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Background  Trimethoprim resistance is increasing in  Enterobacteriaceae . In 2004-2006 an intervention on trimethoprim use was conducted in Kronoberg County, Sweden, resulting in 85% reduction in trimethoprim prescriptions. We investigated the distribution of  dihydrofolate reductase  ( dfr )-genes and integrons in  Escherichia coli  and  Klebsiella pneumoniae  and the effect of the intervention on this distribution.    Methodology/Principal Findings  Consecutively isolated  E. coli  (n = 320) and  K. pneumoniae  (n = 54) isolates phenotypicaly resistant to trimethoprim were studied. All were investigated for the presence of  dfrA1, dfrA5, dfrA7, dfrA8, dfrA12, dfrA14, dfrA17  and integrons class I and II. Isolates negative for the seven  dfr -genes (n = 12) were also screened for  dfr2d ,  dfrA3 ,  dfrA9 ,  dfrA10 ,  dfrA24  and  dfrA26 . These genes accounted for 96% of trimethoprim resistance in  E. coli  and 69% in  K. pneumoniae . The most prevalent was  dfrA1  in both species. This was followed by  dfrA17  in  E. coli  which was only found in one  K. pneumoniae  isolate. Class I and II Integrons were more common in  E. coli  (85%) than in  K. pneumoniae  (57%). The distribution of  dfr -genes did not change during the course of the 2-year intervention.    Conclusions/Significance  The differences observed between the studied species in terms of  dfr- gene and integron prevalence indicated a low rate of  dfr- gene transfer between these two species and highlighted the possible role of narrow host range plasmids in the spread of trimethoprim resistance. The stability of  dfr -genes, despite large changes in the selective pressure, indirectly suggests a low fitness cost of  dfr -gene carriage.

Molecular Characterisation of Trimethoprim Resistance in Escherichia coli and Klebsiella pneumoniae during a Two Year Intervention on Trimethoprim Use