Immunity to exoerythrocytic forms of malaria. I. Course of infection of Plasmodium fallax in Turkeys

Turkeys inoculated intravenously with Plasmodium fallax parasitized erythrocytes developed an initial parasitemia. After the parasitemia crisis, the number of exoerythrocytic forms increased and caused the death of the bird about a week later. When the size of the erythrocytic-form inoculum was decreased tenfold, the day of maximum parasitemia and the day of death due to a high level of exoerythrocytic-form parasitism was delayed approximately 1 day. Turkeys inoculated intravenously with exoerythrocytic forms obtained from erythrocyte-free tissue cultures of parasitized turkey embryo brain cells developed an initial exoerythrocytic-form infection. The growth of exoerythrocytic forms in the poults was not affected by daily drug treatment with chloroquine; the number of exoerythrocytic forms/1000 cerebral cell nuclei was not significantly different in chloroquinetreated or untreated poults. Following the exoerythrocytic-form crisis, the parasitemia increased for several days in nondrug-treated birds. In chloroquine-treated birds, the erythrocytic forms were only detected during the period when exoerythrocytic forms were prevalent. Erythrocytic-form schizonts were not observed in chloroquinentreated birds. The poults stopped gaining body weight when either the exoerythrocytic forms or the erythocytic forms were prevalent. A tenfold decrease in the exoerythrocytic-form inoculum size delayed the exoerythrocytic-form infection 1 day. The development of exoerythrocytic forms was not synchronous in turkeys inoculated with exoerythrocytic forms and examined prior to the exoerythrocytic-form crisis.