Development of Plasmodium chabaudi in mouse red blood cells: structural properties of the host and parasite membranes.

Abstract

ABSTRACTThe structure of both the host and parasite membranes during stages in the asexual development of Plasmodium chabaudi in mouse red blood cells is examined by transmission electron microscopy of thin sections and freeze‐fracture preparations. The erythrocyte's plasma membrane, the membrane of the parasitophorous vacuole, and the plasma membrane of the parasite exhibit different structural properties in terms of membrane width and the frequency and diameter of the typical intramembrane‐particles (IMP) populating the membrane's fracture faces. The difference between the parasitophorous vacuolar membrane and host cell's plasma membrane is remarkable because the vacuolar membrane is formed from an invagination of the erythrocyte's plasma membrane. The vacuolar membrane has significantly reduced frequencies and diameters of IMP's on both faces and reveals a marked temperature response manifesting itself as large IMP‐devoid domains emerging on both faces on chilling to 4°C. In contrast, cooling induces only some very small IMP‐devoid patches on both faces of the host plasma membrane. Neither of these membranes changes significantly as parasite development progresses. In contrast, the parasite's plasma membrane shows local alterations during its development, forming compaction domains with the nuclear envelope in ca. 30% of the ring‐stages and trophozoites. These compaction domains disappear in late uninuclear trophozoites and schizonts. Furthermore, the plasma membrane of the host cell, the vacuolar membrane, and the parasite's plasma membrane do not respond to externally applied Ca2+, and their temperature‐response remains unaltered during the infection cycle. Thus, modification of these three membranes as a consequence of invasion and development of the parasites, as recently found in the primate malaria caused by P. knowlesi, can be detected neither directly nor indirectly via temperature‐ and/or Ca2+‐response in the rodent malaria caused by P. chabaudi.