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 (8)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Richard, R.M.E.
Right arrow Articles by Marshall, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Richard, R.M.E.
Right arrow Articles by Marshall, D.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Journal of Antimicrobial Chemotherapy (1995) 36, 607-618
© 1995 The British Society for Antimicrobial Chemotherapy

other

Mechanism of sulphadiazine enhancement of trimethoprim activity against sulphadiazine-resistant Enterococcus faecalis

R.M.E. Richarda, J. Z. Xinga, D. W. Gregoryb and D. Marshallb

aSchool of Pharmacy The Robert Gordon University, Schoolhill, Aberdeen AB9 1FR bDepartment of Medical Microbiology Medical School Buildings, Foresterhill, Aberdeen AB92ZD, UK

returned 24 March 1995; accepted 9 May 1995

Sulphadiazine had little or no antibacterial effect against three strains of Enterococcus faecalis (MICs of above 3600 mg/L) but it caused approximately six-fold increases in bacterial uptake of trimethoprim, increased release of bacterial ATP and produced ultrastructural damage to both the trimethoprim resistant E. faecalis 463 and the trimethoprim sensitive NCTC 5957. MICs of trimethoprim were 0.6, 0.8 and 76.8 mg/L for E. faecalis NCTC 775, NCTC 5957 and 463 respectively. When log phase E. faecalis 463 and NCTC 5957 were grown for 4 h in trimethoprim 56 and 0.6 mg/L plus sulphadiazine 320 and 100 mg/L respectively there was an approximate ten-fold and nine-fold increase in uptake of sulphadiazine and a two-fold increase in leakage of ATP. Trimethoprim caused more damage to the cell wall and cytoplasmic membrane than sulphadiazine but the combination of sulphadiazine plus tnmethoprim caused the most cell damage. The increased activity observed with the combination seems very likely to have resulted from the increased uptakes of the antibacterials, which in turn had resulted from the cell wall damage and consequent increased cell permeability caused by each antibacterial. It is proposed that a markedly subinhibitory concentration of sulphadiazine enhanced the antibacterial activity of trimethoprim against all three strains of E. faecalis by this mechanism.


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
 J Med MicrobiolHome page
C. J. Ingham, M. van den Ende, P. C. Wever, and P. M. Schneeberger
Rapid antibiotic sensitivity testing and trimethoprim-mediated filamentation of clinical isolates of the Enterobacteriaceae assayed on a novel porous culture support.
J. Med. Microbiol., November 1, 2006; 55(Pt 11): 1511 - 1519.
[Abstract] [Full Text] [PDF]

Home page
 J Antimicrob ChemotherHome page
P. Minkowski, H. Staege, P. Groscurth, and A. Schaffner
Effects of trimethoprim and co-trimoxazole on the morphology of Listeria monocytogenes in culture medium and after phagocytosis
J. Antimicrob. Chemother., August 1, 2001; 48(2): 185 - 193.
[Abstract] [Full Text] [PDF]


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.