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Detecting the Lyme Disease Spirochete, Borrelia Burgdorferi, in Ticks Using Nested PCR
Published on: February 4, 2018
parC mutations in fluoroquinolone-resistant Borrelia burgdorferi
Kendal M Galbraith1, Amanda C Ng, Betsy J Eggers
1Division of Biological Sciences, The University of Montana, Missoula, 59812-4824, USA.
Abstract:
We have isolated in vitro fluoroquinolone-resistant mutants of the Lyme disease agent, Borrelia burgdorferi. Mutations in parC, which encodes a subunit of topoisomerase IV, were associated with loss of susceptibility to sparfloxacin, moxifloxacin, and Bay-Y3118, but not ciprofloxacin. This is the first description of fluoroquinolone resistance in the spirochete phylum.
Insights
Researchers identified fluoroquinolone-resistant mutants of Borrelia burgdorferi, the Lyme disease bacterium. Mutations in parC were linked to resistance against certain fluoroquinolones, marking the first report in spirochetes.
Area of Science:
- Microbiology
- Genetics
- Infectious Diseases
Background:
- Borrelia burgdorferi is the causative agent of Lyme disease.
- Fluoroquinolones are a class of antibiotics used to treat bacterial infections.
Purpose of the Study:
- To investigate the mechanisms of fluoroquinolone resistance in Borrelia burgdorferi.
- To identify specific genetic mutations associated with resistance.
Main Methods:
- Isolation of in vitro fluoroquinolone-resistant mutants of Borrelia burgdorferi.
- Analysis of mutations in the parC gene, which encodes a subunit of topoisomerase IV.
Main Results:
- Mutations in parC were associated with reduced susceptibility to sparfloxacin, moxifloxacin, and Bay-Y3118.
- Ciprofloxacin efficacy was not affected by the identified parC mutations.
Conclusions:
- This study reports the first instance of fluoroquinolone resistance in the spirochete phylum.
- parC mutations are implicated in fluoroquinolone resistance in Borrelia burgdorferi.
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