Lyme disease Borrelia spirochetes are naturally resistant to clinically relevant concentrations of rifampin, trimethoprim, and dapsone

Abstract

ABSTRACT A number of health care providers recommend the antibiotics rifampin, trimethoprim, and/or dapsone for treatment of Lyme disease. In opposition, previous studies found that Lyme disease-causing Borrelia are innately resistant to those antibiotics at concentrations that would be lethal to other bacterial species. To resolve those contradictions, multiple genospecies and strains of Lyme disease-causing spirochetes were assessed for their ability to grow and replicate in the presence of these drugs. For each antibiotic, the minimum concentrations necessary to prevent growth of Borrelia burgdorferi sensu stricto type strain B31 exceeded 300 µg/mL. All of the tested genospecies of Lyme disease, Borrelia , grew and replicated in the presence of 100 µg/mL or more of antibiotic. In contrast, prior studies determined that maximum serum concentrations of these antibiotics in humans and laboratory animals are less than 15 µg/mL. The current study’s results indicate that rifampin, trimethoprim, and dapsone are unlikely to have any positive effect in clearing Lyme disease-causing Borrelia infections. IMPORTANCE There are conflicting reports on the efficacy of using the antibiotics rifampin, trimethoprim, or dapsone against the Lyme disease spirochete, Borrelia burgdorferi ( sensu lato ). The present studies found that the concentration of antibiotic necessary to prevent borrelial growth and replication, alone or in combination, exceeded 200 µg/mL for all tested strains of B. burgdorferi sensu lato . In contrast, previous studies of humans and mice found that clinically relevant dosages of these antibiotics yielded maximum serum concentrations of 15 µg/mL or less. All together, these data indicate that these pharmaceuticals are not likely to be effective in curing B. burgdorferi (sl) infections.

The authors' abstract, as published at the source. Microbiology Spectrum, 2026 · DOI ↗