The first demonstration of infection of chimpanzees with P. ovale indicated that splenectomy was necessary for the animals to support significant parasitemia (11, 12).
Infections with the Nigerian I/CDC strain of P. ovale have been induced in splenectomized chimpanzees (25, 76). Animals previously infected with P. vivax or P. malariae were readily susceptible to infection via intravenous inoculation of infected erythrocytes that had been stored frozen. Maximum parasite counts ranged from 1,240 to 127,224/µl. Anopheles stephensi, A. gambiae, A. freeborni, and A. dirus mosquitoes were infected by feeding through parafilm membranes on heparinized blood from chimpanzees. Mean oocyst counts ranged from 1 to 85.1 per mosquito midgut. One infection was induced in a chimpanzee via the bites of infected A. gambiae; the prepatent period was 16 days.
Attempts to infect intact rhesus monkeys (Macaca mulatta) have been unsuccessful (19, 55). Subsequent attempts to infect splenectomized rhesus monkeys were also unsuccessful. Sporozoites from the salivary glands of infected A. maculipennis mosquitoes were injected into an intact mona monkey (Cercopithicus mona), but no parasitemia developed (37). Attempts to infect splenectomized New World Aotus trivirgatus griseimembra monkeys were also unsuccessful (20). Although Saimiri sciureus boliviensis monkeys were shown to support the development of exoerythrocytic stages, parasitemia was not demonstrated (75). Five splenectomized S. s. boliviensis monkeys were injected with from 77,000 to 500,000 sporozoites dissected from A. dirus mosquitoes; none developed detectable parasitemia during 3 months of observation.
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