Resistance to chloramphenicol and metronidazole in anaerobic bacteria

This paper describes two quite different mechanisms of resistance to clinically important antimicrobial agents in anaerobic bacteria, which also represent two distinct genetic processes. The first is resistance to chloramphenicol (Cm) in Bacteroides species (in particular, Bacteroides fragilis) and Clostridium perfringens, which arises due to the enzymic inactivation of the drug by acetylation. When Cm resistance occurs in other genera, it is typically plasmid determined; it is also plasmid associated in Cm-resistant strains of Cl. perfringens (Sebald and Brfort, 1975) and B. ochraceus (Guiney and Davis, 1978). The second is resistance to a group of antimicrobial agents, the 5-nitroimidazoles, which includes metronidazole (Mz) and tinidazole (Tz). In this case, resistance in strains of B. fragilis and Cl. perfringens is associated with a change in the biochemical pathway normally involved in activation of the drugs. This is a result of a chromosomal mutation which can be induced by treatment with mutagens such as N-methyl-N'-nitro N-nitrosoguanidine (MNNG) (Britz & Wilkinson, 1979). © 1981 The British Society for Antimicrobial Chemotherapy. All Rights Reserved.