[Low-level vancomycin resistance in Enterococcus faecalis].
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Biomedical subjects
Publications and source records attributed to M C García-Iglesias.
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We have studied the clinical efficacy and pharmacokinetics of cefuroxime in 3 children aged 5, 7 and 10 months who were suffering from meningitis due to Haemophilus influenzae group b (beta-lactamase producers). The MICs of chloramphenicol against these three beta-lactamase-producing H. influenzae isolates were 8, 3.1 and 16 micrograms/ml, and those of cefuroxime were 0.25, 0.5 and 0.12 microgram/ml, respectively. The dosage of cefuroxime was 100 mg/kg/day divided in four 6-hourly intravenous doses for 15 days, and 10 mg given intrathecally every 48 h. Blood and spinal fluid levels were determined by microbiological assay. All the 3 children had excellent clinical and bacteriological responses with negative spinal fluid cultures after 48 h of treatment.
The in vitro activity of the new semisynthetic ureidopenicillins azlocillin (AZ) and mezlocillin (MZ), and of the new cephalosporin cefsulodin (CEF) were determined against 50 carbenicillin-sensitive (CARs) and 50 carbenicillin-resistant (CARr) P. aeruginosa clinical isolates. In the CARs group the most active antibiotics are AZ and CEF with MICs between 0.5 and 8 microgram/ml. Ticarcillin (TIC) and MZ showed more activity than CAR with MICs from 2 to 32 mu/ml. In this group there is a predominance of pyocine-type groups 1 and 3. In the CARr group, AZ is the most active antibiotic at low concentrations. At 64 microgram/ml of CEF, 72% of strains are inhibited as compared to 70% with AZ, 62% with MZ and 50% with TIC. In this group there is predominance of non-typeable strains. Interaction with mecillinam (MEC) and these antibiotics was studied on three different culture media (MH, NIH and DST). There were few cases of synergism with MEC and TIC combinations, mostly on DST medium. No appreciable synergism was found with other combinations of antibiotics.
Eleven patients with 16 infections due to Enterobacteriaceae or Pseudomonas that were in most cases refractory to treatment with cephalosporins, kanamycin, gentamicin, tobramycin, carbenicillin, or ampicillin (administered singly or in combinations) received 1 g of amikacin daily by the intramuscular route (10 patients) or 0.4 g daily (one patient with renal insufficiency). The average duration of treatment was eight days. At the beginning of treatment, 18 pathogens were sensitive to amikacin at concentrations of 0.25-2 mug/ml. Of the 16 infections, 10 were cured clinically. Thirteen of the 19 pathogens isolated initially were eradicated, and five persisted during treatment but without change in in vitro sensitivity. A strain of Pseudomonas cepacia recovered from a diabetic patient and sensitive initially to 8 mug of amikacin/ml showed an eightfold increase in minimal inhibitory concentration. Superinfection with P. cepacia resistant to amikacin was noted in one case and urinary colonization with Candida albicans in another. No abnormalities of hematopoietic, hepatic, or renal function were observed in laboratory tests.
The susceptibility of current clinical isolates of Pseudomonas aeruginosa and Enterobacteriaceae to amikacin and other aminoglycosides was tested by a standardized disk sensitivity method. Minimal inhibitory concentrations (MICs) were determined for all 200 isolates tested, and mean MICs were calculated for each of 10 bacterial species. Amikacin proved to be the most effective of six aminoglycosides against nine bacterial species; isolates of Proteus morganii were slightly more sensitive to gentamicin than to amikacin. Whereas 50% of the 200 isolates could be considered resistant to gentamicin (MIC, greater than 16 mug/ml), 94.4% of the 126 enteric gram-negative bacilli and all 74 isolates of P. aeruginosa were sensitive to amikacin. At a concentration of 8 mug/ml, gentamicin inhibited 50% and tobramycin inhibited 67% of the 200 isolates. At 16 mug/ml, amikacin inhibited 96.5% of the 200 isolates; the respective figures for kanamycin, aminosidine, and streptomycin were 28.5%, 26.5%, and 24%. The virtual absence of cross-resistance between amikacin and gentamicin and between amikacin and the other four aminoglycosides was confirmed.
Twenty adult surgical patients aged between 15 and 83 years (mean:45), 10 of whom had wound infections (one complicated with septicaemia), 2 with septicaemia, 1 with gynecological infection complicated with endocarditis, 5 with urinary tract infections and 2 with lower respiratory tract infections, were treated with parentally-administered cefotaxime. Aetiology was Proteus 7, E. coli 4, Pseudomonas 3, Enterobacter 2, Klebsiella 2 and 2 Serratia. Susceptibility testing was determined by the agar dilution method, with MIC values ranging from 0.01 to 5 microgram/ml, with two urinary isolates of Pseudomonas with MIC of 20 microgram/ml. Clinical responses were excellent in 13 (65 per cent) cases, moderate in 2 (10 per cent) and 3 (15 per cent) failed to respond to therapy. Clinical assessment was not possible in three patients. Bacteriological responses were excellent in 14 (70 per cent) cases, poor in 4 (20 per cent) and in two there was no follow-up. Systemic tolerance was good in all patients except one.