The bacteria that cause Lyme disease are able to trick the immune system into not launching a full-blown immune response or developing lasting immunity to the disease, a new study with mice shows.
The discovery may explain why some people remain vulnerable to repeat infections by the same strain of bacteria, especially in regions where Lyme disease is prevalent.
The findings also suggest that blood tests may not be an effective way to detect previous exposure to Lyme disease, by far the most common vector-borne disease in the United States and Europe.
“We demonstrated that an animal infected with Borrelia burgdorferi, the corkscrew-shaped bacteria that cause Lyme disease, launches only a short-lived immune response, and that protective immunity against repeat infections quickly wanes,” says Nicole Baumgarth, professor in the School of Veterinary Medicine and an authority on immune response to infectious diseases at the Center for Comparative Medicine at University of California, Davis.
“This study also suggests a possible mechanism responsible for the disappearance of antibodies following infection and subsequent treatment with antibiotics,” she says.
The Borrelia burgdorferi bacteria are transmitted to humans and animals through bites from infected ticks. Symptoms of the disease include fever, headache, fatigue, and a characteristic skin rash. If left untreated, the infection can spread to the joints, heart, and nervous system. About 300,000 cases of Lyme disease are diagnosed annually in the United States.
The bacteria initially trigger a strong immune response in an infected animal, but findings from this study, published in PLOS Pathogens, indicate that the bacteria soon cause structural abnormalities in “germinal centers”—sites in lymph nodes and other lymph tissues that are key to producing a long-term protective immune response.
For months after infection, those germinal centers fail to produce the specific cells—memory B cells and antibody-producing plasma cells—that are crucial for producing lasting immunity.
In effect, the bacteria prevent the animal’s immune system from forming a “memory” of the invading bacteria and launching a protective immune response against future infections.
Further, following Borrelia burgdorferi infection, the process even prevented induction of strong immune responses to an influenza infection.
The National Institutes of Health and National Institute for Allergy and Infectious Diseases funded the work.
Source: UC Davis