ABSTRACT
Parasitized red blood cells (PRBCs) were sequestered in microvessels of cerebral and subcutaneous tissues of a rhesus monkey infected with Plasmodium coatneyi. A similar sequestration rate (approximately 80%) was observed in both cerebral and subcutaneous microvessels. Electron microscopy showed knobs of the sequestrated PRBCs cytoadhered to endothelial cells. These results are consistent with the finding of PRBC sequestration in subcutaneous tissues in a comatose patient with cerebral malaria. Biopsy specimens of subcutaneous tissue may be useful as indicators of PRBC sequestration in the brain of cerebral malaria patients.
Subject(s)
Brain/parasitology , Erythrocytes/parasitology , Malaria, Cerebral/parasitology , Plasmodium/physiology , Skin/parasitology , Animals , Brain/blood supply , Macaca mulatta , Microcirculation/parasitology , Skin/blood supplyABSTRACT
The ultrastructural changes caused by a new antimalarial drug, pyronaridine, were investigated using mice infected with erythrocytic forms of Plasmodium berghei and P. falciparum cultivated in vitro in human erythrocytes. The first changes observed in both parasites after exposure to pyronaridine occurred in the food vacuoles. This suggests that the target organelle of this drug may be the food vacuole of malarial parasites. In addition, rapid alterations were also noted within the pellicular complex of both plasmodia.
Subject(s)
Antimalarials/pharmacology , Naphthyridines/pharmacology , Plasmodium berghei/drug effects , Plasmodium falciparum/drug effects , Animals , Chemical Phenomena , Chemistry , Erythrocytes/parasitology , Humans , Microscopy, Electron , Organoids/drug effects , Organoids/ultrastructure , Plasmodium berghei/ultrastructure , Plasmodium falciparum/ultrastructure , Vacuoles/drug effects , Vacuoles/ultrastructureABSTRACT
The ultrastructural changes induced by the administration of a recently developed antimalarial drug, mefloquine, were studied in mice infected with Plasmodium berghei and human erythrocytes infected with P. falciparum in vitro. Pronounced changes which occurred in both experiments comprised swelling of the parasites' food vacuoles with gradual loss of pigment granules, which did not form clumps as occurs with chloroquine. These findings suggest that the malarial parasites' food vacuole is the target of this drug.
Subject(s)
Plasmodium berghei/drug effects , Plasmodium falciparum/drug effects , Quinolines/pharmacology , Animals , Malaria/drug therapy , Malaria/parasitology , Mefloquine , Mice , Mice, Inbred ICR , Microscopy, Electron , Plasmodium berghei/ultrastructure , Plasmodium falciparum/ultrastructureABSTRACT
Invasion of erythrocytes by malarial merozoites requires the formation of a junction between the merozoite and the erythrocyte. Migration of the junction parallel to the long axis of the merozoite occurs during the entry of the merozoite into an invagination of the erythrocyte. Freeze-fracture shows a narrow circumferential band of rhomboidally arrayed particles on the P face of the erythrocyte membrane at the neck of the erythrocyte invagination and matching rhomboidally arrayed pits on the E face. The band corresponds to the junction between the erythrocyte and merozoite membranes observed in thin sections and may represent the anchorage sites of the contractile proteins within the erythrocyte. Intramembrane particles (IMP) on the P face of the erythrocyte membrane disappear beyond this junction. When the erythrocytes and cytochalasin B-treated merozoites are incubated together, the merozoite attaches to the erythrocyte membrane and a junction is formed between the two, but the invasion process does not advance further and no movement of the junction occurs. Although there is no entry of the parasite, the erythrocyte membrane still invaginates. Freeze-fracture shows that the P face of the invaginated erythrocyte membrane is almost devoid of the IMP that are found elsewhere on the membrane, suggesting that the attachment process in and of itself is sufficient to create a relatively IMP-free bilayer.
