Re: Borelioza - atb - klidovy rezim?

Jen stručně (/Nelson, Textbook of Pediatrics, 19th edition (2011)
Part XVII - Infectious Diseases
Section 8 - Spirochetal Infections
Chapter 214 - Lyme Disease (Borrelia burgdorferi)
Pathology and Pathogenesis


Similar to other spirochetal infections, untreated Lyme disease is characterized by asymptomatic infection, clinical disease that can occur in stages, and a propensity for cutaneous and neurologic manifestations.

The skin is the initial site of infection by B. burgdorferi. Inflammation induced by B. burgdorferi leads to the development of the characteristic rash, erythema migrans. Early disseminated Lyme disease results from the spread of spirochetes through the bloodstream to tissues throughout the body. The spirochete adheres to the surfaces of a wide variety of different types of cells, but the principal target organs are skin, central and peripheral nervous system, joints, heart, and eyes. Because the organism can persist in tissues for prolonged periods, symptoms can appear very late after initial infection.

The symptoms of early disseminated and late Lyme disease are due to inflammation mediated by interleukin 1 and other lymphokines in response to the presence of the organism. It is likely that relatively few organisms actually invade the host, but cytokines serve to amplify the inflammatory response and lead to much of the tissue damage. Lyme disease is characterized by inflammatory lesions that contain both T and B lymphocytes, macrophages, plasma cells, and mast cells. The refractory symptoms of late Lyme disease can have an immunogenetic basis. Persons with certain HLA-DR allotypes may be genetically predisposed to develop chronic Lyme arthritis. An autoinflammatory response in the synovium can result in clinical symptoms long after the bacteria have been killed.