Induction of streptomycin uptake in resistant strains of Escherichia coli.
Different streptomycin-resistant strains of Escherichia coli, including an R100 plasmid-carrying strain of E. coli W3110, the ribosomally resistant mutant SM10, and the spontaneous revertant from dependence to independence d1023, exhibited poor accumulation capacity for aminoglycoside antibiotics. This was due to a failure of these mutants to induce the general polyamine transport system that is utilized by streptomycin to enter the cell. It is shown that the aminoglycoside kanamycin, which is effective on these streptomycin-resistant strains, was capable of inducing the uptake of streptomycin, thus giving rise to streptomycin accumulation up to wild-type levels. Plasmid-determined resistance, which has been speculated to be the result of a blockage of the uptake system by modified antibiotic molecules, cannot be overcome by the induction of streptomycin transport. Increase in permeability of the antibiotic does not affect the susceptibility of the bacteria. It is shown that all of the antibiotic taken up was enzymatically modified. R-plasmid-conferred resistance to aminoglycosides is therefore explained by the inactivation of the antibiotic entering the bacterial cell.
D004352:Drug Resistance, Microbial; D004926:Escherichia coli / Q000254:growth & development / Q000378:metabolism*; D013307:Streptomycin / Q000378:metabolism* / Q000494:pharmacology; D013997:Time Factors
D013307:Streptomycin