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JAC Advance Access originally published online on May 12, 2005
Journal of Antimicrobial Chemotherapy 2005 56(1):251-252; doi:10.1093/jac/dki149
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© The Author 2005. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oupjournals.org

Correspondence

Hyperproduction of AmpC ß-lactamase in a clinical isolate of Escherichia coli associated with a 30 bp deletion in the attenuator region of ampC

Felipe Fernández-Cuenca1,*, Alvaro Pascual1 and Luis Martínez-Martínez2

1 Department of Microbiology, University Hospital Virgen Macarena and School of Medicine, University of Seville, Apdo. 914, 41009 Seville, Spain; 2 Service of Microbiology, University Hospital Marqués de Valdecilla, Santander, Spain

* Corresponding author. Tel: +34-954-552-862; Fax: +34-954-377-413; Email: felipefc@us.es

Keywords: E. coli , AmpC , mutations , antimicrobial resistance

The first 10% of the full text of this article appears below.

Sir,

The expression of the chromosomally encoded AmpC ß-lactamase of Escherichia coli is not inducible, because of the absence of the regulatory gene ampR. The ampC gene of E. coli is regulated by a weak promoter and a transcriptional attenuator. Hyperproduction of AmpC can arise by gene amplification of ampC or mutations at either the promoter . . . [Full Text of this Article]


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