Researchers Reveal Stubborn Source Behind Lyme Disease

Despite the fact that the Lyme disease-causing bacterium Borrelia burgdorferi does not show antibiotic resistance, the illness continues to prove to be difficult to fight in the late stages.

Despite the fact that the Lyme disease-causing bacterium Borrelia burgdorferi does not show antibiotic resistance, the illness continues to prove to be difficult to fight in the late stages.

Led by Kim Lewis, PhD, a team from Northeastern University discovered what they believe to be the explanation for the perplexing problem. While antibiotics usually clear Lyme disease if caught early on, about 10 to 20% of the 300,000 Americans infected every year continue to suffer with additional diagnoses such as arthritis and neurological issues.

“It hasn’t been entirely clear why it’s difficult to treat the pathogen with antibiotics since there has been no resistance reported for the causative agent of the disease,” Lewis, director of the Antimicrobial Discovery Center at Northeastern, explained in a news release.

So what is to blame for the disease’s stubbornness? Dormant persister cells.

Previous research by Lewis and team has shown this very variable was present in other chronic infections — and now they have proven its existence in B. burgdorferi. According to the study published in Antimicrobial Agents and Chemotherapy, the bacterium has the ability to form persisters. It turns out that since the cells are inactive, that serves as another shield against antibiotics.

Not only did the researchers identify the cause of the challenge, but they also presented 2 potential solutions — one of which shows promise. The first method involved the anti-cancer agent Mitomycin C, and even though it was successful, its toxicity caused the team to advise against its usage for Lyme.

“Combinations of antibiotics did not improve killing,” the study revealed. “Daptomycin, a membrane-active bactericidal antibiotic, killed stationary phase cells, but not persisters.”

The more practical route that they tested consisted of frontloading antibiotic treatment. The initial dose killed the growing cells but not the dormant ones. However, once the medication ran its course the inactive cells were awaken — allowing for the team to swoop in with another course of antibiotics and rid of the B. burgdorferi.

“This is the first time, we think, that pulse-dosing has been published as a method for eradicating the population of a pathogen with antibiotics that don’t kills dormant cells,” Lewis verified.

Furthermore, more research is needed in this area but this study revealed key understandings in the fight against Lyme disease.