Plasmodium falciparum - Pathology
Pathology of Plasmodium falciparum
Typical pathological effects of Plasmodium falciparum malaria infection are seen in organs such as the spleen, liver, lungs, bone marrow, kidney, and brain.
The organs infected by Plasmodium falciparum have the following common features:
the organs are black or slate-grey in color due to pigments
reticuloendothelial cells show hyperplasia
organ capillaries contain free pigments, free plasmodia, infected erythrocytes, etc
in some cases, aggregation of pigments present in thrombi is also seen in capillaries
Spleen
spleen is enlarged
in acute infection, a moderately enlarged spleen is soft, and the splenic substance is congested or hemorrhagic with a thin splenic capsule
the spleen may rupture but is rare
in chronic infection, the enlarged spleen is hard with a thick capsule
as the infection continues, the infected organ becomes grayish, dark brown, or even black- which is termed as ‘ague cake’
Liver
enlarged liver
in acute cases, the liver is also congested
in chronic cases, the organ increases its size, becomes firmer and pigmented
the number of Kupffer cells is increased and their cytoplasm is filled with Plasmodium falciparum, malarial pigment, and cellular debris
parenchymal cells also contain pigments
Bone Marrow
in acute cases, the bone marrow becomes red and hyperplastic
in chronic cases, the bone marrow becomes pale
reticuloendothelial cells become hyperplastic
parasitized RBC fills up the capillaries
Lungs
lungs become pigmented and show hemorrhagic patches
lung capillaries also contain pigments, pigmented leucocytes, phagocytes, and infected erythrocytes
Kidneys
kidneys are enlarged and congested
tubules may contain hemoglobin casts while the glomeruli contain malarial pigments
Brain
the brain becomes congested while the capillaries of the brain are plugged with parasitized RBCs with malaria pigments
parenchyma contains small foci of hemorrhage
around the vessels, malarial or Duck’s granuloma are found
in cases of severe hypoxia, neurons degenerate and occasional inflammatory infiltrates in the meninges are also seen
Hematological changes
Anemia caused by Plasmodium falciparum occurs through the following mechanisms
Enormous destruction of both parasitized and non-parasitized erythrocytes
decreased erythropoiesis in the bone marrow
Enormous destruction of both parasitized and non-parasitized erythrocytes
as parasitized erythrocytes are antigenically different than non-parasitized erythrocytes, erythrocytes bind nonspecifically to non-parasitized erythrocytes which form rosettes and eventually block the venule lumen
compliment mediated and autoimmune hemolysis are responsible for the destruction of non-parasitized erythrocytes
the spleen is responsible for destroying a large number of non-parasitized erythrocytes as well as continuing this process even after the Plasmodium falciparum parasites have been cleared from the circulation
Decreased erythropoiesis in the bone marrow
Due to TNF toxicity and failure of the host to recycle the iron-bound in the hemozoin, decreased erythropoiesis in the bone marrow occurs
in chronic cases, malarial anemia may resemble primary pernicious anemia
hemoglobin level and leucocyte count are decreased
host peripheral blood smear demonstrates free pigments, infected phagocytes, and pigmented white blood
large mononuclear leucocytes are increased in number