B. Sharma, A. Brown, K. Lewis;
Northeastern Univ., Boston, MA
Lyme disease, caused by the spirochete Borrelia burgdorferi, is the most common vector-borne infection in North America and Europe. In 10-20% of cases, patients develop chronic Lyme disease after completing antibiotic treatment. The cause of these chronic symptoms is, however, poorly understood. We have previously shown that high-persister mutants are selected for over the course of relapsing chronic infections of Pseudomonas aeruginosa in cystic fibrosis patients and Candida albicans in oral thrush patients. It seems likely that these high persister mutants may contribute to the recalcitrance of the infection. Persister cells are drug-tolerant phenotypic variants of normal cells and may cause recurrent bacterial infections by resuming growth once antibiotic treatment has ceased. We hypothesize that persister cells play a role in the treatment failure that leads to chronic Lyme disease. Here, using time-dependent and dose dependent survival assays, we show that B. burgdorferi forms persister cells to the antibiotics commonly used for treatment of Lyme disease. Our results indicate that in a B.burgdorferi population, 0.001% to 1% of the cells can survive lethal doses of various antibiotics in vitro. These persister cells may contribute to treatment failure in chronic Lyme patients. Future experiments are aimed at screening for a better antimicrobial therapy to eradicate persisters in B. burgdorferi.