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The Clinical Significance Of The Malaria Parasite: Pathology And Route Of Transmission

Updated on March 27, 2014

How Malaria Is Transmitted

The malarial parasites grow in the erythrocytes and at the end of schizogony, rupture them resulting in hemolysis which coincides with the febrile paroxysm. Plasmodium falciparum invades all stages of red cells and multiplies faster, thereby leading
The malarial parasites grow in the erythrocytes and at the end of schizogony, rupture them resulting in hemolysis which coincides with the febrile paroxysm. Plasmodium falciparum invades all stages of red cells and multiplies faster, thereby leading | Source

The Pathology Of Malaria Infection

The malarial parasites grow in the erythrocytes and at the end of schizogony, rupture them resulting in hemolysis which coincides with the febrile paroxysm. Plasmodium falciparum invades all stages of red cells and multiplies faster, thereby leading to heavier parasitemia and more severe anemia and organ damage than P. Vivax. Plamodium vivax merozoites enter only young erythrocytes. Parasites can be demonstrated in variable numbers in the erythrocytes and tissues such as bone marrow, liver and spleen depending on the severity of infection. Fever develops when the parasite number reaches the required minimum and this is achieved by successive schizogony after the pre-erythrocytic phase. In P.vivax, all stages of the parasites are seen in erythrocytes in peripheral blood. The growing stages of P. falciparum develop in the small vessels of vital organs and, therefore, the peripheral blood usually shows only the ring forms and gematocytes. The alteration in physical state of the erythrocyte leads to sickness of the microcirculation. Such erythrocytes, along with a large number of phagocytic cells, occlude the small blood vessels. Falciparum malaria causes significant mortality, the others do so only rarely. At autopsy, the pathological changes include parenchymal degeneration of the Kidneys and liver, reticuloendothelial hyperplasia, accumulation of parasitized cells and fibrosis in several organs particularly the spleen and liver. Malarial pigment is heavily deposited in these organs, but it does not cause organ damage. Liver and spleen are slate-grey in colour.

They show areas of fibrosis. In the serious form of falciparum, malaria such as pernicious malaria and black water fever, the kidneys show tubular degeneration and necrosis. Acute nephritic syndrome may develop as a result of immunological abnormalities. Plasmodium malariae leads to nephrotic syndrome and this is also immune-mediated. The antigen antibody complexes can be demonstrated in the basement membrane. Continued exposure to the parasites stimulates the production of antibodies- both IgG and IgM.

Affected Children Due To Malaria Infection

Source

The Malaria Patient

The immature status of the individual determines the clinical picture. The classical picture develops in non-immunes. Manifestations are milder in semi-immunes. Maternal antibodies are passively transferred to the fetus and these persist for the first few months of life after which the infant becomes susceptible. Antibodies passed in mother’s milk may have a mild protective role. In general, the normal placenta acts as an effective barrier against congenital transmission, though such transmission has been recorded in non-immunes. The malarial parasite depends on the host’s hemoglobin for its metabolism and therefore abnormalities in the erythrocytes make them unfavourable for the growth and development of particular species of malarial parasites. Falciparum malaria is rare in patients with hemoglobin S-trait, thalassemia or glucose-6-phosphate dehydrogenase deficiency. In population groups, showing high prevalence of these genetic disorders, there is a natural protection against falciparum malaria. This represents a state of balanced polymorphism in nature.

© 2014 Funom Theophilus Makama

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      Diana 3 years ago

      Interesting study. If it weren't for the association with mliaraa endemicity apparently attested in Africa and Europe, the pure gene evolution would point to a migration out of America (ancestral state) through East Asia to Europe and Africa (derived state). India is a bridge between the east and the West and a "swing" continent. Africa still preserves the original state in some pockets such as Madagascar, Horn of Africa and northwest Africa but overall it has shifted away from the original condition. But even with the mliaraa association in Africa and Europe this scenario would work.The map of Hbs distribution reminds me of Y-DNA YAP+ distribution, with Africa being heavy on YAP+ but with pockets of YAP-, Europe intermediary and Asia showing a strange small pocket of YAP+. India has Hbs, Tibetans and Andaman islanders have high frequencies of YAP+. America is devoid of YAP+ completely. There's a parallelism here, I think.

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