BACKGROUND: Loss of sensitivity to betalactamic, quinolones and aminoglucoside antibiotics has been described during treatment of infections produced by strains of Pseudomonas aeruginosa. Sixteen nosocomial strains isolated over a year during which sensitivity to one or several antibiotics of the above mentioned groups had been lost during the course of treatment were studied. METHODS: The strains were identified by conventional techniques. Sensitivity to antibiotics was studied by determination of the minimum inhibitory concentration in solid medium, according to the guidelines of the National Committee for Clinical Laboratory Standards. Plasmidic beta-lactamases were identified by analytic isoelectric focusing. Hyperproduction of chromosomic lactamase was studied by a qualitative technique. The 0 antigens were studied against rabbit antisera. The pyocinetype was determined according to the Fyfe method. Plasmids were detected by alkaline lysis extraction and electrophoresis in agarose gel. RESULTS: The 16 strains in which changes in sensitivity were observed during the course of treatment represent 4.47% of all P. aeruginosa isolates during one year. Loss of sensitivity to betalactamic antibiotics was observed in 10 strains, in one to aminoglucosides, in two to ciprofloxacin, simultaneously to aminoglucosides and ciprofloxacin in one and to betalactamic and ciprofloxacin in another two. Six of the 13 patients (46%) required a change in antibiotic treatment. CONCLUSIONS: The convenience of following the sensitivity of the strains of Pseudomonas aeruginosa isolated in a patients is suggested to thereby avoid therapeutic failure and the potential danger of clonal dissemination of the strains which have lost sensitivity.
BACKGROUND: Loss of sensitivity to betalactamic, quinolones and aminoglucoside antibiotics has been described during treatment of infections produced by strains of Pseudomonas aeruginosa. Sixteen nosocomial strains isolated over a year during which sensitivity to one or several antibiotics of the above mentioned groups had been lost during the course of treatment were studied. METHODS: The strains were identified by conventional techniques. Sensitivity to antibiotics was studied by determination of the minimum inhibitory concentration in solid medium, according to the guidelines of the National Committee for Clinical Laboratory Standards. Plasmidic beta-lactamases were identified by analytic isoelectric focusing. Hyperproduction of chromosomic lactamase was studied by a qualitative technique. The 0 antigens were studied against rabbit antisera. The pyocinetype was determined according to the Fyfe method. Plasmids were detected by alkaline lysis extraction and electrophoresis in agarose gel. RESULTS: The 16 strains in which changes in sensitivity were observed during the course of treatment represent 4.47% of all P. aeruginosa isolates during one year. Loss of sensitivity to betalactamic antibiotics was observed in 10 strains, in one to aminoglucosides, in two to ciprofloxacin, simultaneously to aminoglucosides and ciprofloxacin in one and to betalactamic and ciprofloxacin in another two. Six of the 13 patients (46%) required a change in antibiotic treatment. CONCLUSIONS: The convenience of following the sensitivity of the strains of Pseudomonas aeruginosa isolated in a patients is suggested to thereby avoid therapeutic failure and the potential danger of clonal dissemination of the strains which have lost sensitivity.