A novel chromosomal TEM derivative and alterations in outer membrane proteins together mediate selective ceftazidime resistance in escherichia coli

David A. Weber, Christine C. Sanders, Johan S. Bakken, John P. Quinn

Research output: Contribution to journalArticlepeer-review

33 Scopus citations

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 languageEnglish (US)
Pages (from-to)460-465
Number of pages6
JournalJournal of Infectious Diseases
Volume162
Issue number2
DOIs
StatePublished - 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.

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