Journal Article

Increase in <i>ampC</i> promoter strength due to mutations and deletion of the attenuator in a clinical isolate of cefoxitin-resistant <i>Escherichia coli</i> as determined by RT–PCR

Dobryan M. Tracz, David A. Boyd, Louis Bryden, Romeo Hizon, Sandra Giercke, Paul Van Caeseele and Michael R. Mulvey

in Journal of Antimicrobial Chemotherapy

Volume 55, issue 5, pages 768-772
Published in print May 2005 | ISSN: 0305-7453
Published online May 2005 | e-ISSN: 1460-2091 | DOI: http://dx.doi.org/10.1093/jac/dki074
Increase in ampC promoter strength due to mutations and deletion of the attenuator in a clinical isolate of cefoxitin-resistant Escherichia coli as determined by RT–PCR

More Like This

Show all results sharing these subjects:

  • Medical Oncology
  • Critical Care

GO

Show Summary Details

Preview

Objectives: To characterize the mechanism of cefoxitin resistance in clinical isolate Escherichia coli N99-0001.

Methods: Plasmid analysis, PCR for β-lactamases, and sequencing of the ampC genes was carried out. An RT–PCR method was developed to determine relative ampC expression.

Results: Analysis of the ampC promoter region of E. coli N99-0001 revealed a T→A mutation at −32, a C→A mutation at −11, an insertion of a T between −20 and −21, and a 28 bp deletion including the entire attenuator. RT–PCR showed that ampC was expressed 140-fold higher in E. coli N99-0001 than in E. coli ATCC 25922.

Conclusions: Cefoxitin resistance in E. coli N99-0001 was due to overexpression of ampC caused by an increase in promoter strength.

Keywords: cefoxitin resistance; E. coli; RT–PCR

Journal Article.  2478 words.  Illustrated.

Subjects: Medical Oncology ; Critical Care

Full text: subscription required

How to subscribe Recommend to my Librarian

Users without a subscription are not able to see the full content. Please, subscribe or login to access all content.