[Etiology and pathogenesis of Lyme borreliosis]

Some characteristics of B. burgdorferi which have crucial role in the pathogenesis of Lyme-borreliosis are described. The pathogenesis of Lyme-borreliosis is a complex process resulting from inflammation, release of interleukin-1, dissemination and adherence of borrelia to different tissues. Dissemination of borrelia is facilitated by the increased permeability of the blood vessels and active penetration of borrelia through the endothelial membranes. Invasion of different type of tissues emerges as a result of B. burgdorferi adherence to several types of cells and structures rather evenly distributed in human host. Immune response, normally protective, is not efficient in eradicating the organisms and can contribute to the illness by development of an autoreactive process. Autoreactivity is based on antigenic cross-reactivity between epitopes common to borrelia and human host, especially situated on so called "heat shock proteins".