Blood Loss and Replacement in Plasmodial Infections II. Plasmodium Vinckei in Untreated Weanling and Mature Rats

Abstract

Mature rats had negligible to mild infections followed by anemia greatly in excess of that attributable to red cell destruction by emerging parasites. It is suggested that this excess destruction may be due to the development of autoantibody. No wave of reticulocytosis followed these mild infections. Weanling rats had infections ranging from negligible to severe. Three out of 24 succumbed. Mild infections in weanlings were followed by excessive blood loss similar to but less extensive than that observed in mature rats. Direct rupture of red cells by parasites in severer infections in weanlings may mask excessive destruction by the postulated autoantibody. Waves of repair reticulocytosis occurred in weanlings following infections with peaks 5% or higher; but were not observed in the 3 weanlings which died. Parasitemias below a liminal level induced reticulocytic repair roughly proportional to degrees of parasitemia. Above this liminal level repair was more extensive but was not directly proportional to parasitemia. In contrast to Plasmodium berghei merozoites, which clearly prefer to invade relatively immature reticulocytes whatever the current blood picture, P. vinckei merozoites tend to invade the predominant red cells currently available. Processes of blood loss and replacement accompanying and following P. vinckei infections in rats of varying age were compared in detail with similar infections induced by P. berghei in rats. Loss of blood in excess of that due to direct parasitic rupture of red cells characterized both infections.