[Acquisition of antibiotic-resistance in bacteria by alteration of molecular target, or by the decreased permeability].
The target of an antibiotic is any essential enzyme for bacterial growth and quantitative or qualitative alteration of the enzyme or its substrate may cause resistance to the drug. Thus, the alteration of DNA gyrase and/or topoisomerase IV may result in resistance to fluoloquinolones, and alteration of beta-subunit of RNA polymerase may cause rifampicin-resistance. The cell wall synthesizing enzymes which cross-bridge peptidoglycan units are called PBPs and their alteration cause resistance to beta-lactams, and the alteration of the substrate D ala-D ala to D ala-D lactate causes vancomycin-resistance. In other drug-resistances, various instances of alteration of enzymes are known. Drug-resistances are also brought about by decreased permeability of the drug. Some instances are described.
Hashimoto
H
H
Kitasato Institute.
D000900:Anti-Bacterial Agents / Q000493:pharmacokinetics* / Q000494:pharmacology; D001419:Bacteria / Q000201:enzymology* / Q000378:metabolism; D002463:Cell Membrane Permeability; D027101:DNA Topoisomerase IV; D004250:DNA Topoisomerases, Type II / Q000235:genetics; D012321:DNA-Directed RNA Polymerases / Q000235:genetics; D004352:Drug Resistance, Microbial / Q000235:genetics; D009154:Mutation
D000900:Anti-Bacterial Agents; D012321:DNA-Directed RNA Polymerases; D027101:DNA Topoisomerase IV; D004250:DNA Topoisomerases, Type II