Abstract
The mechanism of tetracycline resistance mediated by R931 (a Pseudomonas aeruginosa R factor not yet successfully transferred to Escherichia coli recipients) was examined. In strain 931 (R931) (minimal inhibitory concentration [MIC] 200 μg/ml) significant tetracycline uptake did not occur until 100 μg of tetracycline per ml was included in uptake studies. The introduction of R931 into strain 280 resulted in a significant decline in 3H-tetracycline uptake. In both strains 931 (R931) and 280 (R931), a further reduction in tetracycline uptake resulted from pre-incubation with 1 μg of tetracycline per ml. Tetracycline resistance in R−P. aeruginosa strains 1731, 1885, and 494, considered to be of chromosomal origin, was associated with a lack of tetracycline uptake until the MIC of the strain was obtained. No evidence of tetracycline inactivation or ribosomal resistance was detected in R− or R+ strains. The MIC for R− strains was generally about 25 μg/ml and that for R+ strains was 75 to 200 μg/ml.
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