Immunity to exoerythrocytic forms of malaria. II. Passive transfer of immunity to exoerythrocytic forms

Abstract

The passive transfer of heat-inactivated or nonheat-inactivated convalescent serum, from turkeys inoculated with Plasmodium fallax exoerythrocytic forms and treated with chloroquine to suppress the development of erythrocytic forms and the development of immunity to them, delayed the exoerythrocytic-form infection in turkeys inoculated intravenously with exoerythrocytic forms. The degree of exoerythrocyticform parasitization in cerebral tissue was significantly less in the experimental groups than the degree of parasitization in control groups, and the experimental birds continued gaining weight for a longer period than the control birds. The passive transfer of immune serum had an effect on the course of the exoerythrocytic-form infection equivalent to killing 90% of the exoerythrocytic-form inoculum. The immunity to exoerythrocytic forms is form-specific, since the infected, chloroquine-treated, serum donors were just as susceptible to an erythrocytic-form challenge infection as normal turkeys. In vitro studies demonstrated that heat-inactivated serum from turkeys immune to exoerythrocytic-form infections caused a precipitate to form at the small end of exoerythrocytic merozoites. This precipitate was not observed on merozoites mixed with control serum.