[EPIDEMIOLOGIC SITUATION BY NATURAL-FOCI INFECTIONS IN THE CRIMEA FEDERAL DISTRICT IN 2014-2015].

AIM: Analysis of epidemic manifestations of natural-foci infections (NFI), clarification of spectrum of their causative agents, determination of epizootic activity of natural foci in the Crimea Federal District (KFD). MATERIALS AND METHODS: Epizootologic examination of 10 administrative districts of KDF was carried out. 291 pools (2705 specimens) of ixodes ticks and 283 samples of organs of small mammals were studied by PCRmethod for the presence of DNA/RNA of causative agents of a number of NFI. RESULTS: Morbidity by NFI in KFD was registered by 6 nosologies: Lyme borreliosis, Marseilles fever, leptospirosis; tularemia, intestine yersiniosis and tick-borne viral encephalitis, wherein, transmissive infections made up 91.6%. Circulation of causative agents of Crimea hemorrhagic fever, Q fever, group of tick-borne spotted fever, Lyme borreliosis, human granulocytic anaplasmosis, human monocytic ehrlichiosis, hemorrhagic fever with renal syndrome, West Nile fever, tularemia and leptospirosis was established. CONCLUSION: Due to activity of natural foci of NFI further monitoring of epidemiologic and epizootologic manifestations of these infections in the Crimea, including using genetic methods of analysis, is necessary for ensuring sanitary-epidemiologic welfare of KFD population.

[Rotavirus: an ubiquitous infection?]. / Rotavirus: une infection ubiquitaire?

Rotavirus is the most frequent virus found in childhood gastroenteritis. A rotavirus viremia is observed in 19 to 63 % of cases, for three days at the beginning of infection. Then, rotavirus can reach several organs as liver (hepatitis in 1/3 of case), nervous central system (2 % of encephalitis could be linked to rotavirus), or more infrequently mesenteric lymph nodes, lung or heart. However, the link between rotavirus and systemic manifestations has not been well established. Further studies are necessary to confirm the role of rotavirus in these organ's lesions.

[The role of focal infections in the pathogenesis of diseases]. / A gócok szerepe a betegségek kialakulásában.

Focal infections have a definite role in various infectious complications. They may cause local propagation, systemic infection (sepsis) and metastatic infections. In such complications eradication of focal infections may have a curative and/or preventive effect. Such a role of focal infections in diseases of immunopathological origin cannot be proven. In these disorders the persistence of focal infection is not necessarily required for the progression of the disease, and eradication of focal infection(s) has no curative effect. There are no sufficient evidence favouring a connection between dental, tonsillar, and urogenital focal infections and allergic or autoimmune diseases. We also lack evidence that eradication of focal infections, apart from rare instances, might influence the prognosis of such patients.

Herpes simplex replication and dissemination is not increased by corticosteroid treatment in a rat model of focal Herpes encephalitis.

Neurological damage in Herpes simplex type 1 encephalitis results from neuronal cell death secondary to viral invasion, and from inflammatory changes and cerebral oedema secondary to the immune response to the virus. Corticosteroids could have an important role in the management of Herpes simplex encephalitis because their anti-inflammatory action reduces cerebral oedema. However their use has been limited by concerns that their immunosuppressive actions could increase viral replication and spread. The present study examined this issue in a rat model in which injection of HSV-1 into the cervical vagus nerve produced a well-defined focal encephalitis, characterised by an orderly progression of the virus through central neural pathways connected with vagal afferent termination sites in the medulla oblongata. After injection of HSV-1, rats were treated twice a day, either with vehicle (saline, 400 microl i.p.), with acyclovir (30 mg/kg i.p.), with dexamethasone (5 mg/kg i.p.), or with both acyclovir and dexamethasone. Animals were sacrificed after 72 h, and viral load in different brain regions was quantified by computer-assisted measurement of the area occupied by immunohistochemical reaction product. Treatment with acyclovir reduced viral load to 17 +/- 5% of the saline value (P < 0.01). After dexamethasone treatment, the viral load (63 +/- 13% of the saline value) was also reduced (P < 0.05). Treatment with both acyclovir and dexamethasone reduced viral load to 26 +/- 8% of the saline value (P < 0.01 compared with saline, and P > 0.05 compared to acyclovir alone). Our results confirm the effectiveness of acyclovir in a new model of HSV-1 infection, and provide evidence that corticosteroids do not inhibit the antiviral action of acyclovir. In addition corticosteroids may decrease the extent of infection in their own right. The acute time course studied in our model parallels the time course of acute Herpes simplex encephalitis in humans. Our data suggests that corticosteroids are not detrimental when combined with acyclovir in the management of this condition.