TY - JOUR
T1 - Resistance to cefamandole
T2 - Derepression of f3-lactamases by cefoxitin and mutation in enterobacter cloacae
AU - Gootz, Thomas D.
AU - Sanders, Christine C.
AU - Goering, Richard V.
N1 - Funding Information:
Received for publication August 20, 1981, and in revised form March 5, 1982. This work was supported in part by Biomedical Research Support grant no. RR-05390 from the National Institutes of Health, awarded to Creighton University. Please address requests for reprints to Dr. Christine C. Sanders, Department of Medical Microbiology, Creighton University School of Medicine, Omaha, Nebraska 68178. * Present address: Department of Microbiology and Immunology, University of Washington, Seattle, Washington.
PY - 1982/7
Y1 - 1982/7
N2 - Studies were performed to characterize resistance to cefamandole in two strains of Enterobacter cloacae. Susceptible wild-type cells were exposed either to cefamandole to select stably resistant mutants or to cefoxitin to induce unstable resistance. The two types of resistant cells inactivated cefamandole, and their fJ-Iactamases had identical isoelectric focusing patterns and substrate profiles. Studies of the fJ-Iactamases of these resistant cells indicated that the enzymes belonged to the Richmond and Sykes Group I and suggested that their production in wild-type cells is under repressor control. The resistant mutants appeared to be stably derepressed at the locus for fJ-Iactamase expression, whereas cefoxitin-induced cells were reversibly derepressed wild-type cells. Transfer of plasmids from one mutant colony to recipient Escherichia coli cells did not transfer resistance. These two types of resistance to cefamandole may explain the widely discrepant results obtained during in vitro and in vivo studies, as well as the rapid emergence of resistance that has been observed during clinical use.
AB - Studies were performed to characterize resistance to cefamandole in two strains of Enterobacter cloacae. Susceptible wild-type cells were exposed either to cefamandole to select stably resistant mutants or to cefoxitin to induce unstable resistance. The two types of resistant cells inactivated cefamandole, and their fJ-Iactamases had identical isoelectric focusing patterns and substrate profiles. Studies of the fJ-Iactamases of these resistant cells indicated that the enzymes belonged to the Richmond and Sykes Group I and suggested that their production in wild-type cells is under repressor control. The resistant mutants appeared to be stably derepressed at the locus for fJ-Iactamase expression, whereas cefoxitin-induced cells were reversibly derepressed wild-type cells. Transfer of plasmids from one mutant colony to recipient Escherichia coli cells did not transfer resistance. These two types of resistance to cefamandole may explain the widely discrepant results obtained during in vitro and in vivo studies, as well as the rapid emergence of resistance that has been observed during clinical use.
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U2 - 10.1093/infdis/146.1.34
DO - 10.1093/infdis/146.1.34
M3 - Article
C2 - 6979593
AN - SCOPUS:0019954958
VL - 146
SP - 34
EP - 42
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
SN - 0022-1899
IS - 1
ER -