Zygotes and ookinetes of the rodent malaria Plasmodium berghei can be enriched 50-fold, from whole blood cultures by ammonium chloride lysis. Three monoclonal antibodies (MoAbs) raised against such enriched preparations specifically bind to a determinant of Mr 21 kD as assessed by 125I-labelled goat anti-mouse IgG probed immunoblots of Western transfers of SDS-PAGE gels. Indirect immunofluorescence indicates that the 21 kD determinant bound by specific MoAbs, whilst not detectable on gametocytes or gametes, appears on the parasite surface within 2 h of exflagellation/fertilization and increases thereafter. The three MoAbs specifically binding the 21 kD determinant block oocyst development in mosquitoes by at least 90%, as assessed either by in-vitro membrane feeds or by live feeds on passively immunized mice. These MoAbs reduce ookinete formation in vitro by between 52 and 100%. Possible mechanisms of action of these MoAbs are discussed.

By using affinity-purified ookinete surface antigen from the rodent malaria parasite Plasmodium berghei, a transmission-blocking immunity was induced in mice. Groups of mice were immunized via different routes, with total quantities of antigen ranging from 0.5 to 40 ,ug (with or without Freund adjuvant). Vaccination by the intramuscular route with 20 ,ug of antigen in the absence of adjuvant and boosted once with the same amount of protein induced a total transmission blockade. Immunoblot analysis confirmed that immune sera invariably recognized Pbs2l antigen. The isotype and titer of the anti-Pbs2l immunoglobulin G (IgG) response was determined by enzyme-linked immunosorbent assay. The antibody isotype was predominantly IgGl. The concentration of specific anti-Pbs2l IgG reached a peak of 182.45 92.13 ,ug/ml by week 7 postimmunization and fell progressively to 38 ,g/ml at week 34 (at which time the transmission was still inhibited by 98%).

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The causal prophylactic activity of the novel hydroxynaphthoquinone, 566C80, was assessed against the exo-erythrocytic (EE) stages of Plasmodium berghei cultured in the human hepatoma cell line, HepG2. 566C80 was found to be highly active as an inhibitor of EE development and was more active than the established causal prophylactic pyrimethamine. A 566C80 concentration of 1.85 x 10(-9) M, added 3 h after sporozoite invasion, reduced the numbers of EE forms visible at 48 h by 50 degrees o, while the equivalent concentration of pyrimethamine was 1.95 x 10(-8) M.

The distribution of the circumsporozoite (CS) antigens in the 24 hour exoerythrocytic trophozoite of P. berghei was studied using Lowicryl immunogold electron microscopy. These antigens were present on the plasmalemma of the parasite, in disrupted areas of the host cell cytoplasm adjacent to the trophozoite and around inclusions of the host cell cytoplasm. There was evidence of a redistribution of the CS antigens away from the pellicular region of the sporozoite.