Publications by authors named "Khavkin T"

Current advances in the understanding of the pathogenicity of the agents of diarrheal infections, Vibrio cholerae, diarrheagenic E. coli, Shigella, Salmonella, and enteropathogenic Yersinia, have, to a great extent, become possible due to morphological studies of host-pathogen interactions in natural and experimental infections. Despite a multigenic nature and a diversity of pathogenic features in the bacterial species and even in serogroups of the same species, it is now possible to delineate four major patterns of interaction of enteric pathogens with their cellular targets, the enterocytes, and with the immune apparatus of the gut.

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The adherence of human red blood cells (RBC) to autologous T-cells does not occur in the body, and in vitro is elicited at 4 degrees. Autologous E-rosetting at 37 degrees has not previously been described. In this work, lymphocyte-RBC adherence has been studied in mixed leukocyte-RBC cultures and in whole blood from healthy donors.

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A histologic, immunofluorescence, and electron microscopic study of the intracellular parasitism of Coxiella burnetii (the Q fever agent) in mouse lungs after intranasal challenge was undertaken. It was shown that this microorganism invades type I and, rarely, type II pneumocytes as well as pulmonary fibroblasts and histiocytes. The infectious process can be described as a focal intra-alveolar inflammation with the macrophages prevailing in the exudate.

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Lymphocyte-monocyte synergistic interaction in cooperative response to mitogens and antigens is well established. This paper describes a less known--antagonistic (effector-target)--lymphocyte-monocyte interaction that came into existence in a leukocyte culture after the commencement of cellular response to concanavalin A, phytohemagglutinin and Wistaria floribunda mitogen. An invasion of lymphocytes into monocytes and monocyte polykaryons has been found 24-48 h after exposure to mitogens.

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Mouse omentum was studied after intraperitoneal challenge with tachyzoites of Toxoplasma gondii. Parasites inhabit omental histiocytes, fibroblasts, mesothelial cells, and free peritoneal macrophages. Recently infected cells showed enhanced metabolic and functional activity.

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Two phase I strains of Coxiella burnetii of different virulence were injected into the yolk sacs of chicken embryos, and the yolk sacs and livers were examined at intervals by light, fluorescent, and electron microscopy. The high absorptive and digestive capacities of the yolk endoderm contributed to he entrance of the organisms into endodermal epithelial cells where C. burnetii multiplied.

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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.

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Fluorescent periodic acid-Schiff reaction (FPR) was used in the study of the normal rabbit ileal epithelium and its changes after injection of living cultures or enterotoxins of enterotoxigenic Escherichia coli. This reaction, with the use of auramine OO-SO2 complex as a Schiff-type reagent, demonstrates gut epithelium periodate-reactive mucosubstances more distinctly and brightly than does the common periodic acid-Schiff (PAS) reaction. It permitted the quantitative assessment of polysaccharide content in the gut sections by microfluorimetry, and examined extensively the mucosal structures, brush border, and mucous cells which participate in the interaction with enteropathogens.

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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.

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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.

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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).

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Comparison of some properties of phase I and phase II Coxiella burnetii cells suggests the presence of lipopolysaccharide (LPS) also in the surface structures of phase II cells. Polysaccharide chains were released from them by mild acid hydrolysis and corpuscular residues resulting from such hydrolysis elicited in rabbits anti-lipid A-antibodies. Toxicity for adrenalectomized and actinomycin D-sensitized mice was demonstrated with phase I cells, but not with much higher concentrations of phase II cells.

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Lysosomes of peritoneal macrophages, selectively pinpointed by aminoacridine-induced fluorescence, do not fuse with vacuoles containing viable Toxoplasma gondii RH strain.

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The article presents a survey of the literature containing reports on lesions of some human organs in Q-fever and on a possible role of the pathogene--Rickettsia burnetii in the development of these lesions. Pathoanatomical findings were compared with those of the experimental investigations of the Q-rickettsial infectious process. The literature data and the author's own investigations confirm the capability of Rickettsia burnetii of parasitizing in cells of the reticulo-endothelial system.

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The lungs of white mice given intranasal injections of various amounts of Rickettsia prowazekii were studied. Agent parasitism, mainly in the alveolar epithelium and nonciliated cells of bronchiolar epithelium, underlies the infectious process developing in the lungs. Rickettsiae may lodge in these cells without inducing both local and general alterations or a leukocyte response.

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