Abstract
A clinical Escherichia coli isolate (MG32) resistant to ceftazidime but susceptible to other third-generation cephalosporins was previously examined and found to harbor TEM-1 and exhibit alterations in outer membrane proteins. Reexamination of this isolate revealed the additional presence of a novel TEM-1 derivative, now designated TEM-12. Evaluation of ceftazidime and cefotaxime minimum inhibitory concentrations for isogenic derivatives demonstrated a major role for TEM-12 in the decreased susceptibility observed. This was selectively enhanced for ceftazidime resistance by the altered porins of E. coli MG32. TEM-12 appeared identical to TEM-101, an in vitro TEM derivative, in both isoelectric point (pI 5.25) and substrate profile. Hybridization and cloning of the TEM-12 determinant revealed that, unlike other TEM derivatives, TEM-12 is chromosomally encoded, not plasmid-encoded.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 460-465 |
| Number of pages | 6 |
| Journal | Journal of Infectious Diseases |
| Volume | 162 |
| Issue number | 2 |
| DOIs | |
| State | Published - Aug 1990 |
Bibliographical note
Funding Information:Received 24 August 1989; revised 9 February 1990. Grant support: Health Future Foundation, Omaha. Reprints and correspondence: Dr. Christine C. Sanders, Department of Medical Microbiology, Creighton University School of Medicine, 2500 California St., Omaha, NE 68178. * Present address: Department of Infectious Diseases, the Duluth Clinic, Duluth, MN.
Copyright:
Copyright 2016 Elsevier B.V., All rights reserved.