Skip Navigation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (19)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Heikkilä, E.
Right arrow Articles by Huovinen, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Heikkilä, E.
Right arrow Articles by Huovinen, P.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Journal of Antimicrobial Chemotherapy (1990) 25, 275-283
© 1990 The British Society for Antimicrobial Chemotherapy


research-article

The emergence and mechanisms of trimethoprim resistance in Escherichia coli isolated from outpatients in Finland

Elina Heikkilä, Olli-Veikko Renkonen, Ritva Sunila, Pirkko Uurasmaa and Pentti Huovinen

Department of Medical Microbiology, University of Turku, Department of Microbiology and Immunology, University of Helsinki, National Institute of Public Health, Rovaniemi and Turku Regional Laboratories Finland

Received 1 August 1989; accepted 25 September 1989


Trimethoprim (TMP), either alone or in combination with sulphonamides, is commonly used for treating urinary tract infections. In Finland, TMP alone has been in clinical use since 1973. TMP resistance in the major outpatient urinary tract pathogen, Escherichia coli, increased during 1978–1988 from 5% to 16% in the Turku area, during 1980–1988 from 3% to 19% in the Helsinki area and also during 1980–1988 from 3% to 14% in the Rovaniemi area. The majority (91%) of TMP-resistant strains were highly-resistant to TMP (MIC ≥ 1024 mg/l). The most common (57%) TMP resistance gene, detected by DNA hybridization, was the type I dihydrofolate (DHFR) gene. The type II DHFR genes were found in less than 3% of the strains studied. No positive hybridizations were detected with the type III DHFR probe, and only a few positive hybridizations were found with the type V DHFR probe. Forty percent of the isolates did not hybridize with any of the DHFR probes used, suggesting additional unknown resistance mechanisms responsible for the high-level TMP resistance. These unknown TMP resistance mechanisms, together with the type I DHFR-mediated resistance, were responsible for the increase of TMP resistance among the E. coli strains studied.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Antimicrob. Agents Chemother.Home page
P. V. Adrian, C. J. Thomson, K. P. Klugman, and S. G. B. Amyes
New Gene Cassettes for Trimethoprim Resistance, dfr13, and Streptomycin-Spectinomycin Resistance, aadA4, Inserted on a Class 1 Integron
Antimicrob. Agents Chemother., February 1, 2000; 44(2): 355 - 361.
[Abstract] [Full Text]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.