Abstract
Stable resistance to metronidazole in a nontoxigenic Clostridium difficile strain was investigated at both the genomic and proteomic levels. Alterations in the metabolic pathway involving the pyruvate-ferredoxin oxidoreductase were found, suggesting that reduction of metronidazole, required for its activity, may be less efficient in this strain. Proteomic studies also showed a cellular response to oxidative stress.
Copyright © 2014, American Society for Microbiology. All Rights Reserved.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Anti-Infective Agents / metabolism
-
Anti-Infective Agents / pharmacology
-
Bacterial Proteins / genetics
-
Bacterial Proteins / metabolism*
-
Clostridioides difficile / classification
-
Clostridioides difficile / drug effects
-
Clostridioides difficile / enzymology*
-
Clostridioides difficile / genetics*
-
Drug Resistance, Bacterial / genetics*
-
Enterocolitis, Pseudomembranous / drug therapy
-
Enterocolitis, Pseudomembranous / microbiology
-
Gene Expression
-
Genome, Bacterial*
-
Humans
-
Metabolic Networks and Pathways / genetics
-
Metronidazole / metabolism
-
Metronidazole / pharmacology
-
Microbial Sensitivity Tests
-
Oxidative Stress
-
Phylogeny
-
Proteomics
-
Pyruvate Synthase / genetics
-
Pyruvate Synthase / metabolism*
-
Ribotyping
Substances
-
Anti-Infective Agents
-
Bacterial Proteins
-
Metronidazole
-
Pyruvate Synthase