This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. This project studies the pathogenesis of Borrelia burgdorferi that causes Lyme disease, the most common vectorborne illness in North America and Europe. Over 20,000 people contract Lyme disease annually in the United States alone. Lyme disease is a multi-system disorder that can result in arthritis, neurological abnormalities, carditis and cutaneous lesions such as erythema migrans and acrodermatitis chronica atrophicans. Up to 10% Lyme disease patients may develop post-treatment Lyme syndrome, a mysterious illness that can not be cured. As a slow growing extracellular bacterium with a doubling time of approximately 8 hours in the best in vitro conditions, B. burgdorferi has a 50% infectious dose (ID50) of less than 100 organisms in the murine host, and can also cause persistent infection despite the development of vigorous immune responses against the pathogen, making itself one of the most invasive microbial pathogens in both humans and animals. The focus is on the following three aspects of the pathogenesis of B. burgdorferi. 1. How B. burgdorferi evades initial elimination by phagocytes 2. How B. burgdorferi evades specific humoral responses 3. How B. burgdorferi causes Lyme arthritis
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