Open AccessMolecular genetic analysis of cephalosporinase production and its role in beta-lactam resistance in clinical isolates of Enterobacter cloacae
Author(s) -
M. H. Nicolas,
Nadine Honoré,
Vincent Jarlier,
A. Philippon,
Stewart T. Cole
Publication year - 1987
Publication title -
antimicrobial agents and chemotherapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.07
H-Index - 259
eISSN - 1070-6283
pISSN - 0066-4804
DOI - 10.1128/aac.31.2.295
Subject(s) - enterobacter cloacae , escherichia coli , biology , gene , microbiology and biotechnology , moxalactam , strain (injury) , enterobacteriaceae , plasmid , enterobacter , enterobacter aerogenes , overproduction , cephalosporin , antibiotics , genetics , anatomy
Two strains of Enterobacter cloacae were isolated from a patient before (strain MHN1) and during (strain MHN2) treatment with moxalactam and gentamicin. Strain MHN1 exhibited inducible ampC cephalosporinase production. In contrast, strain MHN2 expressed the enzyme constitutively at a 3,000-fold higher level. With the Escherichia coli ampC gene as a hybridization probe it was shown that the genomic arrangement of the ampC region was the same in both strains. To gain more insight into regulatory phenomena, the ampC genes were cloned, and their expression was studied in E. coli K-12. The ampC gene from MHN1 behaved normally and conferred inducible beta-lactam resistance. A regulatory region of at least 800 base pairs involved in controlling repression-induction was located immediately upstream of ampC. Surprisingly, when present in E. coli the ampC gene from MHN2 no longer overproduced the cephalosporinase, and inducible expression was observed. This indicates that in MHN2 stable cephalosporinase overproduction is controlled by another factor which is not linked to the ampC gene.