High Expression of Chromosomal Dihydrofolate Reductase in Campylobacter Is Related to Its Trimethoprim Resistance
The antifolate agent trimethoprim is not used in the clinical treatment of infections with Campylobacter spp. because pathogenic strains of these bacteria are regarded as endogenously resistant to pharmacokinetic concentrations of this drug.5 This property of innate resistance could be explained in several ways. One is the occurrence, in pathogenic strains, of plasmid-borne genes expressing insensitive variants of the drug target enzyme dihydrofolate reductase. This is the most common type of resistance among clinical isolates of enterobacteria.2 Sixteen different types of these plasmid-mediated genes have presently been found.2 Another explanation of antifolate resistance in Campylobacter spp. could be an endogenous insensitivity to trimethoprim of its chromosomal dihydrofolate reductase, in much the same way as the human enzyme is insensitive, allowing selectivity in antibacterial use of the drug.2
KeywordsNalidixic Acid Dihydrofolate Reductase Parent Isolate Trimethoprim Resistance Antifolate Resistance
Unable to display preview. Download preview PDF.
- 3.Maniatis T., Fritsch E.F., and Sambrook J. (1989) Molecular cloning: a Laboratory Manual. Cold Spring Harbor Laboratory, Cold Spring Harbor, New York.Google Scholar