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Malaria

Malaria
Malaria
  • Malaria affects 100 million people and kills 1.5million every year. The etiologic agent is a protozoa called plasmodium and the anopheles mosquito acts as a vector.
  • The massive antimalaria campaign from 1950 to 1980 failed and produced resistant mosquito for DDT and resistant plasmodium to chloroquine.
Life cycle and pathogenesis
  • The sporozoites transmitted by the mosquito bites pass into the blood stream and invade the hepatocytes by binding hepatocyte receptors for serum proteins thrombospondin and properdin. this occurs because the sporozoites have similar domains to these proteins. Within the liver cell they multiply rapidly and as many as 30,000 merozoites (asexual haploid blood form) are released into the blood when hepatocyte ruptures.





·       The HLA-B53 associated resistance to PF. Infection showed by many Africans appears caused by the ability of HLA-B53 to present liver stage malaria Ag to cytotoxic T cells which kill malaria infected hepatocytes.
·       Once in the blood, the merozoites of PF bind on a glycophorin molecule on the surface of RBC, P   vivax on Duffy Ag on the RBC (many African are resistant to P vivax infection because they lack the Duffy Ag)
·       In the RBC the merozoites replicate in digestive vacuoles hydrolyzing the HB with aspartate protease homologues to that of the HIV VIRUS.
·       Individual with sickle cell anemia are resistant to malaria parasites because parasited sickled RBC are more readily removed from the circulation when the blood passes in the spleen.


  • After rupture of the RBC, the merozoites reinfect other RBC but some merozoites develop in sexual forms, gametocytes that can infect the mosquito and are responsible for the perpetuation of the disease.
  • As the parasites mature inside the RBC they change from ring form to schizont form and secret protein called sequestrin encoded by var genes. The protein forms 100nm humps on the cell surface called knobs.
  • The sequestrin binds to the endothelial cell by ICAM-1, the thrombospondin receptor and glycophorin CD46 causing malaria infected RBC to be removed from the circulation in the spleen. So in the peripheral smear we see only ring form containing RBC which are flexible but not the schizont forms


  • The cerebral malaria with 80% death in children, there are an increased number of ICAM-1, thrombospondin receptors and CD46 on their cerebral endothelial cells ( perhaps activated by cytokines like TNF) to which bind to infected RBC.
  • The organs most commonly affected are spleen, liver with congestion and enlargement due to macrophage proliferation (hepatospleenomegaly)
  • In non immune patients, pulmonary edema and shock with DIC cause death of the individual.

Cerebral malaria.
  • Brain vessels are plugged with parasited RBC containing dots of HEMOZOIN pigment.
  • There are a ring hemorrhage due to local hypoxia from the vascular stasis and focal inflammatory reaction known as malaria granuloma. When the hypoxia is severe enough there is neuron degeneration, focal ischemic softening and occasionally scant inflammatory infiltrate in the meninges

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