**2. The overall clinical and anatomical characteristics of tick-borne encephalitis**

For the duration of the disease, all patients were divided into four groups in which the death occurred respectively in the first, second, third and fourth week of the onset of clinical symptoms. In all cases there was an acute onset of temperature increase to high numbers 38 º - 39 º C, quickly joined the general brain symptoms as headache, nausea, vomiting, stupor, and disorders of consciousness and sometimes convulsions. In the early days of the onset of the disease appeared meningeal syndrome and focal symptoms of central nervous system involvement: paresis and paralysis of the limbs, neck, bulbar disorders, due to which almost all patients at different times transferred to a ventilator.

or horn of the spinal cord, mainly in the cervical region (Fig. 1b, d). In the cerebellar cortex is constantly met the degeneration and loss of Purkinje cells. At the nucleus of Semmering

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The attention is drawn to the distinct focal reaction of microglia and oligodendroglia with neuronophagia and the formation of glial nodules on the site of dead nerve cells. In areas of inflammation was observed a significant admixture of polymorphonuclear leukocytes. There was also a diffuse infiltration of the brain substance by lymphocytes, polymorphonu‐ clear leukocytes and glial cells. In the white matter of the brain and spinal cord was detected fragmentation of nerve fibers, were seen clusters of large, basophilic-stained cells. The in‐ flammation around blood vessels of the brain substance were not common, however, in some places were found loose histiocytic and lymphocytic perivascular infiltrates, in which

In general, the pathological process in the CNS of patients with the first group can be characterized as meningo-polioencephalomielitis with a predominance of exudative phe‐ nomena and alterative changes in the nerve cells. The severe damage to the wall of blood vessels, edematous hemorrhagic component of inflammation with exudation of polymor‐ phonuclear leukocytes showed marked sensitization of the organism in response to the in‐ troduction of the virus in the CNS with the presence of morphological reactions of

*The second group* of deaths was the most numerous (17 cases) and was 48.5% of cases. All died patients in the second week of the disease were observed in the brain the pronounced breach of hemocirclulation: eritrostasis, the presence of fibrin in the lumen of blood vessels, the expressive swelling of the brain tissue of spongy type. Vascular endothelium was in a state of proliferation, there was damage to the endothelial layer, porosity of the wall of blood vessels, often identified microhemorragii in different parts of the brain (Fig. 2 a). The elastic membrane of blood vessels had the irregular thickness, stratification, and sometimes not detected. There were the mucoid and fibrinoid swelling, the fibrinoid necrosis and

In the meninges, in addition to plethora, revealed swelling, stratification, proliferation of arahnoidendotelium, loose perivascular infiltrates of lymphocytes, histiocytes, with a small

In the vascular plexus of the brain ventricles were observed the rough swelling of the villi, the plethora and the homogenization of capillary wall, the degeneration, and in some places proliferation of the epithelium lining the villi. Ependyma cells were able to hyperplasia with

As in the previous period, the neuronal pathology was significantly expressed at different stages of damage. There were the diffuse chromatolysis, cell death and neuronophagia, focal loss of neurons with microglial reaction in these areas (Fig. 2b). Processes of nerve cells are often not reviewed, observed their destruction - klazmatodendrosis. Often hyperchromic

black substance the part of neurons was reduced the content of the pigment melanin.

there was an admixture of neutrophils (Fig. 1 c).

immediate hypersensitivity (IH).

aneurysmal expansion of vessels wall.

admixture of plasma cells.

areas of proliferation.

cells were seen.

From the brain of all died patients was isolated tick-borne encephalitis virus, and sera were determined by specific antibodies in diagnostic titers. At autopsy, macroscopic changes in the CNS manifested by edema and vascular injection of the meninges and brain substance, sometimes point hemorrhages scattered in different parts of the brain. The boundary of gray and white matter was somewhat effaced, especially in the cervical spinal cord and parts of the brain stem. There were congestion and degenerative changes in parenchymal organs (heart, kidney, liver), hyperemia of spleen. According to our observations, pathoanatomical diagnosis of tick-borne encephalitis should continue to be based on microscopic examina‐ tion of brain and spinal cord. At the same time the crucial importance to the diagnosis has an analysis of pathological changes in the so-called indicator areas of the brain.
