Biomedical subjects
Publications and source records attributed to A K Shustrov.
A motion picture study of macrophage culture infected with the endozoits of Toxoplasma gondii revealed an enhanced locomotor activity in afected cells: regular contractions of the cell resulting in an incomplete extrusion of the parasitophorous vacuole or host-cell destruction, formation of excessive undulating membranes and pinocytotic vesicles.
Macrophages with lysosomes pinpointed by quinacrine-induced fluorescence were infected with the endozoits of Toxoplasma gondii RH strain (peritoneal exudate of infected mouse), or treated with liquid (acellular) fraction of the same exudate. Dead toxoplasmas ingested by macrophages come into contact with the stained lysosomes of the cell and acquire a diffuse fluorescence. Viable toxoplasmas do not give fluorescence, which means that they do not come into contact with lysosomes, either primary or secondary. This supports the hypothesis that toxoplasmas can prevent lysosomes from fusing with the phagosomes of the host cell. Moderate doses of soluble products of toxoplasmas contained in peritoneal exudate cause an excessive output of macrophage lysosomes which points to the activation of macrophages; high doses of challenge inhibit the phagocytosis of toxoplasmas and damage macrophages. The pathogenicity of toxoplasmas due to their ability to inhibit the fusion of lysosomes and phagosomes and the cellular action of their soluble products is discussed.
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Toxoplasma gondii was found to cause an appearance of cells with a changed number of chromosomes in the bone marrow of infected white rats. Besides the increase of aneuploid and polyploid cells the infection with toxoplasms inhibits the mitotic activity in bone marrow of rats. The similar changes were observed in blood leucocytes of toxoplasmosis patients.
The omentum of 8 white mice was examined 24--96 hours after the intraperitoneal infection. Endozoites are capable of intensive intrusion not only into phagocytizing cells (hystocytes, peritoneal macrophages) but also into the cells which are not phagocytes (mesothelium). Just after the intrusion metabolism of the host-cell intensifies and in it are formed special structures which facilitate metabolic processes between the cell and the parasite (microvilli on the membrane of the parasitophore vacuole). At the final stage of the interaction with the cell endozoites cause the lysis of the membrane of the parasitophore vacuole that facilitates their transition into new cells. The ability to intrude into the cells, which are not phagocytes, and to cause the lysis of parasitophores vacuole is a factor of pathogenicity of virulent strains of toxoplasms which determines the generalized character of the infection caused by them.
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The spleen of 73 white mice was studied (15 mice were studied by electron microscopy) from 24 to 120 hours after intraperitoneal infection. The successive stages of interaction of parasites with cells of mononuclear phagocytes system were observed. At the early stages of the infection the activation of these cells takes place. During the dissemination of endozoites over the host organism they penetrate the activated mononuclear phagocytes. Activation, however, is not effective enough since in these cells the parasites preserve the ability to hinder the fusion of lysosomes with phagosomes containing endozoites and at later stages of the infection of lyse the membrane of parasitophore vacuole. The ability to reproduce in activated mononuclear phagocytes and to lyse the membrane of parasitophore vacuole is regarded as a factor of the virulence of endozoites of RH strain toxoplasms.
The dynamics of the distribution and concentration of toxoplasms of strain RH in organs and tissues of white mice infected subcutaneously was studied by the titration method during the toxoplasmatic infection. The distribution of toxoplasms in the organism was found to be active in the first 30 to 60 minutes with a subsequent fall of their concentration. In 24 hours no parasites were discovered by the bio-assay method. On the next days toxoplasms in the organs reached such abundance that caused the death of the animal. In the brain toxoplasms were found only after 3 days.