Open AccessIsolation and Properties of Metronidazole-resistant Mutants of Clostridium Perfringens
Author(s) -
Peppa Sindar,
ML Britz,
R.G. Wilkinson
Publication year - 1982
Publication title -
journal of medical microbiology/journal of medical microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.91
H-Index - 117
eISSN - 1473-5644
pISSN - 0022-2615
DOI - 10.1099/00222615-15-4-503
Subject(s) - clostridium perfringens , mutant , microbiology and biotechnology , strain (injury) , biology , biochemistry , metronidazole , mutagenesis , tinidazole , nalidixic acid , lactate dehydrogenase , chemistry , enzyme , bacteria , antibiotics , tetracycline , gene , genetics , anatomy
Clostridium perfringens strains resistant to metronidazole and tinidazole were isolated from the sensitive parent strain CM288 after mutagenesis with N-methyl-N'-nitro-N-nitrosoguanidine. Strain CM288 was already resistant to rifampicin and nalidixic acid; these genetic markers helped to confirm the identity of mutants. All mutants showed similar characteristics: they grew more slowly than the parent strain and failed to reach the same maximum turbidity; uptake of metronidazole and tinidazole from culture fluids was slow and end products of glucose metabolism were different from those of the parent. Pyruvate dehydrogenase activity was not detected in broken cell preparations of the mutant strains although this enzyme was readily detected in the parent strain. Changes in end products of glucose metabolism were consistent with the absence of pyruvate dehydrogenase activity because pyruvate was accumulated during growth and lactate levels were higher whereas acetate, CO2 and ethanol levels were diminished.