DAVIS, CALIF. — Bacteria that cause Lyme disease can hide in lymph nodes, triggering immune responses not quite strong enough to kill the
infection, according to a new study from the University of California-Davis (UC-Davis).
The study may explain why some people experience repeat infections of the disease, the report states in Public Library of Science Pathogens.
"Our findings suggest for the first time that Borrelia burgdorferi, the bacteria that cause Lyme disease in people, dogs and wildlife, has developed a novel strategy for subverting the immune
response of the animals they infect," says Dr. Nicole Baumgarth of the UC-Davis Center for Comparative Medicine. "At first
it seems counter intuitive that an infectious organism would choose to migrate to the lymph nodes where it would automatically
trigger an immune response in the host animal. But B. burgdorferi has apparently struck an intricate balance that allows the bacteria to both provoke and elude the animal's immune response."
The study sought to answer why lymphadenopathy is so closely associated with Lyme disease infection. And researchers sought
to investigate the resulting immune response.
Researchers found that when mice were infected with B. burgdorferi, live spirochetes accumulated in the animals' lymph nodes. The lymph nodes responded with a strong, rapid accumulation of
B cells, according to the study. The presence of B. burgdorferi also prevented the lymph node from functioning normally. B cells accumulated in large numbers and made some specific antibodies
against B. burgdorferi, but they did not form "germinal centers," structures that are needed for the generation of highly functional and long-lived
"Overall, these findings suggest that B. burgdorferi hinder the immune system from generating a response that is fully functional and that can persist and protect after repeat
infections," Baumgarth says. "Thus, the study might explain why people living in endemic areas can be repeatedly infected
with these disease-causing spirochetes."
Other members of the research team included Drs. Stephen Barthold, director of the Center for Comparative Medicine; Emir Hodzic,
director of the Real-Time PCR Research and Diagnostics Core Facility; staff scientist Sunlian Feng; graduate student Christine
Hastey; and Stefan Tunev, formerly of the Center for Comparative Medicine and now at Medtronic Inc. Funding was provided by
the National Institutes of Health.