Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 34-42 |
| Number of pages | 9 |
| Journal | Journal of Infectious Diseases |
| Volume | 146 |
| Issue number | 1 |
| DOIs | |
| State | Published - 1982 |
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All Science Journal Classification (ASJC) codes
- Infectious Diseases
- Immunology and Allergy
- Immunology
- Public Health, Environmental and Occupational Health
Cite this
Resistance to cefamandole : Derepression of f3-lactamases by cefoxitin and mutation in enterobacter cloacae. / Gootz, Thomas D.; Sanders, Christine C.; Goering, Richard V.
In: Journal of Infectious Diseases, Vol. 146, No. 1, 1982, p. 34-42.Research output: Contribution to journal › Article
}
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.
PY - 1982
Y1 - 1982
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.
UR - http://www.scopus.com/inward/record.url?scp=0019954958&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0019954958&partnerID=8YFLogxK
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 -