Chronic, patent Plasmodium berghei malaria in splenectomized mice.
It was shown that splenectomized mice could develop a certain resistance to Plasmodium berghei but usually no real immunity, since the infection became chronic, often with high parasitemias. A patent infection lasting at least 2 weeks was necessary for the development of this degree of protection. Prolonged suppression to subpatent levels (sulfonamide treatment), rather than radical cure (chloroquine), after 2 weeks of patency yielded a higher proportion of mice resistant to superinfection. An increasing proportion of B10LP, but not C57BL/Rij or BALB/c, mice cleared their chronic infection spontaneously in time. Chronic patent infections were accompanied by anemia, elevated serum glutamate oxaloacetate transaminase levels, indicating liver pathology, and decreased immune reactivity, but the magnitude to these pathological changes was limited compared with changes in primary, lethal infections in intact controls. Parasitemia and pathology did not always develop synchronously.
D000818:Animals; D000917:Antibody Formation; D001219:Aspartate Aminotransferases / Q000097:blood; D002738:Chloroquine / Q000627:therapeutic use; D006400:Hematocrit; D007114:Immunization; D008288:Malaria / Q000097:blood / Q000188:drug therapy / Q000276:immunology*; D051379:Mice; D008815:Mice, Inbred Strains; D010962:Plasmodium berghei; D013156:Splenectomy; D013411:Sulfadiazine / Q000627:therapeutic use; D013997:Time Factors
D013411:Sulfadiazine; D002738:Chloroquine; D001219:Aspartate Aminotransferases