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Biomedical subjects

T N Khavkin

Publications and source records attributed to T N Khavkin.

At least 19 recordsLinked to original sources
PubMed1980

Fluorescent PAS-reaction study of the epithelium of normal rabbit ileum and after challenge with enterotoxigenic Escherichia coli.

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. Fluorescent periodic acid-Schiff reaction showed that noninvasive enterotoxigenic E. coli O148:H28 B7A organisms caused restricted damage to the intestinal epithelium brush border. Invasive enterotoxigenic E. Coli O26:K60:H11 N3 organisms penetrated the epithelium and caused extensive brush border lesions and mucous cell hyperproduction. Importance of FPR in the complex morphologic analysis of enteric infections, pathogenesis of escherichoses under study, and some aspects of the intestinal epithelium histology are discussed.

Animals↗
PubMed1980

Motion picture study of the response of cultured peritoneal macrophages to the invasion of endozoits of toxoplasma gondii, RH strain.

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.

Animals↗
PubMed1980

Vital fluorescence microscopy of lysosomes in cultured mouse peritoneal macrophages during their interactions with microorganisms and active substances. III. Interactions of macrophages with endozoits of Toxoplasma gondii RH strain and their soluble substance.

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.

Acid Phosphatase↗
PubMed1978

Attempts at demonstration of lipopolysaccharide in phase II Coxiella burnetii.

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. By contrast, the extent of protection against formation of ascitic tumour in mice with comparable concentrations of phase I and phase II cells was similar.

Animals↗
PubMed1977

[Pathologo-anatomic and experimental study of the morphology of Q-fever].

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. This is an important factor in the pathogenicity of this causative agent and lies at the root of the pathogenesis of Q-rickettsial infection.

Animals↗
PubMed1976

[Toxoplasmosis].

Explore the source record for details and available documents.

Animals↗
PubMed1974

Infectious process in the lungs after intranasal challenge of white mice with Rickettsia prowazekii. A histologic immunoluminescent and electron microscopic study.

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. After being released from the cells they inhabit, rickettsiae evoke acute exudative inflammation. The inflammation is accompanied by marked circulatory disorders, necrosis of exudate cells and vascular thrombosis, which are induced by toxic products of the agent. Polymorphonuclear leukocytes and macrophages represent the main defense mechanism of a host. They ingest and destroy rickettsial organisms. If infection runs a favorable course, phagocytes destroy the rickettsiae, and the organisms are entirely cleared from the lungs.

Administration, Intranasal↗