In investigations on the role of the spleen in host defense against malaria, we studied the course of murine malaria in three groups of mice with altered splenic function: congenitally asplenic mice, adult-splenectomized mice, and adult-splenectomized mice which were reconstituted with spleen-cell suspensions. Intact mice infected with either Plasmodium yoelii or P. chabaudi adami experienced infections which resolved spontaneously, with low mortality. Congenitally asplenic and splenectomized-reconstituted mice were unable to clear their primary infections, and experienced high mortality; infections in the latter two groups of mice differed little from those in splenectomized, nonreconstituted controls. However, when asplenic and splenectomized mice were treated with cloroquine during their primary infections and then rechallenged with the homologous Plasmodium species, they experienced mild infections similar to those of intact controls. These observations support the concept that the host defense in primary malaria infections requires an architecturally intact spleen, and therefore is not solely dependent upon the presence of a subpopulation of immune spleen cells.
Present address: Division of Communicable Diseases and Immunology, Department of Immunology, Walter Reed Army Institute of Research, Washington, D.C. 20012.
Present address: Division of Geographic Medicine, Department of Medicine, Tufts-New England Medical Center, Boston, Massachusetts 02111.