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Pathology study of 32 patients who died of tick-borne encephalitis (TBE) in the Ural Region in 1990s revealed differences with this infection registered in 1940-1950s. Pathological changes in the central nervous system by their severity and location are like those observed in the Far East TBE. Apart from grave alterative changes in the nerve cells of motor nuclei of the spinal cord and brain, three types of pathological changes are observed: productive inflammation, exudative inflammation without pronounced inflammatory reaction. Differences in the organism reactions to the infectious process are explained by differences in the virus virulence and organism immunological status.

Congenital respiratory viral infection is followed in the CNS of fetuses and newborns by grave dyscirculatory disturbances with glia proliferation and nervous tissue edema. The process is mainly localized in the periventricular regions of the brain ventricles. Neurologic and morphologic consequences of these damages in the CNS of fetuses and newborns need further studies.

Clinicomorphological characteristics of intrauterine chlamydiasis (IUC) are given. The authors describe a cottonwool-like meningochorioiditis the observation of which at necropsy allows IUC suspection. Chlamydial etiology of this condition is confirmed by means of electron microscopy and immunofluorescence. Fibroblast proliferation of the pia mater followed by intensive fibrillogenesis plays a most important role in morphogenesis of cottonwool-like nodules. The occurrence of IUC at the necropsies varies depending on the age of foetuses and newborns from 6.2 to 38.7%.

Lymph nodes of humans and experimental animals with tick-borne encephalitis (TBE) were studied using electron microscopy. TBE virus reproduction occurred in macrophages, reticular and plasma cells. Severe organelle destruction was found in the above cells and lymphocytes. The results suggest that macrophage, reticular and plasmatic cell death is due to the virus reproduction, while lymphocyte death is due to the toxic effect. It is evident that the outcome is determined by pathological process in lymphoid organs.

The ultrastructural study of fetal and newborn lungs in the intrauterine infection caused by respiratory viruses showed the virus reproduction to take place in type II alveolocytes with destructive changes in cell organelles. Each type of virus results in a certain picture of ultrastructural changes. Progressing cell organelles destruction with an intensive cytoplasm vacuolization and virion presence in the cytoplasmic matrix and on the endoplasmic network membranes is characteristic for influenza. Severe cytoplasm vacuolization with lipid formation, homogenization and condensation of membranous bodies, nuclear pyknosis are observed in parainfluenza. RS-infection is characterized by virion formation on the cytoplasmic cell membrane, numerous deformed membranous bodies, filling intercellular spaces and alveolar lumen with rough granular electron-dense material, massive release of organelles into the alveolar lumen. Edema and vacuolization of endothelium, edema and focal disappearance of basal membrane are observed in the capillary walls.

The paper systematizes the data of the literature on ultrastructural changes in the central nervous system (CNS) of experimental animals infected with arboviruses of the Togaviridae family. The main site of virus reproduction in the CNS was found to be nerve cells in which the ultrastructural lesions typical for this group of viruses developed. The main features of these lesions consist in degeneration of rough membranes, ribosomes, and polysomes of the cell, hyperplasia and hypertrophy of smooth membranes, formation of various vacuoles and vesicles in the cell hyaloplasm. Mature virions accumulate in cisterns and cavities of the endoplasmic reticulum, lamellar complex, in vacuoles and vesicles. Each of arboviruses produces in the cells not strictly specific but typical ultrastructural lesions. In the CNS the viruses spread hematogenically, in intercellular and perivascular spaces and dendrites of the nerve cells.

Light and electron microscopies were applied to examine liver punctates from 10 patients with typhoid fever. Both in the full swing of the disease and in clinical recovery (convalescence), dystrophic and necrobiotic changes along with focal cell death were found to occur in the hepatocytes, endothelial and Kupffer cells covering the sinuses. The protein-synthesizing system and mitochondria were demonstrated to be primarily destroyed. The microbes of typhoid fever were located in the hepatocytes, endothelial and Kupffer cells.

The monkey eyes infested by inoculation into the eye anterior chamber of the ECHO-19 virus from children with uveitis were studied morphologically. It was established electron microscopically that the inoculated virus is replicated in the capillary endothelium and stromal cells of the uveal tract. Crystal-like accumulation of virions and degenerative changes in the organelles are observed in these cells. Acute granulomatous alterative-exudative-hemorrhagic uveitis with the destruction of the iris, ciliary body and processes and secondary changes in the cornea and crystalline lens with the symptoms of keratitis and cataract develop in the anterior part of the eye as observed in the light microscope. The anterior and posterior goniosynechia develop. An acute inflammatory process is further transformed into a progressing autoimmune inflammation.

Tick-borne encephalitis virus is localized in nerve cells and intracellular spaces. According to the nature of ultrastructural changes, the pathological process in nerve cells may be divided into three stages connected with the stages of virus reproduction. In the first stage, the protein-synthesizing systems of the cell are degraded. In the second stage specific virus inclusions form in the cell cytoplasm as aggregates of mature and immature virions alongside with destruction of ultrastructures and growth of smooth membranes. In the third stage degradation of neurons is accompanied by necrobiosis and discomplexation of the surrounding glial elements, processes, cells of the inflammatory infiltrate and capillary walls. A certain combination of nonspecific changes in organelles of various cells with viral inclusions makes the ultrastructural picture of the focus of lesions in tick-borne encephalitis sufficiently characteristic for differential pathological diagnosis.

An account of the findings resulting from the study of experimental poliomyelitis in M. rhesus after several immunizations with Sabin live vaccine is given. The challenge of the vaccinated monkeys with the virulent strain of poliomyelitis virus, type I, was shown to result in the development of a disease with clinical and morphological characteristics typical of poliomyelitis in some of these monkeys. The incidence of the infection was found to decrease with the growth of antibody level in the blood of the monkeys. The virus was isolated from the tissues of the vaccinated animals showing the symptoms of the disease less frequently than from the tissues of the control animals.

The central nervous system of monkeys with chronic tick-borne encephalitis (TBE) shows the following ultrastructural alterations which differ from those in acute TBE: widespread destructive changes in neurons, astrocytes, oligodendrocytes, processes, myelin, vascular walls, severe edema of brain tissue with the signs of a so-called spongious degeneration and the absence of cell proliferation and perivascular cell infiltrations, glial nodules as well as circulatory disorders (hyperemia, stasis, hemorrhages). Few virions with or without and altered supercapsid membrane are detected in the neuronal cytoplasm or in the intercellular spaces; the signs of active virus reproduction in the cells are lacking. Pathologic process is of a degenerative but not of an inflammatory nature; the latter is typical for acute TBE.

The ultrastructure of cells of the central nervous system of Rhesus monkeys in experimental poliomyelitis caused by virus of poliomyelitis Type 3 was studied. It was found out that the virus of poliomyelitis was localized in nerve cells, astocytes, oligodendrocytes, the endothelium of capillaries and macrophages. This justifies the conclusion that pathological changes in the cells referred to the above result from reproduction of the virus therein. Ultrastructural changes in infected cells are divided into three stages: the first stage corresponded to eclipse-phase of infection; the second -- to the period of reproduction of the virus and composition of viral particles; and the third -- to the period following the escape of the virus from the cell. A definite combination of nonspecific changes in organoids of various cells with specific viral inclusions makes the ultrastructural picture of cells in poliomyelitis sufficiently characteristic for differential diagnosis. Pathogenesis of the developing lesions is discussed.

Synthesis and the content of RNA and protein in cells of the pig embryo kidneys infected with tick--borne encephalitis virus were studied by means of autoradiography and cytophotometry. Acceleration of synthesis and accumulation of RNA (in cellular structures) were estimated as over 125--200% of the initial level followed by a decrease in 12 hr when the virus release from the cells occurred. By the 2nd and 6--8th hr of infection (in the period of synthesis of early and late virus material), two peaks of protein contents over 123--131% were observed. The RNA and protein shifts are well correlated with the virus reproduction stages.