Trimethoprim resistance in enterococci: microbiological and biochemical aspects.
Synergy was found between sulphonamide and trimethoprim in ratios 1:1 and 20:1 against both trimethoprim-sensitive enterococci (17 strains) and trimethoprim-resistant enterococci (23 strains). Many of these strains were resistant to kanamycin, tetracycline, streptomycin and/or erythromycin. Resistance to kanamycin, but not to trimethoprim, was clearly associated with the presence of a plasmid of molecular weight 35-45 Md. Elimination of this plasmid in three out of four highly trimethoprim resistant strains brought about loss of resistance to both kanamycin and trimethoprim. Furthermore, it was possible to transfer trimethoprim resistance from three of five highly resistant strains, but not from three strains with low-grade resistance. It is concluded that resistance to trimethoprim in enterococci can be encoded on a plasmid, and that the gene responsible may be on a transposon. No significant differences were found between the specific activities of dihydrofolate reductase from trimethoprim-sensitive and -resistant strains. The enzyme from resistant strains was several orders of magnitude less susceptible to inhibition by trimethoprim than was the enzyme from sensitive strains.
Hamilton-Miller
J M
JM
Department of Medical Microbiology, Royal Free Hospital School of Medicine, London, Great Britain.
Stewart
S
S
D003227:Conjugation, Genetic; D004352:Drug Resistance, Microbial; D008826:Microbial Sensitivity Tests; D010957:Plasmids; D013291:Streptococcus / Q000187:drug effects* / Q000235:genetics; D013449:Sulfonamides / Q000494:pharmacology; D013762:Tetrahydrofolate Dehydrogenase / Q000032:analysis; D014295:Trimethoprim / Q000494:pharmacology*
D013449:Sulfonamides; D014295:Trimethoprim; D013762:Tetrahydrofolate Dehydrogenase