Abstract
One mechanism for generation of multiple antibiotic resistance in enteric bacteria involves the global regulatory system marRAB. The operon, when induced, encodes for resistance to structurally and functionally unrelated antibiotics. Exposure of Escherichia coli O157:H7 to increasing levels of chloramphenicol (CHL) resulted in survival of mutants that were resistant to the inducing agent and to tetracycline (TET), nalidixic acid (NAL), and ciprofloxacin (CIP). A mutant (RU122) that lacks MarR, the transcriptional repressor of the multiple antibiotic resistance ( mar) operon, served as a genetic tool to study the role of MarR in growth of E. coli O157:H7. No significant difference ( P>0.05) was observed in growth curves of the wild-type or the mutant under the conditions examined (rich and minimal media, acidic conditions, and temperatures from 24 to 42 C). A preconditioned mutant (indRU122; cultured for 17 h in Luria–Bertani (LB) containing chloramphenicol and then examined) exhibited greater growth under all treatments tested compared to the mutant. marCRAB of E. coli O157:H7 was sequenced and compared to other known mar sequences to determine divergence from other bacteria ( Salmonella, Klebsiella, and Enterobacter).
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