國家衛生研究院 NHRI:Item 3990099045/1989

NHRI > National Institute of Infectious Diseases and Vaccinology > Leung-Kei Siu > Periodical Articles > Item 3990099045/1989

Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/1989

Title:	High-level expression of AmpC beta-lactamase due to insertion of nucleotides between-10 and-35 promoter sequences in Escherichia coli clinical isolates: Cases not responsive to extended-spectrum-cephalosporin treatment
Other Titles:	High-Level Expression of AmpC ß-Lactamase Due to Insertion of Nucleotides between -10 and -35 Promoter Sequences in Escherichia coli Clinical Isolates: Cases Not Responsive to Extended-Spectrum-Cephalosporin Treatment
Authors:	Siu, LK;Lu, PL;Chen, JY;Lin, FM;Chang, SC
Contributors:	Division of Clinical Research
Abstract:	Two Escherichia coli isolates were recovered from the blood of two cancer patients and were demonstrated to produce high levels of the AmpC beta-lactamase with isoelectric points of >9.0. The hypertranscription of ampC RNA was observed by Northern blot hybridization in both isolates. One isolate (isolate EC44) had a point mutation (G-->A at position -28) and insertion of thymidine between positions -20 and -19 of the ampC promoter gene (GenBank accession no. AE000487). The single nucleotide insertion of T between positions -19 and -20 created an optimal distance (17 bp) in the Pribnow box for ampC hyperproduction. The other isolate (isolate EC38) had two point mutations (G-->A at position -28 and C-->T at position +58) and a 2-base (GT) insertion between positions -14 and -15. Although the insertion of GT between positions -14 and -15 may create a new promoter next to the original promoter, cloning of the ampC region with truncated nucleotides of the original -35 region of EC38 failed to verify the hypothesis that a new promoter would be created by such a nucleotide insertion. Instead, multiple start sites for ampC transcription at -1, +1, +2, and +3 were observed in an S1 nuclease protection assay. These results suggest that the RNA polymerase is flexible in the selection of a start site in ampC hypertranscription. In conclusion, nucleotide insertions between the -35 and -10 ampC promoter sequences was the mechanism for the hyperproduction of AmpC P-lactamase and resistance to oxyimino-cephalosporins. The failure of the two patients to respond to treatment with oxyimino-cephalosporins highlights the important role of such a resistance mechanism in the clinical setting.
Keywords:	Microbiology;Pharmacology & Pharmacy
Date:	2003-07
Relation:	Antimicrobial Agents and Chemotherapy. 2003 Jul;47(7):2138-2144.
Link to:	http://dx.doi.org/10.1128/AAC.47.7.2138-2144.2003
JIF/Ranking 2023:	http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0066-4804&DestApp=IC2JCR
Cited Times(WOS):	https://www.webofscience.com/wos/woscc/full-record/WOS:000183786700012
Cited Times(Scopus):	http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0038338397
Appears in Collections:	[Leung-Kei Siu] Periodical Articles

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