once equilibrium is achieved between synovia and extracellular fluid in the peripheral compartment, the decrease in drug concentrations in synovia parallels that in serum. Therefore, after 6 hours, synovial concentrations of gentamicin sulfate can be predicted based on peripheral-compartment pharmacokinetics, using an appropriate correction factor. The significance of these findings need to be correlated with clinical conditions so that a pharmacostatistical model for the prediction of synovial concentrations of drug(s) during treatment of horses with septic arthritis can be developed.

Ampicillin↗
PubMedDate not supplied

[Development of gentamicin-resistant Small Colony Variants of S. aureus after implantation of gentamicin chains in osteomyelitis as a possible cause of recurrence].

AIM: Recently, S. aureus small colony variants (SCVs) were reported to persist within cultured endothelial cells and to cause persistent and antibiotic resistant infections in humans. Because gentamicin can very reproducably select for electron transport deficient SCVs as shown in earlier in vitro experiments, we searched for SCVs in a patient with chronic osteomyelitis, who received gentamicin beads. METHOD: Special culture and identification procedures for determination of SCVs were used, including testing of the S. aureus specific nuc gene, pulsed field gel electrophoresis (PFGE) as a typing method and characterization of the auxotrophism of the SCVs. RESULTS: In a case of a 34-year-old patient with chronic osteomyelitis who had previously been treated with gentamicin beads, menadione auxotrophic S. aureus SCVs as well as wild type S. aureus were recovered in multiple bone specimen. All different colony types isolated from simultaneous or from sequential specimen were shown to be clonal by PFGE. CONCLUSION: Recovery of S. aureus SCVs from a patient treated with gentamicin beads suggests that the slow release of gentamicin into the local environment may be an efficient way to select for and/or induce SCVs. These data should alert physicians to also consider SCVs when a treatment failure occurs in a patient that has received gentamicin beads.

Adult↗
PubMed1985

Stratified outcome comparison of clindamycin-gentamicin vs chloramphenicol-gentamicin for treatment of intra-abdominal sepsis.

A randomized, prospective trial was conducted of 93 patients with operatively confirmed intra-abdominal sepsis. The study compared clindamycin-gentamicin and chloramphenicol-gentamicin for treatment of carefully stratified patient groups. Malnutrition, age over 65 years, shock, alcoholism, gastrointestinal tract bleeding, steroid administration, diabetes, obesity, and organ malfunction were present with equal frequencies in each group. The duration of antibiotic treatment averaged 8 1/2 days, and the average length of postoperative hospitalization was 29 days. Study antibiotics were changed for bacteriologic reasons in 11 patients taking clindamycin-gentamicin and 12 patients taking chloramphenicol-gentamicin (25% of the total), and two patients in the clindamycin-gentamicin group had a minor adverse reaction. Initial satisfactory clinical responses were obtained in 59 (63%) patients. Twenty-five patients (27%) subsequently developed unsatisfactory courses, but 48 (52%) patients remained well through the 30-day period. Septic-related mortality occurred in 18 (19%) patients, and two (2%) patients had unrelated deaths. There were no significant differences between the study regimens by the outcome criteria evaluated.

Abdomen↗
PubMed1998

Gentamicin resistance in clinical strains of Enterobacteriaceae associated with reduced gentamicin uptake.

Seven strains of Enterobacteriaceae resistant to gentamicin obtained as representatives of the predominant resistance profiles in the clinical laboratories of Rafeidia and Al-Watani Hospitals in Nablus (Palestine) were included. Five strains showed a broad aminoglycoside resistance profile but contained no evidence of gentamicin acetylation, adenylation, or phosphorylation. Gentamicin uptake in two tested strains was significantly reduced, compared to that of gentamicin-sensitive E. coli (MIC, 0.5 microgram/mL). These strains are likely resistant due to a relative reduction of the amount of gentamicin and other aminoglycosides entering the bacterial cell. Two strains showed evidence of adenyltransferase ANT(2")-I activity.

Anti-Bacterial Agents↗
PubMed1994

Bactericidal action of gentamicin against enterococci that are sensitive, or exhibit low- or high-level resistance to gentamicin.

Treatment of serious enterococcal infection involves the use of penicillin-aminoglycoside combination therapy if the aminoglycoside minimum inhibitory concentration (MIC) is < or = 2000 micrograms/ml, and the organism is susceptible to penicillin or ampicillin. We evaluated killing of 15 enterococci that differ in their susceptibility to gentamicin using time-kill studies at different gentamicin concentrations. Sensitive strains had a uniform population killed by gentamicin concentrations equal to or above the MIC. Low-level resistant strains (MIC > or = 8 but < or = 2000 micrograms/ml of gentamicin) had a diverse population with large numbers of cells killed at one-half the MIC, while the highly resistant strains (MIC > 2000 micrograms/ml) showed no killing by any concentration of gentamicin.

Drug Resistance, Microbial↗
PubMed1997

A randomized, prospective study comparing once-daily gentamicin versus thrice-daily gentamicin in the treatment of puerperal infection.

OBJECTIVE: The efficacy, safety, and antibiotic-related charges for once-daily gentamicin with twice-daily clindamycin were compared with those of thrice-daily dosing of these antibiotics. STUDY DESIGN: Patients with puerperal endometritis or with chorioamnionitis in labor assessed to be at risk for endometritis were randomized to receive gentamicin 4 mg/kg intravenously every 24 hours with clindamycin 1200 mg intravenously every 12 hours (experimental arm) or gentamicin 1.33 mg/kg intravenously and clindamycin 800 mg intravenously every 8 hours (conventional dosing interval arm). Primary outcomes included cure rates, mean length of treatment, antibiotic-related charges, and nephrotoxicity. Multiple logistic regression analysis was used to control for confounding variables. RESULTS: There were 135 and 137 patients randomized to the experimental and conventional interval arms, respectively. Cures were obtained in 94.1% and 87.6% of patients in the experimental and conventional arms, respectively (p = 0.06). The experimental arm had mean antibiotic charges of $250.79 versus $442.49 in the conventional arm (p < 0.0001). There was no permanent nephrotoxicity in either group. CONCLUSIONS: Once-daily gentamicin dosing with twice-daily clindamycin dosing is as efficacious and safe as the thrice-daily dosing of gentamicin and clindamycin for peripartum uterine infection. The experimental regimen results in substantial cost savings. The incidence of nephrotoxicity is low.

Adult↗
PubMedDate not supplied

Gentamicin treatment associated with later nosocomial gentamicin-resistant Serratia marcescens infections.

During a hospital epidemic of infections with gentamicin-resistant Serratia marcescens (GRS), we studied the relation between receiving antibiotics and acquiring GRS. In a five-month period, 22 patients acquired GRS, whereas 18 patients acquired gentamicin-sensitive Serratia (GSS). When compared with patients with nosocomial GSS infection, patients with nosocomial GRS had been in the hospital (p = 0.04) and the intensive care unit (p = 0.003) longer before infection and more had received gentamicin (p = 0.001) or ampicillin (p = 0.02) before infection. To control for the influence of underlying disease, we matched all 12 ICU patients with GRS infection and 12 patients without GRS infection for underlying illness and duration of intensive care. Use of any antibiotic (p = 0.04), or a combination of gentamicin plus ampicillin or cephalosporin (p = 0.047) was more common among patients with GRS infection. The hospital had not significantly increased the use of aminoglycosides from the previous year. We conclude that for the individual patient antimicrobial therapy, especially with gentamicin or ampicillin, creates a risk for later infection by GRS that is independent of the severity of the underlying illness.

Aged↗
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↗
PubMedDate not supplied

Simple combined agar-strip test for detection of enterococcal susceptibility to ampicillin, moderate- or high-level gentamicin resistance and potential additive activity of ampicillin plus gentamicin.

A simple combined agar-strip test (CAST), involving filter paper strips charged with 20 micrograms of ampicillin or 40 micrograms of gentamicin, accurately detected high-level gentamicin resistance among 43 of 146 isolates of Enterococcus faecalis and additive activity of ampicillin plus gentamicin against 101 of 103 (98%) isolates of E. faecalis with moderate-level gentamicin resistance (MLGR). All 15 MLGR Enterococcus faecium isolates were moderately to highly resistant to ampicillin; 5 isolates with moderate resistance to ampicillin (minimal inhibitory concentrations = 16 micrograms/ml) were additively inhibited by ampicillin plus gentamicin, whereas the highly ampicillin-resistant E. faecium isolates yielded an indifferent effect with the CAST procedure.

Ampicillin↗
PubMedDate not supplied

Comparison of in vitro inhibitory and bactericidal activities of daptomycin (LY 146032) and four reference antibiotics, singly and in combination, against gentamicin-susceptible and high-level-gentamicin-resistant enterococci.

The in vitro inhibitory and bactericidal activities of daptomycin and reference antibiotics were determined by serial macrobroth dilution for 23 gentamicin-susceptible (MIC: < 2,000 mg/l) and 21 high-level-gentamicin-resistant (HLGR) Enterococcus faecalis, Enterococcus faecium, and Enterococcus avium isolates. The activities of daptomycin, vancomycin, and teicoplanin were independent of the gentamicin susceptibility profile and species tested. For all the isolates, the inhibitory activity of daptomycin (MIC90: 2 mg/l) was comparable to vancomycin (MIC90: 2 mg/l), but less than that of teicoplanin (MIC90: 0.5 mg/l). Daptomycin demonstrated excellent bactericidal activity against all enterococci tested (MBC90: 8 mg/l). In contrast, all microorganisms were tolerant to vancomycin and teicoplanin. Ampicillin and ciprofloxacin MICs and MBCs were dependent on enterococcal gentamicin resistance profile and species, with MICs and MBCs that ranged between 1 and > 64 mg/l. By time-kill curves, the combination of daptomycin plus ampicillin demonstrated synergistic bactericidal activity against gentamicin-susceptible and HLGR E. faecalis. Daptomycin, singly and in combination, may be useful in treating enterococcal infections, including those caused by HLGR microorganisms.

Ampicillin↗
PubMed1990

Mechanism of protection afforded by polyaspartic acid against gentamicin-induced phospholipidosis. I. Polyaspartic acid binds gentamicin and displaces it from negatively charged phospholipid layers in vitro.

Coadministration of polyaspartic acid protects rats against aminoglycoside-induced nephrotoxicity, with respect to functional and pathological changes as well as to early signs of renal alterations (lysosomal phospholipidosis of proximal tubular cells, increased proliferation of proximal tubular and peritubular cells), without reduction, but actually by increasing the drug cortical content (Williams et al., J. Pharmacol. Exp. Ther. 237: 919, 1986; Gilbert et al., J. Infect. Dis. 159: 945, 1989; Beauchamp et al., 1990). Because aminoglycoside accumulation in kidney cortex involves their segregation in lysosomes, we have examined the possibility of formation of intracellular aminoglycoside-polyaspartic acid complexes that would render the drug less toxic. We found that in vitro polyaspartic acid (MW 9-15,000) 1) binds gentamicin with an optimum at acidic pH (5.4), 2) displaces it from negatively charged liposomes and 3) restores the activity of gentamicin-inhibited lysosomal phospholipase A1 toward phosphatidylcholine included in negatively charged liposomes. In parallel, we also observed that at pH 7.0, polyaspartic acid binds and displaces gentamicin from purified brush-border membrane vesicles, causing an apparent decrease of affinity of gentamicin for these membranes, which was falsely interpreted by Williams et al., J. Pharmacol. Exp. Ther. 237: 919, 1986 as "competition for a common membrane binding site." Assuming that, after its administration in vivo, polyaspartic acid gains access to lysosomes of proximal tubular cells, as many low molecular weight proteins and polypeptides do, our results suggest that protection against gentamicin-induced nephrotoxicity is obtained by the binding of the aminoglycoside to the polyanion in lysosomes, preventing thereby the development of phospholipidosis and therefore interfering with the cascade of events leading from drug accumulation to nephrotoxicity.

Animals↗
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↗
PubMed1983

Replacement of gentamicin by amikacin as a means of decreasing gentamicin resistance of gram-negative rods in a neonatal intensive care unit.

The emergence of resistance in bacteria that colonize infants in a neonatal intensive care unit (NICU) is of great concern and a serious therapeutic problem. During the years 1980 to 1981, continuous surveillance of bacterial colonization was carried out on 499 infants admitted to the NICU of the Beilinson Medical Center. Antibiotic sensitivity testing was performed on all organisms isolated. At the end of 1980 and the beginning of 1981, an increased number of gram-negative rods became gentamicin-resistant. It was assumed that the discontinuation of gentamicin usage and replacement with another aminoglycoside, amikacin, would bring about a reduction in gentamicin resistance. Replacement of gentamicin by amikacin resulted in a significant decrease in gentamicin-resistant Escherichia coli and Klebsiella within 3 to 6 months. The emergence of resistant strains can be detected by surveillance methods and overcome by a change in the antibiotic regimen.

Amikacin↗
PubMedDate not supplied

Gentamicin-carbenicillin synergy among gentamicin resistant Pseudomonas aeruginosa.

Forty-five isolates of gentamicin resistant Pseudomonas aeruginosa were evaluated for gentamicin-carbenicillin synergy. Only 9 percent (4/45) showed synergy. Of nine isolates with demonstrable zones around a gentamicin disc (8 to 12 mm), none showed a synergistic response. Effective treatment of gentamicin resistant Ps. aeruginosa with gentamicin and carbenicillin should not be assumed without additional test procedures.

Carbenicillin↗
PubMed1980

The effect of combined gentamicin-corticosteroid treatment on gentamicin-resistant Pseudomonas keratitis.

In an experimental model of Pseudomonas keratitis caused by a gentamicin-resistant strain of Ps aeruginosa, the results of treatment with gentamicin alone and a gentamicin-steroid combination were evaluated. Treatment with steroids did not reduce the amount of corneal inflammation when compared to eyes treated with gentamicin alone. Eyes treated with the gentamicin-steroid combination were, however, infected with a statistically significant greater number of organisms at the end of a 3-day treatment period. Corticosteroids probably should not be used in the treatment of Pseudomonas keratitis during the early period when the antibiotic sensitivities of the organism are not known.

Animals↗
PubMed1980

A comparative study of the ototoxicity of gentamicin and gentamicin C1.

Dose-response experiments comparing the ototoxic liability of the aminoglycoside antibiotics gentamicin sulfate and gentamicin C1 sulfate were conducted on guinea pigs. Measures of cochlear electrophysiology, histology, and the pharmacokinetic disposition of the drugs in the plasma and perilymph were made. Electrophysiological and histological measures indicated that gentamicin is more ototoxic than is gentamicin C1.

Animals↗
PubMed1985

Methylation of 16S ribosomal RNA and resistance to the aminoglycoside antibiotics gentamicin and kanamycin determined by DNA from the gentamicin-producer, Micromonospora purpurea.

When DNA fragments from Micromonospora purpurea (the producer of gentamicin) were cloned in Streptomyces lividans, a gentamicin-resistant strain was obtained in which the ribosomes were highly resistant both to gentamicin and to kanamycin. Reconstitution analysis revealed that such resistance resulted from some property of their 16S RNA. Extracts from the clone contained methylase activity which acted on 16S RNA within E. coli 30S ribosomal subunits and rendered them resistant to gentamicin and kanamycin.

DNA, Bacterial↗
PubMed1991

Antimicrobial activity of isepamicin (SCH21420, 1-N-HAPA gentamicin B) combinations with cefotaxime, ceftazidime, ceftriaxone, ciprofloxacin, imipenem, mezlocillin and piperacillin tested against gentamicin-resistant and susceptible gram-negative bacilli and enterococci.

Isepamicin, formerly SCH21420 or 1-N-HAPA gentamicin B, is an aminoglycoside that was tested alone or in combination with one of seven broad spectrum drugs against 80 clinical isolates. Half of the strains were gentamicin-resistant but only one isolate (1.3%) was resistant to isepamicin. The broadest spectrum comparison drugs tested alone (ciprofloxacin at 3.8% resistance and imipenem at 5.0% resistance) were associated with the lowest synergy rates when combined with isepamicin. The rank order of synergy (complete or partial) was; cefotaxime = ceftazidime = ceftriaxone = mezlocillin = piperacillin (75% to 80%) greater than imipenem (66%) greater than ciprofloxacin (38%). Isepamicin/ampicillin combinations produced synergistic killing of those enterococci not having high-grade resistance to gentamicin or kanamycin. Enterococcus faecium strains were also refractory to isepamicin/ampicillin synergy. Isepamicin appears to be widely useable against gentamicin-resistant gram-negative bacilli either alone or combined with most commonly used broad spectrum beta-lactams.

Cefotaxime↗