Czynniki odpowiedzialne za rozwój Lyme carditis
1. Wstęp. 2. Lyme carditis – objawy, rozpoznanie i leczenie. 3. Patomechanizm zapalenia serca. 3.1. Ruch krętków. 3.2. Chemotaksja i adhezja. 3.3. Reakcje autoimmunologiczne. 4. Podsumowanie
Abstract: Borrelia burgdorferi sensu lato spirochetes are unique in many aspects. They are the etiological agents of Lyme borreliosis, meta-zoonotic, tick-borne disease of mammals, including humans. Ixodes spp. ticks are the vector. With the exception of erythema chronicum migrant (EM), manifestations of the disease may vary depending on the genospecies of Borrelia burgdorferi sensu lato. One of the symptoms is Lyme carditis. To date, the causative factors and the mechanisms of pathogenesis have not been well-described.
Borrelia burgdorferi spirochetes are considered as one of the most invasive mammalian pathogen. They are able to move through the skin, as well as break into and out of blood vessels, easily crossing the blood-brain barrier. Genes encoding various motility forms are bound with chemotaxis signaling system which leads and coordinates motion functions. The attachment of bacteria to host cells or extracellular matrix may promote colonization and disease development. Lyme disease spirochetes encode several surface proteins including decorin binding adhesion (DbpA), which varies among strains contributing to strain-specific differences in tissue tropism. The strains demonstrating the greatest decorin-binding activity promote the greatest colonization of heart and cause the most severe carditis. Moreover, the manifestation of Lyme carditis in certain hosts may be a result of an autoimmunological reaction due to molecular mimicry between B. burgdorferi and host self-components. In mammals, infection with B. burgdorferi induces the development of antibodies which may cross-react with myosin and neural tissue.
1. Introduction. 2. Lyme carditis – symptoms, recognition and treatment. 3. Patho-mechanism of Lyme carditis. 3.1. Spirochetes motility. 3.2. Chemotaxis and adhesion. 3.3. Autoimmunological reactions. 4. Summary