Plasmodium malariae: parasite and disease

Abstract

A review of the life history of Plasmodium malariae, the quartan malaria parasite of humans, is presented. Much of the information is based on data obtained from induced infections in humans who were given malaria therapy for the treatment of neurosyphilis between 1940 and 1963. Prepatent periods (i.e., the time until the first day of parasite detection) fever episodes, and maximum parasitemias as a result of infection with P. malariae were obtained and are presented. Experimental and known vectors of the parasite are also discussed. Splenectomized chimpanzees and New World monkeys are readily infected and serve as sources of parasites and antigens for diagnostic and molecular studies. South American monkeys are naturally infected with a parasite known as Plasmodium brasilianum. This parasite appears to be P. malariae that has adapted from humans to grow in monkeys, probably within the last 500 years. Infection with P. malariae is associated with the production of immune complexes in the kidneys and the associated nephrotic syndrome. The essential lesions are a thickening of the glomerular basement membrane and endocapillary cell proliferation. Studies of monkeys infected with P. malariae indicate the same pathology as that demonstrated in humans.

FIG. 1.

Daily peak parasite counts and fever peaks in a patient infected with Plasmodium malariae, showing the synchronous quartan pattern of fever and peak parasite count.

FIG. 2.

Median parasite counts during the first 40 days of patent parasitemia for 69 patients infected with Plasmodium malariae. Maximum parasite counts are limited in infections with P. malariae due to the low number of merozoites produced, 72-hour developmental cycle, and preference for older erythrocytes.

FIG. 3.

Development of oocysts of Plasmodium malariae in Anopheles freeborni mosquitoes. Top row, 10-, 11-, 12-, and 13-day oocysts; bottom row, 14-, 15-, and 17-day oocysts and sporozoites.

FIG. 4.

Development of the erythrocytic stages of Plasmodium malariae. 1, normal red cell; 2 to 5, young trophozoites; 6 to 11, growing trophozoites; 12 and 13, nearly mature and mature trophozoites, respectively; 14 to 20, developing schizonts; 21 and 22, mature schizonts; 23, developing gametocyte; 24, mature macrogametocyte; 25, mature microgametocyte. (Reprinted from reference .)

FIG. 5.

Development of the IFA response in a patient following infection and recrudescence of an infection with Plasmodium malariae. Recrudescence of infection began at day 84.

FIG. 6.

Daily parasite counts and percent infection of Anopheles freeborni mosquitoes when fed on a splenectomized Aotus lemurinus griseimembra monkey infected with the Uganda I strain of Plasmodium malariae.

FIG. 7.

Top row, trophozoite stages of Plasmodium malariae; middle row, trophozoite stages of Plasmodium knowlesi; bottom row, trophozoite stages of Plasmodium inui.