| Autor: |
Skripchenko EY; Children's Research and Clinical Center for Infectious Diseases, St. Petersburg, Russia.; Saint Petersburg State Pediatric Medical University, St. Petersburg, Russia., Ivanova GP; Clinical Hospital «Russian Railways-Medicine», St. Petersburg, Russia., Skripchenko NV; Children's Research and Clinical Center for Infectious Diseases, St. Petersburg, Russia.; Saint Petersburg State Pediatric Medical University, St. Petersburg, Russia., Egorova ES; Children's Research and Clinical Center for Infectious Diseases, St. Petersburg, Russia. |
| Abstrakt: |
The analysis of publications on the websites PubMed, ClinicalKey, devoted to the pathogenesis of neuroborreliosis (NB), using keywords for search: «pathogenesis of neuroborreliosis», «neuroborreliosis in children», «pathogenesis of Lyme disease», as well as an analysis of the results of the published research results of the staff of the Research Institute of Pediatric Infections, St-Petersburg, Russia is presented. Syndromes of early and late NB are more often observed among the forms without migrating erythema, and their development can be caused by all representatives of the species B. burgdorferi s.l. ( B.b. ), but more often - B. garinii , since it most effectively suppresses the factors of innate and adaptive immune response, reducing interferon production, phagocytosis and complement synthesis. The cause of immunosuppression with the development of NB may be simultaneous infection with several genovids and borrelia species or pathogens of other infections transmitted by Ixodes ticks, for example, infection with B.b. and tick-borne encephalitis virus. The ability to move along peripheral nerves, the change of surface antigens of the VlsE protein, as well as the formation of atypical cysts and granular forms allows B.b. to affect different structures of the peripheral and central nervous system, avoid an immune response and persist for a long time, causing chronic neuroinfection. Both the B.b. themselves, capable of being outside and inside glial cells and neurons, and inflammatory reactions developing in response to their introduction and associated with the synthesis of cytokines and chemokines and mimicry, cause damage to the vascular endothelium, vasculitis and impaired blood supply to the brain, demyelination, autoimmune inflammation and degeneration, leading to the development of NB syndromes, the spectrum of which varies depending on the duration of neuroinfection. In the development of NB and its outcomes, the following are also important: early initiation of treatment, the effectiveness of antibacterial drugs, the use of immunotropic agents that optimize the patient's immune response to the fight against neuroinfection, as well as the timely use of pathogenetic drugs, such as Cytoflavin, which have a complex effect on the vascular endothelium. |
