Isolation and characterization of isoniazid-resistant mutants of Mycobacterium smegmatis and M. aurum.
INH-resistant mutants of Mycobacterium aurum and M. smegmatis were isolated and characterized in an attempt to provide fresh insight into the activity of isoniazid (INH), a key antibiotic in the treatment of tuberculosis. In both cases, high levels of resistance were accompanied by slower growth rate, by loss of peroxidase and reduced catalase activities, although mycolic acid production was unaffected. A gene homologous to the katG gene of M. tuberculosis, encoding peroxidase-catalase, was detected in wild-type and INH-resistant strains and it appears that INH resistance may stem from the loss of its product.
Heym
B
B
Laboratoire de Génétique moléculaire bactérienne, Institut Pasteur, Paris.
Cole
S T
ST
D002374:Catalase / Q000378:metabolism; D002855:Chromatography, Thin Layer; D004352:Drug Resistance, Microbial; D004591:Electrophoresis, Polyacrylamide Gel; D066298:In Vitro Techniques; D007538:Isoniazid / Q000494:pharmacology*; D007612:Kanamycin / Q000494:pharmacology; D016296:Mutagenesis; D009161:Mycobacterium / Q000187:drug effects / Q000201:enzymology / Q000254:growth & development / Q000302:isolation & purification*; D009171:Mycolic Acids / Q000032:analysis; D010544:Peroxidases / Q000378:metabolism; D012293:Rifampin / Q000494:pharmacology; D013307:Streptomycin / Q000494:pharmacology
D009171:Mycolic Acids; D007612:Kanamycin; D010544:Peroxidases; D002374:Catalase; D007538:Isoniazid; D012293:Rifampin; D013307:Streptomycin