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Int J Antimicrob Agents. 2007 Dec;30(6):496-504. Epub 2007 Oct 1.

Evidence of a conjugal erythromycin resistance element in the Lyme disease spirochete Borrelia burgdorferi.

Author information

1
Antimicrobial Resistance Research Unit, ARS, SAA, USDA, Russell Research Center, Athens, GA 30602, USA.

Abstract

We report the identification of isolates of Borrelia burgdorferi strain B31 that exhibit an unusual macrolide-lincosamide (ML) or macrolide-lincosamide-streptogramin A (MLS(A)) antibiotic resistance pattern. Low-passage isolates were resistant to high levels (>100 microg/mL) of erythromycin, spiramycin and the lincosamides but were sensitive to dalfopristin, an analogue of streptogramin B. Interestingly, the high-passage erythromycin-resistant strain B31 was resistant to quinupristin, an analogue of streptogramin A (25 microg/mL). Biochemical analysis revealed that resistance was not due to antibiotic inactivation or energy-dependent efflux but was instead due to modification of ribosomes in these isolates. Interestingly, we were able to demonstrate high-frequency transfer of the resistance phenotype via conjugation from B. burgdorferi to Bacillus subtilis (10(-2)-10(-4)) or Enterococcus faecalis (10(-5)). An intergeneric conjugal system in B. burgdorferi suggests that horizontal gene transfer may play a role in its evolution and is a potential tool for developing new genetic systems to study the pathogenesis of Lyme disease.

PMID:
17905571
PMCID:
PMC2175076
DOI:
10.1016/j.ijantimicag.2007.07.013
[Indexed for MEDLINE]
Free PMC Article

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