Ca2+-Dependence of Conoid Extrusion in Toxoplasma gondii Tachyzoites

The internal pH (pHi) of Toxoplasma gondii was estimated by measuring the accumulation of the weak base 9-aminoacridine in buffers with various ionic compositions. The pHi of the metabolizing parasite increased when the extracellular K+ was elevated in alkaline medium or when the external pH (pHe) was substantially increased in medium employing high external K+ (90 mM). The parasite in mouse peritoneal fluid, or in potassium sulfate buffer (pH 8.2), where the pHi was demonstrated to be increased to 7.9, became motile when acidic buffer was substituted for the original suspension medium. This acid-induced independent movement subsided within 5 min but was repeatedly induced if the pHe was serially lowered to 6.0. Basic buffers, on the other hand, abolished motility when applied to the moving parasites. Nigericin, which is known to collapse pH gradients across the membrane, also abolished motility.

Toxoplasma gondii, an obligate intracellular protozoal parasite, is the etiologic agent of toxoplasmosis. A main event in the pathologic course of this organism is the infection of both phagocytic cells and "nonprofessional phagocytes"--e.g., heart cells--and the subsequent destruction of these cells following massive multiplication of the parasite therein. There are two mechanisms of invasion. The parasite may enter a cell such as a macrophage by the well-known mechanism of phagocytosis without triggering its own death inside the cell. By the other process, communication of the parasite's apical pole and the host cell membrane may evoke a sequence of invasion steps different from that of phagocytosis. This invasion process involves the cooperation of the host cell and the parasite. The entry of the parasite is characteristically a rapid process that requires the input of energy by both of the cells involved. A series of cytochalasin-sensitive morphologic changes that are undergone by the parasite and the host cell lead to the interiorization of the parasite. Chemical factors, as well as membrane composition, microviscosity, and membrane structures on the host cell membrane, modulate the parasite's entry.