Mechanism of chloramphenicol-resistance mediated by kR102 factor in Pseudomonas aeruginosa.
The chloramphenicol (CP)-resistance mechanism of five-drug-resistant R factor (kR102) of Pseudomonas aeruginosa K-Ps 102 derived from a clinical specimen was investigated. Neither inactivation by acetyltransferases of CP nor induced resistance by CP was recognized. Reduced affinity of the ribosome to the drug was not seen in the result of incorporation experiment of 14C-valine by phage f2 RNA and risosome of K-Ps 102. However, on spheroplasts by glycine treatment, remarkable increase of CP susceptibility was observed. From the above evidence, it was considered that the CP-resistance barrier controlled by kR102 factor would be in the cell wall and the surface layer of cytoplasma and that the mechanism of CP-resistance was possibly by decreased membrane permeability of CP. However, the susceptibility to CP of the susceptible strain still increased by the formation of spheroplasts. Consequently, it was considered that R factor might be controlling the function of membrane permeability of the cells.
D000123:Acetyltransferases / Q000378:metabolism; D002474:Cell-Free System; D002701:Chloramphenicol / Q000494:pharmacology*; D003470:Culture Media; D004352:Drug Resistance, Microbial / Q000187:drug effects*; D008826:Microbial Sensitivity Tests; D011550:Pseudomonas aeruginosa / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D011815:R Factors / Q000187:drug effects*; D013104:Spheroplasts / Q000187:drug effects; D014633:Valine / Q000378:metabolism
D003470:Culture Media; D002701:Chloramphenicol; D000123:Acetyltransferases; D014633:Valine