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A new microorganism, tentatively named "Montezuma" was detected in ticks and in specimens (blood, bioptic specimens of the primary affect) taken from patients with an acute fever disease, etiologically linked with the bites of Ixodes ticks in the Far East of the Russian Federation. After sequencing the products of the amplification of DNA isolated from ticks with wide-spectrum primers new primers were developed, highly specific to the unusual sequence thus obtained. The study revealed that ticks of the species Ixodes persulcatus (97%) and Haemophysalis concinnae (5%) contained DNA of this microorganism. The same DNA was detected in materials taken from the patients. The phylogenetic analysis of the gene showed that this organism formed an independent and well defined branch within the order Rickettsiales. The nearest homology (89%) was observed with recently detected endosymbiotes Acanthamoeba. The similarity with their relatives from the families Rickettsiaceae and Anaplasmataceae of the order Rickettsiales was within 81-86%, which made it possible to infer the existence of, probably, only a new genus, but also a family. The isolated DNA belonged, supposedly, to the new microoganism which caused a tick-borne disease in humans, transmitted through bites of Ixodes ticks, and was, supposedly, widely spread in the southern area of the Khabarovsk Territory.

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A serological survey of a patient admitted to the Clinic of Infectious Diseases, Far-East State Medical University, for suspected North Asian tick-borne rickettsiosis (NATBR) revealed antibodies in the increasing titers to Ehrlichia phagocytophila and no antibodies to other causative agents of natural and focal infections in the Far East. The disease presented with significant intoxication and maculopapular eruption. This disease differed from the standard NATBR in that there was neither primary affect at the site of pathogen entry, regional lymphadenitis, nor involvement of the liver in the pathological process (elevated levels of AIAT, AsAT, pigment metabolic disturbance), and that there was a steady-state tendency to leukopenia.

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A case of a male patient with chronic Lyme borreliosis running with marked neurological symptoms (Garin-Bujardoux-Bannwarth syndrome) is reported. Two years before the disease manifestation the patient was infected by the tick with both borrelia and Rickettsia sibirica. The latter infection provoked an acute fever in tick-borne rickettsiosis immediately after the tick's bite. This masked development of Lyme borreliosis which manifested only 5 months later as a neurological disease. It is thought necessary to propose a rational scheme of antibiotic treatment of patients with tick-transmissible diseases.

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AIM: To evaluate effects of antibiotics in the treatment of hemorrhagic fever with renal syndrome (HFRS). MATERIAL AND METHODS: Clinico-laboratory comparisons were conducted in patients with HFRS who received antibiotics (n = 153) and did not (n = 104) in combined treatment of their disease. RESULTS: HFRS patients treated with antibiotics had weakness, poor appetite, hyperemia of the face, enanthema, hemorrhagic eruption, coated tongue, abdominal distention, thirst, xerostomia, oligoanuria, polyuria significantly longer. Antibiotics raise blood levels of urea and creatinine, urinary levels of protein, ESR, later normalization of renal function, number of plasmic cells and eosinophils, etc. CONCLUSION: This study evidently shows a negative influence of antibiotics on the course of hemorrhagic fever with renal syndrome.

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In 150 patients with epidemic hemorrhagic fever hyperserotoninemia, thrombocytopenia, increase in the activity of monoamine oxidase, ceruloplasmin and serotonin pectic effect were found. However only during mild cases of the disease inactivation of serotonin was effective and changes of its concentration in plasma were absent.

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Differences in the concentrations of serotonin in whole blood and plasma of patients with hemorrhagic fever with the renal syndrome prompted measurements of serotonin in different components of the blood. The concentration of serotonin in whole blood was found to depend on its hemoconcentration: the higher is the hematocrit, the greater is the difference between serotonin content in the plasma and whole blood. In case of hemoconcentration or hemodilution it is impossible to assess serotoninemia from the level of serotonin in whole blood.

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High concentrations of histamine and serotonin were found in the blood, cerebral and cortical substance of the kidney from 8 patients who had died of HFRS. These elevated levels may be responsible for renal edema and loss of function. Underlying causes of the above changes are considered.

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Fluorometry of histamine and serotonin in cadaveric blood revealed a threefold increase of their concentrations in comparison with those in whole blood of live subjects. This indicates liberation of amines in the course of death and after it when factors inactivating them cease to function. However, the authors consider it possible to validate their conclusions about changes in the content of histamine and serotonin in cadaveric tissues in different diseases, provided certain conditions of selecting the material are adhered to. The distribution of amines in the viscera is not sex-dependent, little depends on the blood content of tissues, and is determined by the organ-specific features of metabolism of these bioactive substances. To illustrate this, the authors consider the content of histamine and serotonin in the organs of patients dead from hemorrhagic fever with the renal syndrome.

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173 case records have been analyzed to specify the role of early therapy (antipyretics, antibiotics, sulphanilamide drugs) on further development of hemorrhagic fever with renal syndrome. Early treatment of the above patients was found uneffective and not safe as to possible complications, for instance antipyretics occasionally brought hypotonia and shock.

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Whether preventive antibiotics are beneficial in hemorrhagic fever with renal syndrome was checked up by the evidence obtained from 303 relevant case histories. The analysis showed undesirability of antibiotics, as they promote emergence of nonspecific complications and prolong the patients' stay in hospital.

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The authors detected impaired urinary excretion of some amino acids in 20 patients suffering from moderate hemorrhagic fever with renal syndrome. The excretory changes depended on the kind of amino acid, the disease period and renal function. The causes of the above abnormality are discussed.

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Changes in amino acids in blood, daily urine as well as amino acid clearance were studied in 20 patients with moderate hemorrhagic fever and renal syndrome. The amino acid balance was impaired and the degree of impairment depended on the type of an amino acid and the duration of a disease. Dysaminoacidemia at the peak of the disease is associated with excretion and reverse transport of some amino acids. It is suggested that hyperaminoacidemia of early and late periods of the disease is compensatory.

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According to the data contained in the materials provided by the hospital of infectious diseases of the Khabarovsk Medical Institute, in the recent decade hemorrhagic fever with the renal syndrome, together with pseudotuberculosis, played the leading role in the structure of morbidity caused by natural foci of infections. The distribution of patients in social groups and different important factors of the epidemiology of this disease are considered. Taking into account a high morbidity level in this disease and its social grounds, the necessity of further improvement of the system of nonspecific prophylaxis is substantiated.

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Eight patients suffering from hemorrhagic fever with renal syndrome (HFRS) running a severe course complicated by pulmonary edema developed absolute hyperhistaminemia and hyperserotoninemia, histamine and serotonin accumulation in tissues. These amines inactivation in blood and lungs and excretion of catecholamines with urine got disturbed. High blood and lung tissue levels of biologically active substances resultant in enhanced permeability of the vascular wall and alveolar epithelium, hemodynamic disturbances due to hypoexcretory hypercatecholaminemia are thought to underlie the occurrence of this grave HFRS complication.

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Comparison of the parameters that characterize the activity of the sympathoadrenal system (urine adrenalin and noradrenalin) and the severity of hypoxia (lactic acid in blood and urine, pyruvic acid in blood and urine, lactate/pyruvate) in patients suffering from hemorrhagic fever with the renal syndrome (HFRS) showed them to be significantly and directly correlated. The time-course of changes in the study parameters mirrors the gravity of the pathological process. The authors hold that the sympathoadrenal system plays the leading role in the development of different types of tissue hypoxia in HFRS patients.

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The known methods for simultaneous measurements of blood histamine and serotonin have prompted the authors to search for approaches to simultaneous measurements of monoamine oxidase and diamine oxidase, the enzymes contributing to serotonin and histamine inactivation. The authors suggest a method for simultaneous measurements of the blood serum monoamine oxidase and diamine oxidase activities that permits cut down the time of the blood and substrate incubation to 10 min, essentially shortens the procedure and simplifies it. The method is recommended for research and practice.

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Hyperhistaminemia, hyperserotoninemia and activation of the kinin system followed by a decrease in the system reverse capacities and inadequate compensatory reactions were detected in 86 patients with various forms of hemorrhagic fever and renal syndrome. The data obtained suggest that these biologically active substances are of importance in pathogenesis of the disease.

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In order to explore possible involvement of histamine and serotonin in acute renal failure related to hemorrhagic fever with renal syndrome (HFRS), selected markers or renal lesions have been compared with biochemical findings in highly severe cases. Literature reports and the study results lead the authors to conclude that histamine and serotonin are obviously pathogenetic determinants of HFRS since their concentrations in plasma of these patients are increased 3-fold. It is suggested that the biologically active substances may be a link between renal disease and hyperergy in severe and critical disease forms.

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To judge the possible causes of the impairment of blood vascular permeability in hemorrhagic fever associated with the nephrotic syndrome (HFNS), 86 patients were examined over time for the blood content of histamine, serotonin and kallikrein. The patients were found to have hyperhistaminemia, hyperserotoninemia and activation of blood serum kallikrein, which attests to undoubted participation of these biologically active substances in the pathogenesis of HFNS.

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