[POPULATION MORBIDITY BY INFECTIONS TRANSMITIED VIA IXODES PER- SULCATUS IN THE NORTH AND SOUTH OF IRKUTSK REGION].

AIM: Evaluate the degree of epidemic risk of emergence of tick-borne encephalitis (TBE) and ixodes ticks' borreliosis (ITB) in municipalities (MPs) of Irkutsk region with various natural- climate conditions. MATERIALS AND METHODS: Morbidity was compared for TBE and ITB during 2001 - 2015 in MPs of Irkutsk region located, to the north or south of the 55th parallel, i.e. in the con- ditions of different severity of sharply continental climate. 5-year average data were analyzed. RESULTS: ITB morbidity was 2 - 3 times higher than TBE for all the 5-year periods in the north of the region, whereas in the south -differences were not present. Moreover, in MPs located to the north of the 55th parallel in 2001 - 2015 a decrease of TBE and ITB morbidity did not occur, as in the south of the region. CONCLUSION: The lack of population morbidity reduction by TBE and ITB in the north and prevalence of the latter nosoform requires enhancement of a complex of prophylaxis measures in these MPs with an accent in development of non-specific means, includ- ing acaricidic treatment, enhancement of operations of centers of express diagnostics of transmissible infections, familiarizing of the population with the use of protective suits during periods of high activity of ticks.

Interleukin 10 protects the brain microcirculation from spirochetal injury.

Spirochetal infections are an important cause of neurological disease. In previous studies of the pathogenesis of spirochetal brain infection, mice inoculated with Borrelia turicatae, an agent of tick-borne relapsing fever in North America, developed mild meningitis and parenchymal activation/infiltration by interleukin 10 (IL-10)-producing microglia/macrophages. Here, we investigated the neuroprotective effects of IL-10 during spirochetal infection by comparing the outcomes of B. turicatae infection in wild-type and IL-10-deficient RAG2-deficient mice. Mice were infected with either serotype 1 (Bt1), which causes more brain infection but lower bacteremia, or Bt2, which causes less brain infection but higher bacteremia. Interleukin 10 deficiency resulted in early death from subarachnoid/intraparenchymal brain hemorrhage in Bt2-infected mice. These mice had marked apoptosis of brain microvascular endothelial cells as assessed by terminal transferase-mediated DNA nick end-labeling staining. In contrast, Bt1 infection caused milder subarachnoid hemorrhage. Neuronal apoptosis was observed in mice infected with both serotypes and was prominent in the cerebellum. Neutralization of tumor necrosis factor prevented death and reduced morbidity and brain injury in mice infected by both serotypes. We conclude that IL-10 plays a critical role protecting the cerebral microcirculation from spirochetal injury possibly by inhibition effects of tumor necrosis factor.