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Development of antibiotic resistance in Pseudomonas aeruginosa during two decades of antipseudomonal treatment at the Danish CF Center
Author(s) -
CIOFU O.,
GIWERCMAN B.,
HØIBY N.,
PEDERSEN S. S.
Publication year - 1994
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1699-0463.1994.tb05219.x
Subject(s) - carbenicillin , microbiology and biotechnology , pseudomonas aeruginosa , piperacillin , ceftazidime , tobramycin , antibiotics , ciprofloxacin , antibiotic resistance , biology , medicine , ampicillin , gentamicin , bacteria , genetics
At the Danish CF Center patients with chronic Pseudomonas aeruginosa lung infection were treated 3–4 times a year (from 1976) with a 2‐week intravenous antipseudomonal course which included preferentially an aminoglycoside and a β‐lactam antibiotic. We investigated the development of antibiotic resistance in P. aeruginosa strains isolated from Danish CF patients over a period of 18 years by testing the in vitro efficacy of carbenicillin, piperacillin, ceftazidime, tobramycin and ciprofloxacin against P. aeruginosa strains collected in 1973 (51 strains), 1980 (80 strains), 1985 (58 strains), and 1991 (100 strains). All the strains were screened and assayed semiquantitively for β‐lactamase activity by use of nitrocefin. We found a significant (p<0.005) increase in the MIC values of the P. aeruginosa strains against piperacillin and ceftazidime. However, no significant correlation was found between the MIC and the number of antipseudomonal courses of antibiotics. The proportion of resistant in vivo selected P. aeruginosa strains, presumed to be stably derepressed producers of chromosomal β lactamase, also increased significantly during the period studied. Our results confirm that the β lactamase production is an important mechanism of antibiotic resistance in P. aeruginosa.