Search PubMed⌕ Search

Biomedical subjects

M Aikawa

Publications and source records attributed to M Aikawa.

At least 343 records · Page 19Linked to original sources

Experimental infection of Aotus monkeys with Plasmodium falciparum Light and electron microscopic changes.

Six splenectomized Aotus owl monkeys were infected with P. falciparum. The animals were sacrificed when they became moribund and tissues were faken for light and electron microscopic studies. Electron microscopy revealed marked structural changes in both the liver and the heart. In the liver there was glycogen depletion, lipid droplet infiltration mitochondrial disorganization with reduction in numbers and alterations of the microvilli in the sinusoidal pole and the bile canaliculi. In the heart, there was lipid droplet infiltration and focal disorganization of the myofibrils around the intercalated disc. There was focal mitochondrial disorganization and mitochondrial concentration around the muscle lesion. The ultrastructural changes in liver and heart were similar to those described in animals dying of shock, of at least two hours duration, in different experimental models. Ultrastructural lesions found in other organs were less marked. In the kidneys there was mainly a moderate lipid infiltration of the tubular epithelium. This change is probably the early precursor of that seen at four hours in animals dying in experimental shock. The above changes are discussed in light of the known pathophysiology of both experimental infections in animals and natural human malarial infections.

Animals↗

Chediak-Higashi syndrome in a black infant. A light and electron microscopic study with special emphasis on erythrophagocytosis.

Clinicopathologic observations in the case of a black infant with Chediak-Higashi syndrome are reported. Light and electron microscopic examination of spleen, liver and lymph nodes revealed abnormal large lysosomes as well as marked erythrophagocytosis without hemosiderosis in infiltrating histiocytes and Kupffer cells. In addition, there were abnormal ocular findings. It is suggested that the erythrophagocytosis without hemosiderosis might also be a specific anatomic expression of this disease due to defective lysosomal digestion of phagocytosed erythrocytes.

Black People↗

Antibody-induced ultrastructural changes of malarial sporozoites.

Immunization with irradiated sporozoites produces a considerable degree protection against rodent, simian, and human malaria. This protection is in part antibody mediated. Antibodies neutralize sporozoites (SNA), i.e. abolish their infectivity, and cause, in vitro, the formation of a thread-like precipitate on the parasites (CSP reaction). The present study was undertaken to characterize the ultrastructural aspects of antibody-sporozoite interaction.

Animals↗

Malaria (Plasmodium knowlesi) merozoites: immunity and the surface coat.

Immune serum agglutinated merozoites of Plasmodium knowlesi in culture. Agglutinated merozoites attached to erythorcytes but were usually unable to invade. Marked aggregation of merozoites was associated with reduced invasion of erythrocytes in these cultures. The agglutination and reduced invasion were immunologically specific, for the effect of serum was greatest against homologous strains of P. knowlesi. Merozoite agglutination was caused by the binding of surface coats on adjacent parasites. This coat appeared on the plasma membrane of merozoites after it was exposed to culture medium, both with and without immune serum. The coat consisted of protein or glycoprotein, since it was susceptible to trypsin treatment. It appears that antibodies directed against this surface coat are crucial for reduced invasion of erythrocytes, at least in vitro.

Agglutination↗

Erythrocyte membrane alterations induced by Plasmodium simium infection in Saimiri sciureus: relation to Schüffner's dots.

The nature of erythrocyte membrane alterations in Plasmodium simium infections was determined employing light microscopy, carbon replication and transmission electron microscopy. Light microscopy of Giemsa stained preparations shows that infected cells initially acquire a faint stippling (schuffnerization) which becomes pronouced with subsequent parasite development. Enlargement of the host cell usually accompanied stippling. Both phenomena appear to depend on host cell age since infected mature erythrocytes were neither stippled nor enlarged. Carbon replicas show numerous indentations over the outer membrane surface of most infected cells. Their distribution suggests that they account for Schuffner's granules. The surface indentations are manifest as small infundibular which open to the infected cell's surface. Cytoplasmic microvesciles in the infected cell's stroma frequently are observed adjacent or catenated to the surface infundibula. Images suggest their funsion with the surface infundibula thus adding membrane to the cell's surface and accounting for host cell enlargement.

Animals↗

Caveola--vesicle complexes in the plasmalemma of erythrocytes infected by Plasmodium vivax and P cynomolgi. Unique structures related to Schüffner's dots.

Erythrocytes infected with Plasmodium vivax and P cynomolgi, characterized by Schüffner's dots on Giemsa-stained thin films, were studied by electron microscopy and immunocytochemistry. A caveola-vesicle complex, which consisted of a caveola surrounded by vesicles, in an alveolar fashion, formed along the erythrocyte plasmalemma. Horseradish-peroxidase-labeled immunoglobulin from a monkey infected with P vivax bound to the vesicle membrane. Cationized ferritin appeared within the vesicles after incubation with viable parasitized erythrocytes, suggesting that these vesicles were pinocytotic in origin. This caveola-vesicle complex probably corresponds to Schüffner's dots because the alteration is unique to vivax- and ovale-type malarias, and its size and distribution are consistent with Schüffner's dots. Clefts observed within the cytoplasm of infected erythrocytes are present in all malarias and are unlikely candidates for Schüffner's data.

Animals↗

Surface properties of extracellular malaria parasites: morphological and cytochemical study.

Morphological and cytochemical surface characteristics of isolated malaria parasites (Plasmodium berghei) and host erythrocytes were compared by electron microscopy by using thin section and carbon replica techniques. Erythrocytes were uniform in shape and had fine, granular surfaces. In contrast, free parasites exhibited a variety of sizes, shapes, and surface textures. Fine surface stippling was a common topographical feature of isolated parasites. Small, infective forms often had patterned surfaces resulting from the protuberance of an underlying thick intermediate layer. Results of cytochemical analysis using a sialophilic colloidal iron stain indicated that the malaria parasite's surface lacked exposed sialic acid groups which would normally give rise to a net negative surface charge common to erythrocytes. Biochemical assay demonstrated that malaria parasites contained about one-half the amount of sialic acid per unit weight as did control red cell extracts. Similarly, external acidic mucopolysaccharide coats of free parasites, as revealed by ruthenium red staining were extremely thin as compared with the thick glycocalyx layer of red cells. Lipid plaques at the surface of parasites and red cells were localized by lipophilic iron colloid staining. Although the gross patchwork distribution of plaques was somewhat similar for the two cell types, the parasites were stained more intensely and had a closer-knit patchwork pattern than those exhibited by the erythrocytes. Such findings indicate that there are slight differences in the arrangement of phospholipids at the surfaces of limiting membranes of host cells and parasites. The significance of the above cytochemical surface properties of the malaria parasite (which are seemingly akin to those of intracellular organelles is discussed in relation to certain host-parasite interactions, such as parasite adhesion to target cells and enhanced clearance of extracellular parasites.

Cell Membrane↗