LYME BORRELIOSIS - HOST RESPONSES TO BORRELIA-BURGDORFERI

Lyme disease is a chronic inflammatory disorder resulting from infection by the tick-borne spirochete Borrelia burgdorferi. The pathogenesis of this disease is a complex process resulting from host responses to a limited number of organisms. Once introduced into the skin at the site of a tick bite, the spirochetes disseminate to distant locations. This step involves adherence to and penetration across endothelium, a process which has been observed in vitro. The organism's ability to adhere to different eucaryotic cell types in vitro and the wide distribution of the spirochete in infected humans and experimentally infected animals lead to the conclusion that B. burgdorferi can invade successfully and remain associated with many different organs. While phagocytosis and complement activation have been observed in vitro, the specific immune response that develops in humans is inefficient in eradicating the organisms, which may possess some mechanism(s) to evade this response. There is significant evidence for host autoreactivity based on antigenic cross-reactivity between proteins of the organism and endogenous host cell components. The study of the pathogen-host interactions in this disease should increase our understanding of this chronic bacterial infection, provide insight into vaccine protocols, and improve therapeutic approaches.