High Expression of Chromosomal Dihydrofolate Reductase in Campylobacter Is Related to Its Trimethoprim Resistance

  • Amera Gibreel
  • Ola Sköld


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


Nalidixic Acid Dihydrofolate Reductase Parent Isolate Trimethoprim Resistance Antifolate Resistance 
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Copyright information

© Springer Science+Business Media New York 1996

Authors and Affiliations

  • Amera Gibreel
    • 1
  • Ola Sköld
    • 1
  1. 1.Division of Microbiology, Department of Pharmaceutical BiosciencesUppsala UniversityUppsalaSweden

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