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PubMed1996

[Comparative susceptibility of 10 antimicrobials against Pseudomonas aeruginosa isolated from complicated urinary tract infection on 1992 & 1993 vs. 1994 & 1995].

The susceptibility of 10 antimicrobials against P. aeruginosa isolated from complicated UTI during 1992-1995 was determined, and the yearly trend was examined. The drug tested included 3 cephems (ceftazidime [CAZ], cefpirome [CPR], cefclidin [CFCL]), 1 monobactam (aztreonam [AZT]), 2 carbapenem (imipenem/cilastatin [IPM/CS], biapenem [BIPM]), 2 aminoglycosides (netilmicin [NTL], gentamicin [GM]) and 2 new quinolones (ofloxacin [OFLX], ciprofloxacin [CPFX]). A total number of isolates of which MIC were determined was 77 in 1992/1993 and 70 in 1994/1995. MIC50/MIC90(micrograms/ml) on the isolates were as follows (1992/1993 1994/1995); 3.13/ 100 12.5/50 in CAZ, 12.5/100 12.5/100 in CPR, 3.13/25 1.56/25 in CFCL, 6.25/50 12.5/100 in AZT, 6.25/25 3.13/25 in IPM/CS, 1.56/6.25 0.78/50 in BIPM, 12.5/100 6.25/100 in NTL, 6.25/ 50 6.25/100 < in GM, 25.100 < 25/100 < in OFLX, 6.25/100 6.25/100 < in CPFX. When the susceptibility of the yearly trend is compared, no significant changes were detected among the drugs tested expect the decrease of susceptibility on CAZ, AZT and increase of it on IPM/CS. From the data obtained, against complicated UTI infected by P. aerugunosa, CFCL, IPM/CS and BIPM are considered to drugs of first choice in the treatment.

Anti-Bacterial Agents↗
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↗
PubMed1977

Assay of gentamicin in serum by high-pressure liquid chromatography.

A procedure is described that uses high-pressure liquid chromatography for assay of gentamicin in serum. The technique involves extraction of gentamicin from serum by using a CM-Sephadex column and analysis by reverse-phase, ion-pair chromatography. Continuous-flow, post-column derivatization with o-phthaladehyde is used to form fluorescent products for detection. The possible scope of this method for analysis of other aminoglycoside antibiotics is illustrated by application to sisomicin and netilmicin.

Anti-Bacterial Agents↗
PubMed1978

Infections due to gentamicin-resistant Staphylococcus aureus strain in a nursery for neonatal infants.

An apparently homogeneous strain of Staphylococcus aureus resistant to gentamicin (Gmr), kanamycin, tobramycin, and sisomicin, but susceptible to amikacin and netilmicin, caused multiple infections in neonatal infants in a special care nursery. Nasal cultures revealed a high rate of carriage of the Gmr staphylococcus in infants without clinical infection. Segregating patients according to a modified cohort system and use of careful aseptic techniques led to apparent elimination of the Gmr strain. The resistance to aminoglycosides in this strain was mediated by an aminoglycoside 6'-N-acetyltransferase and a gentamicin phosphotransferase. Genetic determinants for these enzymes were borne on a circular covalently closed plasmid of approximately 11 megadaltons. These resistance determinants closely resemble those found in isolates of S. aureus that have caused nosocomial infections in patients in Europe.

Gentamicins↗
PubMed1978

Aminoglycoside modification by gentamicin-resistant isolates of Staphylococcus aureus.

Three clinical isolates of Staphylococcus aureus, which were previously shown to contain a 50S plasmid conferring resistance to several aminoglycosides, were examined for modifying enzymes. Both the wild-type and heat-cured derivatives of the isolates were screened for acetyl-, adenylyl-, and phosphotransferase activities. The substrates were gentamicin, amikacin, and netilmicin; the results indicated that even though all three activites were present, the phosphotransferase reaction was most responsible for resistance to these antibiotics. The absence of any of the modifying activites in cured derivatives of the three isolates supports the conclusion that aminoglycoside resistance in these strains is conferred by a plasmid.

Aminoglycosides↗
PubMed1978

In vitro studies with Sch 21420 and Sch 22591: activity in comparison with six other aminoglycosides and synergy with penicillin against enterococci.

In vitro tests were performed with Sch 21420 and Sch 22591 to determine (i) their activity in comparison to six other aminoglycosides against 343 clinical isolates, and (ii) whether synergy with penicillin G could be demonstrated with enterococci. In broth dilution tests, Sch 22591 was more active than the seven other aminoglycosides against Staphylococcus aureus, Enterobacteriaceae, and most nonfermenting gram-negative bacilli. Sch 22591 was as active as tobramycin against Pseudomonas aeruginosa. The activity of Sch 21420 was comparable to gentamicin, sisomicin, netilmicin, and tobramycin but greater than amikacin or kanamycin against S. aureus and most genera of Enterobacteriaceae. Sch 21420, amikacin, and kanamycin were (i) more active than the other five aminoglycosides against Proteus rettgeri and Providencia stuartii, but (ii) less active than the other five aminoglycosides against Neisseria gonorrhoeae, enterococci, most nonfermenting gram-negative bacilli, Proteus mirabilis, and Proteus morganii. Studies on the bactericidal activity of Sch 22591 with penicillin indicated a synergistic interaction against enterococci, including strains highly resistant to streptomycin and kanamycin. This could be demonstrated with combinations containing 3.0 to 6.0 mug of Sch 22591 per ml and was comparable to that observed with penicillin/gentamicin. Penicillin plus Sch 21420 (25 mug/ml) also demonstrated synergy against enterococci, including strains highly resistant to streptomycin. However, synergy did not occur against strains highly resistant to kanamycin. These latter results were similar to those obtained in tests with penicillin/kanamycin.

Aminoglycosides↗
PubMed1978

Recovery from aminoglycoside nephrotoxicity with continued drug administration.

To examine the nephrotoxicity of prolonged gentamicin administration compared to the effect obtained when a less toxic aminoglycoside is substituted during the course of treatment, we gave gentamicin (67.5 mg/kg per day) to rats for 21 days, gentamicin for 14 days followed by either netilmicin or tobramycin for 7 days, or gentamicin for 14 days followed by saline diluent. After initial tubular, necrosis, the animals recovered from renal injury whether the drug was continued or discontinued or another drug was substituted. These data are consistent with the observation that regenerating renal epithelium is resistant to continued or additional nephrotoxic insults. These findings suggest that improvement in renal function during aminoglycoside therapy cannot necessarily be attributed to the substitution of another aminoglycoside or other therapeutic interventions.

Animals↗
PubMed1978

In vitro activity of 5-episisomicin in bacteria resistant to other aminoglycoside antibiotics.

Eighty-seven isolates of Pseudomonas, Enterobacteriaceae, and Staphylococcus, chosen because of their resistance to other aminoglycosides, were tested for susceptibility to 5-episisomicin. Tests were performed in Mueller-Hinton agar and also, with 38 of these isolates, in Mueller-Hinton broth. Of Enterobacteriaceae, 85 and 95.5% were inhibited by 5 and 10 mug of 5-episisomicin per ml, respectively. Amikacin inhibited 74 and 91% of the strains at 10 and 20 mug/ml, respectively. Fifty-four percent of P. aeruginosa were inhibited by 5-episisomicin and amikacin. Eighty-three percent of S. aureus were inhibited by netilmicin and amikacin, whereas only 50% were inhibited by 5-episisomicin. Isolates resistant to 5-episisomicin were most often resistant to the other aminoglycosides and occurred in gram-negative bacilli that did not carry aminoglycoside-modifying enzymes. Five of 23 isolates that carried a 6'-N-acetyltransferase (AAC-6') and one of two that carried an aminoglycoside 3-acetyltransferase were resistant to and acetylate 5-episisomicin. Strains carrying other aminoglycoside-modifying enzymes were inhibited by 5-episisomicin. Thus, 5-episisomicin is a promising aminoglycoside not attacked by most aminoglycoside-modifying enzymes. Resistance will probably most often be based upon nonenzymatic mechanisms which will also affect other aminoglycosides.

Drug Resistance, Microbial↗
PubMed1978

Anaerobic resistance of clinical isolates of Staphylococcus aureus to aminoglycosides.

The anaerobic minimum inhibitory concentration of six aminoglycosides (amikacin, gentamicin, kanamycin, netilmicin, sisomicin, and tobramycin) averaged over 10-fold greater than the aerobic minimum inhibitory concentration for 50 clinical isolates of Staphylococcus aureus. Cultures from osteomyelitis and blood generally showed a somewhat greater increase in minimum inhibitory concentration due to anaerobiosis than did cultures from abscesses and wounds, and amikacin activity was most affected by anaerobiosis.

Aminoglycosides↗
PubMed1979

Investigations of the occurrence of gentamicin-resistant Staphylococcus aureus.

During the 19-month period from June 1976 to December 1977, 90 patients became colonized or infected with gentamicin-resistant Staphylococcus aureus (GRS). Of 63 adults, 56 had hospital-acquired GRS, whereas only 9 of 27 children had hospital-acquired GRS (P < 0.001). The other 7 adults and 18 children had GRS present on admission. More than half of those who acquired GRS in the hospital had received prior aminoglycoside therapy. Attack rates were higher in adults than in children and significantly higher on the plastic surgery service than on any other adult service. Phage typing revealed a single-strain outbreak on the plastic surgery ward involving 11 patients, whereas other isolates were of several phage types. Community-acquired GRS occurred more frequently in rural native communities (P < 0.02) and may be related to the use of topical gentamicin. Of 17 native children, 10 were from the same area but there was no common phage type. Agar dilution minimal inhibitory concentration (MIC) testing confirmed that all isolates were gentamicin resistant (MIC >/= 8 mug/ml) and almost all were tobramycin resistant (MIC >/= 8 mug/ml). Although the MIC distribution between gentamicin disk-susceptible and -resistant strains was significantly different, MIC's for 90% of gentamicin disk-resistant strains were </=8 mug of amikacin per ml, and MIC's for 92% of the strains were </=4 mug of netilmicin per ml.

Adolescent↗
PubMed1979

High-level, plasmid-borne resistance to gentamicin in Streptococcus faecalis subsp. zymogenes.

Each of three isolates of Streptococcus faecalis subsp. zymogenes harbored three R plasmids and a hemolysin-bacteriocin plasmid. The plasmids carried by one of these strains were physically characterized after their conjugative transfer. In each strain one of the plasmids carried genetic markers for resistance to gentamicin, kanamycin, sisomicin, netilmicin, and tobramycin.

Anti-Bacterial Agents↗
PubMed1980

Comparative susceptibilities of Pseudomonas aeruginosa to 1-oxacephalosporin (LY 127935) and eight other antipseudomonal antimicrobial agents (old and new).

In vitro susceptibilities of 53 clinical isolates of Pseudomonas aeruginosa to nine antipseudomonal antibiotics were determined. From 96 to 100% of the isolates were susceptible to piperacillin, ticarcillin, and 1-oxacephalosporin (LY 127935). Of the aminoglycosides, 89, 82, 79, and 29% were susceptible to amikacin, tobramycin, gentamicin, and netilmicin, respectively. A total of 96% and 78% of the isolates were susceptible to 1-oxacephalosporin (LY127935) and cefotaxime, respectively, at concentrations of 62.5 micrograms/l. Supplementation of testing media by calcium and magnesium not only markedly increased the minimal inhibitory concentrations of the aminoglycosides, but also raised those of cefotaxime and the penicillins; no significant effect was noted with 1-oxace-phalosporin. Synergy was not demonstrated consistently in vitro with 1-oxace-phalosporin combined with either carbenicillin, ticarcillin, gentamicin, or tobramycin.

Anti-Bacterial Agents↗
PubMed1980

Compound A49759, the 3-O-demethyl derivative of fortimicin A: in vitro comparison with six other aminoglycoside antibiotics.

O-Demethylfortimicin A (compound A49759) was tested against 445 bacteria, and the results were compared with those obtained with fortimicin A, amikacin, gentamicin, netilmicin, sisomicin, and tobramycin. A49759 was found to be active and bactericidal against the Enterobacteriaceae, nonfermentative gram-negative bacilli, and Staphylococcus aureus. A49759 was two- to fourfold more active than fortimicin A against most species tested, but generally fourfold less active than amikacin against this population of Pseudomonas aeruginosa (85% inhibited at less than or equal to 16 microgram of amikacin per ml and 85% inhibited at less than or equal to 64 microgram of A49759 per ml). Only amikacin and A49759 were resistant to most aminoglucoside-inactivating enzymes and also had significant antipseudomonal activity. Amikacin was inactivated by aminoglycoside 6'-acetyltransferase, and A49759 was inactivated by aminoglycoside 3-acetyltransferase. The minimal inhibitory concentrations of all tested aminoglycosides were increased by augmenting the inoculum size.

Aminoglycosides↗
PubMed1981

Prevention of acute and chronic ascending pyelonephritis in rats by aminoglycoside antibiotics accumulated and persistent in kidneys.

Gentamicin, because it is stored in renal tissues, can prevent acute retrograde pyelonephritis. Since different aminoglycosides accumulate and persist to various degrees in the kidney parenchyma, the prophylactic activities of gentamicin, tobramycin, amikacin, and netilmicin were compared. The four antibiotics were given intramuscularly to rats 3 days before initiating ascending unilateral pyelonephritis with Escherichia coli. Despite different degrees of renal accumulation at the time of infection (tobramycin and amikacin accumulated significantly less), all four aminoglycosides displayed similar protection against ascending pyelonephritis. This protection was conferred in the absence of active antibiotic detectable in the urine and was therefore attributed to antibiotic stored in the renal parenchyma. Those animals that developed pyelonephritis despite aminoglycoside prophylaxis had less severe acute kidney infection and inflammation. This resulted 3 months later in an almost complete protection against renal scarring (chronic pyelonephritis). These results in rats suggest that renal accumulation and persistence of aminoglycosides may be used to advantage in the prophylaxis or in the treatment of kidney infections.

Aminoglycosides↗
PubMed1982

Ribosomal resistance in the gentamicin producer organism Micromonospora purpurea.

The mechanism of resistance of the gentamicin-producing organism Micromonospora purpurea was analyzed. Determination of minimal inhibitory concentrations revealed high resistance to the 4,6-substituted deoxystreptamine aminoglycosides amikacin, gentamicin, kanamycin, netilmicin, sisomicin, and tobramycin and also to lividomycin A and hygromycin B, but susceptibility to streptomycin, dihydrostreptomycin, paromomycin, and neomycin during all phases of the growth cycle. The nonproducing, closely related Micromonospora melanosporea was susceptible to these compounds. In agreement with results from previous studies (R. Benveniste and J. Davies, Proc. Natl. Acad. Sci. U.S.A. 70:2276-2280, 1973), extracts from M. purpurea showed no activity of enzymes specifically modifying gentamicin. 70S ribosomes from M. purpurea but not from M. melanosporea were resistant to inhibition by gentamicin, kanamycin, tobramycin, and lividomycin in a polyuridylic acid-dependent polyphenylalanine synthesis system and susceptible to those compounds which were inhibitory in vivo. The former antibiotics were also unable to induce misreading. Subunit exchange experiments between M. purpurea and M. melanosporea showed that the main site for inhibition and induction of misreading is the 30S subunit (up to gentamicin concentrations of 10 micrograms/ml).

Aminoglycosides↗
PubMed1982

Synergism between aminoglycosides and cephalosporins with antipseudomonal activity: interaction index and killing curve method.

Combinations of gentamicin with cefotaxime, moxalactam, and ceftazidime were tested against 43 bacterial strains, most of them blood isolates. With an interaction index of less than or equal to 0.5 as borderline, synergism was demonstrated against 30 to 40% of the strains by the fractional inhibitory concentration index and against 50 to 70% by the fractional bactericidal concentration index. The reproducibility of the index was within +/- 0.2 for two-thirds of 40 repetitive assays and within +/- 0.4 to 0.5 for all of these assays. Similar results were obtained when netilmicin was substituted for gentamicin. The killing curve system for studying antibiotic synergism was standardized to give results comparable to those obtained with the interaction index. This was achieved when one-half of a previously determined minimum bactericidal concentration was used for single drugs and the amount of antibiotic was at least halved again when drugs were used in combination. An initial bacterial concentration of 10(5) to 10(6) colony-forming units per ml is recommended. Given these conditions, synergism could be defined as a 2-log 10 or more decrease in viable count given by both drugs together, as compared with the more active of the pair after 24 h. Prediction of killing curve results could then be obtained with the fractional bactericidal concentration index. When cephalosporins and gentamicin were combined from the start, the beta-lactam antibiotics were less susceptible to inactivation, as demonstrated in time-killing assays. If one of the antibiotics were added after 24 h, synergism was not demonstrable. The results indicate that the new cephalosporins may be advantageously combined with aminoglycosides.

Aminoglycosides↗
PubMed1983

Susceptibility of Pseudomonas paucimobilis to 24 antimicrobial agents.

Pseudomonas paucimobilis (group IIK, biotype 1) clinical isolates showed in vitro resistance to ampicillin, carbenicillin, cephalothin, cefoxitin, cefamandole, moxalactam, cefotaxime, cefoperazone, mezlocillin, azlocillin, piperacillin, and ticarcillin. Those agents to which the microbes were shown to be susceptible were tetracycline, chloramphenicol, gentamicin, tobramycin, kanamycin, amikacin, netilmicin, sisomicin, trimethoprim-sulfamethoxazole, ceftazidime, ceftriaxone, and ceftizoxime.

Anti-Bacterial Agents↗
PubMed1983

Pharmacokinetics and bacteriological effect of ceftazidime in experimental Streptococcus pneumoniae, Haemophilus influenzae, and Escherichia coli meningitis.

The pharmacokinetics and bacteriological effect of ceftazidime were evaluated in rabbits experimentally infected with Streptococcus pneumoniae, Haemophilus influenzae type b, and Escherichia coli K1. The mean penetration of ceftazidime into cerebrospinal fluid after single-dose or constant-infusion administration ranged from 7.8 to 14.9%. The median cerebrospinal fluid bactericidal titers were 1:64 against S. pneumoniae and H. influenzae and 1:128 against E. coli. The bacterial colony counts in cerebrospinal fluid were reduced by 58% to 100% (-2.3 to -3.9 log10 CFU/ml) in 3 h and by 100% (-3.2 to -5.1 log10 CFU/ml) in 9 h of constant infusion, whereas in untreated infected animals, bacterial counts increased from +1.4 to +2.1 log10 CFU/ml in 9 h. These data on ceftazidime compare favorably with those on penicillin, chloramphenicol, netilmicin, and moxalactam in this experimental meningitis model.

Animals↗