A possible role of R plasmids in bacterial permeability for beta-lactam antibiotics.
Four strains of clinical isolates of Serratia marcescens (13039, 13090, 13093, 14093) harboring R plasmids were highly resistant to ampicillin (ABPC) and cephaloridine (CER). With elimination of R plasmids from these strains by acriflavine treatment, ABPC-resistance levels of these strains were markedly reduced. Reduction of CER-resistance levels was also demonstrated in strains 13039 and 13093, but not in strains 13090 and 14093. The permeability of the former strains for CER was also decreased, but not in the latter strains. At the same time, beta-lactamase activity of these strains also almost completely disappeared when the R plasmids were eliminated. By broth matings with these strains. The recipient strains of S. marcescens 13031 (rif), Escherichia coli K-12 (rif), and E coli 15046 (rif) all acquired a high permeability barrier against CER with inheritance of the R plasmids from strains 13039 and 13093, but not from strains 13090 and 14093. The transconjugant of strain 13031 that inherited R plasmid 13093 was resistant not only to CER but also to cefazolin, cephalothin, and cephalexin. Its permeability to these antibiotics was significantly lower than that of the original strain. This fact suggest the possibility that the R plasmid from strain 13093 may be involved not only in production of beta-lactamases, but also in regulation of bacterial permeability for cephalosporins.
D000667:Ampicillin / Q000494:pharmacology; D000900:Anti-Bacterial Agents / Q000502:physiology*; D018407:Bacterial Physiological Phenomena; D002509:Cephaloridine / Q000494:pharmacology; D004926:Escherichia coli; D010403:Penicillin Resistance; D010539:Permeability; D010957:Plasmids; D011815:R Factors; D012706:Serratia marcescens / Q000166:cytology; D001618:beta-Lactamases / Q000378:metabolism; D047090:beta-Lactams / Q000502:physiology
D000900:Anti-Bacterial Agents; D047090:beta-Lactams; D000667:Ampicillin; D001618:beta-Lactamases; D002509:Cephaloridine