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PubMed1977

The effect of concomitant mercuric chloride and gentamicin on kidney function and structure in the rat.

In order to define the possible effects of gentamicin on the course of experimental acute renal failure, the interaction between gentamicin and mercuric chloride was studied in rats. Acute renal failure was induced with 1 mg. of HgCl2 per kilogram intravenously. When given alone, HgCl2 produced a uniform, reproducible, nonoliguric, acute renal failure with a low mortality rate. Animals receiving gentamicin over the course of HgCl2-induced acute renal failure, in doses sufficient to produce a 1 hour postinjection serum concentration of 10 mug/ml., recovered glomerular filtration in a fashion similar to animals receiving only HgCl2(p greater than 0.05). Animals that recovered from HgCl2-induced acute renal failure were given 10 mg./Kg. of gentamicin every 4 hours for 15 days and developed proteinuria and decline in urine osmolality to the same degree as animals given gentamicin alone, but failed to develop azotemia. Nevertheless, morphological changes associated with gentamicin nephrotoxicity were found which were similar in severity to those seen with gentamicin alone. Animals pretreated with 10 mg./Kg. of gentamicin every 4 hours for 7 days were then given HgCl2. Acute renal failure in these animals was more severe than in animals receiving HgCl2 alone, as manifest by a greater degree of azotemia and death (p less than 0.05). The data indicate that in the rat the concomitant administration of gentamicin did not interfere with recovery from HgCl2-induced renal failure. Rats recovering from HgCl2-induced acute renal failure were resistant to a depression in glomerular filtration when given gentamicin. The prior administration of gentamicin enhanced the nephrotoxicity of HgCl2.

Acute Kidney Injury↗
PubMed1978

Comparison of silver sulfadiazine and gentamicin for topical prophylaxis against burn wound sepsis.

Daily prophylactic application of either 1.0% silver sulfadiazine cream or 0.1% gentamicin cream was compared for effectiveness in preventing bacterial colonization of burn wounds and sepsis. Pseudomonas aeruginosa colonized the wounds of 37% of the 38 patients treated with silver sulfadiazine and 30% of the 33 patients treated with gentamicin; gentamicin-resistant P. aeruginosa colonized the wounds of 21% of the patients treated with gentamicin. Staphylococcus aureus colonization occurred in 55% of the patients treated with silver sulfadiazine, whereas colonization with Candida species occurred in 58% of the patients treated with gentamicin. Although gentamicin-resistant organisms caused no deaths their repeated appearance resulted in discontinuation of prophylaxiz with gentamicin cream. The next year P. aeruginosa strains resistant to gentamicin were isolated from burn wounds of only two patients who had not previously received parenteral therapy with gentamicin or tobramycin. Gentamicin cream should be reserved for treating patients with wounds infected by gentamicin-sensitive P. aeruginosa and those allergic to sulfa drugs. For most patients with burn wounds silver sulfadiazine is safe and effective as an antibacterial agent for topical prophylaxis.

Administration, Topical↗
PubMed1979

Patient factors contributing to the emergence of gentamicin-resistant Serratia marcescens.

One hundred forty nosocomial Serratia marcescens infections (including 76 cases of bacteremia) were identified by prospective surveillance from 1975 through 1977 and retrospective chart review from 1968 through 1974. Thirty-four cases (24 per cent) involved gentamicin-resistant strains. All gentamicin-resistant strains appeared after 1974. Ninety per cent of the patients had undergone surgery, and 88 per cent had received prior antimicrobial therapy. The emergence of gentamicin-resistant S. marcescens paralleled the increase in usage of gentamicin. Prior use of gentamicin for more than two days in an individual patient was a significant risk factor (P = 0.0002) for being infected with a Serratia that was gentamicin-resistant. Other factors which separated gentamicin-resistant Serratia infections from gentamicin-sensitive Serratia infections were (1) urinary site of infection (P = 0.0005), (2) urinary catheter (P = 0.002), (3) endotracheal tube or tracheotomy (P = 0.03) and (4) increasing duration of hospitalization (P less than 0.05). Thirty-three of 34 (97 per cent) patients with gentamicin-resistant strains had urinary catheters. Specific measures to control infection were effective in decreasing the incidence of infections caused by gentamicin-resistant Serratia.

Adolescent↗
PubMed1977

Emergence of gentamicin-resistant Klebsiella in a general hospital.

Gentamicin had been in use in a general hospital for over 7 years before any gentamicin-resistant Klebsiella were observed. In 1974 and 1975, nine different gentamicin-resistant serobiotypes of Klebsiella were isolated from 35 patients. The first strain to appear had R-factor-mediated gentamicin resistance, and it infected 19 patients during a period of almost 2 years, spreading largely by case-to-case infection in patients with urinary catheters. It appeared to lose the capacity to transfer its gentamicin resistance after it had infected five of the patients. We had previously isolated on the same ward a gentamicin-susceptible Klebsiella of identical type, and it was found to be capable of acquiring an R-factor for gentamicin resistance. All of the other types of gentamicin-resistant Klebsiella infected few patients and did not persist in the hospital; four of them had R-factor-mediated resistance to gentamicin and all four, as did the original strain, cotransferred kanamycin, neomycin, and tobramycin resistance. Every gentamicin-resistant Klebsiella was susceptible to amikacin and netilmicin.

Aminoglycosides↗
PubMed1976

Emergence of gentamicin- and carbenicillin-resistant Pseudomonas aeruginosa in a hospital environment.

Strains of Pseudomonas aeruginosa resistant to either gentamicin or carbenicillin have been noted since their introduction into clinical use. During a 6-month period, twice-weekly cultures were obtained from all patients treated with either gentamicin or carbenicillin and from all patients with a positive culture for P. aeruginosa. Susceptibility testing to gentamicin and carbenicillin and pyocine typing were performed on all isolates. Organisms with a minimal inhibitory concentration greater than 12.5 mug of gentamicin per ml or greater than 100 mug of carbenicillin per ml were defined as resistant. P. aeruginosa was cultured from 238 patients. One patient was initially infected with a gentamicin-resistant isolate. In 11 other patients, serial cultures revealed the emergence of resistance to gentamicin. All but one of these resistant isolates occurred in patients treated with gentamicin. In eight instances the pyocine and/or serological types before and after the change in sensitivity pattern were the same. Gentamicin-resistant P. aeruginosa emerged significantly more often in patients treated with gentamicin than in those who did not receive gentamicin. Carbenicillin-resistant P. aeruginosa emerged in four of 14 patients treated with carbenicillin. Seventeen of the 238 patients were infected de novo with carbenicillin-resistant P. aeruginosa. Carbenicillin-resistant P. aeruginosa emerged significantly more often in patients treated with carbenicillin than in those who did not receive carbenicillin. No evidence was found for in-hospital spread of resistant P. aeruginosa.

Adult↗
PubMed1979

Gentamicin- and silver-resistant pseudomonas in a burns unit.

In 1977-8 gentamicin-resistant strains of Pseudomonas aeruginosa became very common in a burns unit, over 90% being resistant at the peak of the outbreak. Some strains were also resistant to silver nitrate, though silver resistance was not found in any other strains of Ps aeruginosa isolated. Unlike the gentamicin resistance, the silver resistance was unstable, and strains became sensitive on repeated subculture. All the gentamicin-resistant strains of Ps aeruginosa were of the same serotype (O:11, H:2,5). Though gentamicin resistance could be transferred in vitro from resistant strains of Ps aeruginosa to one sensitive strain of Ps aeruginosa, there was no evidence of in-vivo transfer of gentamicin resistance between strains of pseudomonas in the patients' burns, nor was there evidence of transfer of gentamicin resistance between Ps aeruginosa and enterobacteria. Carbenicillin-resistant and gentamicin-resistant Ps aeruginosa were sometimes found in the same burns, but no gentamicin-carbenicillin (doubly) resistant strains were found among the 986 strains tested during the outbreak. The outbreak of gentamicin-resistant Ps aeruginosa from burns was not reduced by stopping treatment with gentamicin and its analogues but only by segregating all patients with Ps aeruginosa in one of the two wards of the unit and admitting new patients only to the other ward.

Burns↗
PubMed1978

Gentamicin-cephalothin drug reaction.

A case report describing the occurrence of nephrotoxicity in a 26-year-old black male with sickle cell anemia after concurrent i.v. administration of gentamicin sulfate and cephalothin sodium is presented. Cephalothin 1 g.i.v. every six hours was given for three days for a Klebsiella infection demonstrated by urine and blood culture to be cephalosporin sensitive. Cephalothin was then discontinued and gentamicin, after an i.v. loading dose of 2.6 mg/kg, was given for 14 days in a dosage of 1.3 mg/kg every eight hours. After cultures of pus aspirated from the right thigh demonstrated Klebsiella, 2 g of cephalothin was administered i.v. every six hours and gentamicin sulfate was discontinued. Gentamicin therapy was reinstituted two days later, at a dosage of 5 mg/kg/day. The gentamicin-cephalothin therapy was continued for nine days. The gentamicin dosage interval was increased from every eight to every 16 hours when serum creatinine and gentamicin levels became elevated. Gentamicin was discontinued entirely two days later because serum gentamicin levels were not decreasing. Previous case reports and studies of nephrotoxicity associated with concurrent gentamicin-cephalothin therapy are reviewed. Pharmacists should be alert to the possible increased incidence of nephrotoxicity occurring with concurrent genticin-cephalothin therapy.

Adult↗
PubMed1979

Urinary myelin figures in gentamicin nephrotoxicity.

The nephrotoxicity of gentamicin is associated with formation of myelin figures within the proximal convoluted tubules of experimental animals and man. By electron microscopy, the authors studied urinary sediments of patients who were treated with gentamicin to detect the occurrence of myelin figures. All three patients who had renal impairment and were treated with gentamicin had numerous urinary myelin figures. By contrast, myelin figures were not observed in urinary sediments of four patients who had no renal impairment despite gentamicin therapy, or nine patients who had no renal impairment and did not receive gentamicin therapy. Occasional myelin figures were detected in a urinary sediment of one of eight patients who had renal impairment and no gentamicin therapy. When the urinary sediments of patients who had gentamicin nephrotoxicity were compared with those of patients with Fabry disease, morphologic differences between the myelin figures of the two groups were detected. The study demonstrates the presence of myelin figures in urines of patients with acute renal failure receiving gentamicin, and suggests that the finding of these myelin figures within urine samples may contribute to the diagnosis of gentamicin-induced nephrotoxicity.

Cell Membrane↗
PubMed1977

In vitro activity of netilmicin, gentamicin, and amikacin.

The in vitro activity of netilmicin (Sch 20569), a new semisynthetic derivative of gentamicin, was compared with that of gentamicin and amikacin. One hundred and ninety-two clinical isolates of Enterobacteriaceae, Pseudomonas aeruginosa, and Staphylococcus aureus were tested using both agar and broth dilution techniques. Netilmicin was comparable to gentamicin, with the following exceptions: (i) for Serratia marcescens and P. aeruginosa, gentamicin was more active than netilmicin; (ii) all strains of Escherichia coli, Klebsiella, Enterobacter, Proteus mirabilis, and Citrobacter freundii, which were resistant to gentamicin, were susceptible to netilmicin; (iii) some strains of S. marcescens, indole-positive Proteus, and Providencia, which were resistant to gentamicin, were susceptible to netilmicin. Netilmicin was more active than amikacin for all Enterobacteriaceae and S. aureus and equal to amikacin in activity against gentamicin-susceptible strains of P. aeruginosa. All strains of P. aeruginosa, resistant to gentamicin, were also resistant to netilmicin but were susceptible to amikacin. Minimal inhibitory concentrations (MICs) obtained with broth and agar showed no significant differences except for P. mirabilis, where broth MICs were twofold greater than agar MICs, and for P. aeruginosa, where agar MICs were twofold higher than broth MICs. The minimal bactericidal concentration (MBC) was either identical to or within one twofold dilution of the MIC for the strains tested. A 100-fold increase in inoculum size produced less increase in MIC and MBC with netilmicin than with gentamicin or amikacin.

Amikacin↗
PubMed1978

Effects of hydration on gentamicin excretion and renal accumulation in furosemide-treated rats.

The effect of furosemide on gentamicin excretion and tissue accumulation was studied with clearance techniques in anesthetized rats, at two different infusion rates of saline or Ringer solution. Gentamicin ( approximately 20 mg/kg) was administered by constant intravenous infusion over a period of 3 h. With the low fluid infusion rate, furosemide (25 mg/kg intravenously) caused severe reduction in glomerular filtration rate and diminished urinary output of gentamicin. Serum and renal tissue levels of the antibiotic were significantly elevated. High fluid infusion prevented the decline of the glomerular filtration rate, with near normalization of all measurements. A fluid deficit incurred by furosemide was noted at both the low and high infusion rates. Complete correction of this fluid deficit by continuous adjustment of the infusion rate fully restored normal renal handling of gentamicin. These results suggest that furosemide had no direct effect on renal excretion of gentamicin. In comparison, renal handling of gentamicin in rats did not respond to changes in the rate of fluid infusion in the absence of furosemide therapy. It appears that gentamicin excretion and gentamicin accumulation in the renal cortex in furosemide-treated rats, in contrast with those in untreated rats, are influenced significantly by the rate of fluid infusion. Fluid administration sufficient to maintain the glomerular filtration rate was found to be necessary for appropriate gentamicin elimination, with consequent reduction in serum and renal tissue levels of the drug.

Animals↗
PubMed1976

[Gentamicin-susceptibility of various pathogens isolated from clinical materials].

We studied on the antibacterial activity of gentamicin against various pathogens isolated from clinical materials mainly isolated during 1974 and 1975, comparing with other antibiotics. Beta hemolytic streptococci, pneumococci and enterococci are less susceptible to gentamicin than staphylococci. Staph, aureus and Staph. epidermidis resistant to various antibiotics are very susceptible to gentamicin, and no resistant strain to this drug was found. Haemophilus influenzae, H. parainfluenzae and H. parahaemolyticus are very susceptible to gentamicin, and there is no resistant strain to this drug. Escherichia coli, Klebsiella, Citrobacter, Serratia and five species of Proteus are more susceptible to gentamicin and tobramycin than dibekacin and amikacin. A few resistant or less susceptible strains to gentamicin are found in E. coli, Citrobacerr, Serratia, Pr. morganii and Pr. rettgeri. Pr. inconstans is less susceptible to gentamicin than other species of Proteus. Antibacterial activity of gentamicin against Pseudomonas aeruginosa is very strong, but dibekacin and tobramycin are stronger. Gentamicin-resistant strains of Pseudomonas aeruginosa are now rather few.

Citrobacter↗
PubMed1975

Postoperative endophthalmitis: a comparison of methods for treatment and prophlaxis with gentamicin.

Toxicity of gentamicin and its use in the treatment of experimentally induced Pseudomonas aeruginosa endophthalmitis were studied in the postoperative aphakic eye. The retinal toxicity of intravitreal gentamicin was different from toxicity in the intact eye and varied with the method of injection. Successful prophylaxis of induced postoperative infection was obtained with an intravitreal injection of 30 mu-g of gentamicin but not with sub-Tenon's administration of gentamicin. Treatment for progressive endophthalmitis was effective with high dose (200 mu-g) gentamicin alone, or a combination of low-dose (30 mu-g) gentamicin with topical and systemic gentamicin. Either sub-conjunctival and systemic gentamicin or low-dose gentamicin alone was ineffective once endophthalmitis was in progress. Although vitrectomy removed abscess products, it failed in this experiment to provide better results than the other modes of therapy.

Animals↗
PubMed1975

A controlled trial of parenteral prophylactic gentamicin therapy in biliary surgery.

This trial has investigated the value of gentamicin therapy in patients requiring biliary surgery. One hundred consecutive patients were randomly allocated to receive either gentamicin or no antibiotic. Post-operative infection was assessed by an independent observer. Cultures and gentamicin assays were performed on bile and blood sampled during and after operation. The minimum inhibitory concentrations of gentamicin were measured with isolated bacterial. In 80 per cent of patients biliary organisms were inhibited by 2 mug/ml of gentamicin. Twice this concentration was found in the serum at operation in 88 per cent, but in the bile in only 18 per cent. Nevertheless, gentamicin lowered the incidence of bacteria in the bile from 42 to 25 per cent. There was a reduction in wound sepsis from 21 to 6 per cent (P less than 0-05). Bacteriaemia was demonstrated in only 1 patient receiving gentamicin compared with 5 controls and 1 death occurred from endotoxaemia in the control group. These data suggest that gentamicin will reduce the morbidity of biliary surgery, particularly in patients in whom the bile is infected at operation.

Aged↗
PubMed1975

Drug-biomolecule interactions: interaction of gentamicin with lipid monomolecular films.

The interaction of gentamicin with monomolecular films of a series of biologically important lipids spread on an aqueous buffered subphase was studied. The surface pressure, pi, of these films was determined by the Wilhelmy plate method as a function of surface area, A, and pi-A curves were constructed. Changes in the pi-A characteristics in the presence of gentamicin were used as a measure of antibiotic-film interaction. No interaction was observed between gentamicin and films of cholesterol, egg lecithin, dipalmitoyl lecithin, phosphatidyl ethanolamine, stearyl alcohol, and bovine ceramides at all pH values studied. Stearic acid films showed no interaction with gentamicin at pH 5. At pH 7 and 8, a small increase in pressure (approximately 3 dynes/cm) was noted. A dramatic increase in surface pressure was observed in the presence of stearyl aldehyde films ranging from approximately 9 dynes/cm at pH 7,2 to 23 dynes/cm at pH 8.4. This effect was attributed to a Schiff-base reaction between the nonprotonated primary amino groups on the gentamicin molecule and the stearyl aldehyde. Further evidence was reported by the fact that the addition of glucose (which has been reported to participate in Schiff-base formation with amines) to the subphase inhibited the stearyl aldehyde-gentamicin interaction. Sucrose did not show a corresponding effect. The addition of sodium bisulfite, which reacts with aldehydes to form alpha-hydroxysulfonic acid, also inhibited the gentamicin-stearyl aldehyde interaction. It is postulated that Schiff-base formation is a step in the in vivo transport of gentamicin across the membrane of sensitive organisms.

Chemical Phenomena↗
PubMedDate not supplied

Factors associated with acquisition of Pseudomonas aeruginosa resistant to gentamicin.

Concern over the increased occurrence of Pseudomonas aeruginosa resistant to gentamicin colonizing and/or causing disease in patients prompted our review of the years 1974 and 1975 for all P aeruginosa isolates, both gentamicin-resistant and gentamicin-sensitive. In this period, 39 patients had gentamicin-resistant P aeruginosa recovered from clinical specimens while 683 patients had gentamicin-sensitive strains. Compared to both matched and/or randomly selected controls with gentamicin-sensitive infections, patients with gentamicin-resistant infections had a higher incidence of (1) prior antibiotic therapy (p less than 0.01), (2) prior therapy with gentamicin (p less than 0.005), and (3) exposure to multiple antibiotics.

Adult↗
PubMed1978

Gentamicin use and Pseudomonas and Serratia resistance: effect of a surgical prophylaxis regimen.

An outbreak of prosthetic valve endocarditis due to methicillin-resistant Staphylococcus epidermidis prompted a change in antimicrobial prophylaxis for open heart surgery in a general hospital from a regimen of aqueous penicillin G, methicillin, and kanamycin to a 5-day regimen of cefazolin and gentamicin. As a result, total gentamicin use in the hospital more than doubled. Increased resistance of pseudomonas and serratia isolates paralleled the increased total use of gentamicin. For pseudomonas species, the incidence of gentamicin resistance increased from 3 to 15%; for serratia species, from 8 to 88%; and for the total of both organisms, from 4 to 28%. Resistance decreased rapidly after removal of gentamicin from the prophylaxis regimen. Review of serratia isolates from the urinary tract showed that gentamicin resistance was associated with prior antibiotic therapy, especially with gentamicin, care on the surgical services, especially the surgical intensive care unit, and presence of indwelling bladder catheters. Gentamicin use in a 5-day antimicrobial prophylaxis regimen for open heart surgery can represent a large proportion of the total hospital use of that antibiotic, with potential adverse effects on hospital flora.

Drug Resistance, Microbial↗
PubMed1979

Effect of protein binding on the activity of penicillins in combination with gentamicin against enterococci.

To assess the effect of protein binding by human serum on the synergistic interaction of penicillins with gentamicin, time-kill curves were determined for four penicillins alone and in combination with gentamicin against 10 blood isolates of enterococci. Killing curves demonstrated synergism with penicillin G plus gentamicin against all 10 strains in either broth or 50% human serum. In broth the combinations of nafcillin plus gentamicin and oxacillin plus gentamicin were synergistic against 10 of 10 strains and 4 of 10 strains, respectively. However, in serum, nafcillin plus gentamicin was synergistically bactericidal against only two strains and oxacillin plus gentamicin against none. Methicillin plus gentamicin was synergistic against none of the enterococci in either medium. Thus, the semisynthetic, penicillinase-resistant penicillins are unlikely to be effective in the therapy of patients with enterococcal endocarditis.

Blood Bactericidal Activity↗
PubMed1976

Bactericidal efficacy of Sch 20569 and amikacin against gentamicin-sensitive and -resistant organisms.

Sch 20569 is a semisynthetic derivative of gentamicin with activity against many gentamicin-resistant gram-negative bacilli. We compared its bactericidal action with that of gentamicin and amikacin against 171 clinical isolates of Enterobacteriaceae, Staphylococcus aureus, and Pseudomonas aeruginosa. Sch 20569 and amikacin showed markedly greater activity than gentamicin against Escherichia coli, Klebsiella, Enterobacter, Citrobacter, and indole-positive Proteus, primarily by virtue of their lethal effect on gentamicin-resistant strains (minimal bactericidal concentration >/= 12.5 mug/ml). Indole-negative Proteus isolates were uniformly sensitive to Sch 20569, whereas several were resistant to both gentamicin and amikacin. Amikacin was most active against Providencia, as was gentamicin against Serratia. All three agents exhibited similar activity against Pseudomonas. Staphylococcus aureus was more sensitive to gentamicin and Sch 20569 than to amikacin.

Amikacin↗