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Case study (30) – Plasmodium falciparum Malaria

Case study (30) – Plasmodium falciparum Malaria 


Q1. What abnormality is seen in the peripheral blood film? 

Q2. What are the important hematological complications of this condition? 

Q3. What treatment should be offered? 


A1. Malaria. The existence of more than one ring form per red cell strongly suggests Plasmodium falciparum. 

A2. Anemia, which is principally due to hemolysis of infected erythrocytes but is also due to immune hemolysis, splenomegaly, and impaired marrow production. 

Thrombocytopenia is usually present, partly because of an enlarged spleen (splenomegaly). 

Low-grade disseminated intravascular coagulation may also occur. 

This can be serious in an overwhelming infection. 

Leukopenia may arise from splenomegaly. Hypergammaglobulinemia is frequent. 

Chronic malaria infection may cause substantial splenomegaly ("tropical splenomegaly"), and chronic immune stimulation may be a factor in the development of lymphoid malignancies (e.g. lymphoma). 

Neutrophil leukocytosis and monocytosis may also occur. 

A3. Falciparum malaria is commonly resistant to chloroquine and is best treated with quinine (by intravenous infusion in severely ill patients). 

If resistance to quinine is suspected, it should be followed by either fansidar or tetracycline. 

Mefloquine and halofantrine are also currently recommended for falciparum malaria. 

Infections caused by Plasmodium ovale, Plasmodium vivax, and Plasmodium malariae are usually less serious, and resistance to chloroquine is not common. 

Peripheral blood film (2) shows a mature schizont from a patient with P. vivax infection and Peripheral blood films 3 and 4 show gametes of P. falciparum and P. vivax, respectively. 

Peripheral blood film (2)

Peripheral blood film (3)

Peripheral blood film (4)

A variety of hereditary red blood cell abnormalities may provide a certain degree of protection from malaria, which helps explain the widespread prevalence of "balanced polymorphism" in the population. 

Heterozygosity for the sickle gene is beneficial as the invasion of the red cell is followed by parasite metabolism and reduced oxygen tension within the cell. 

The resultant sickling causes deformed cells which can be filtered by the reticuloendothelial system. 

Homozygosity for the sickle cell gene is usually related to hyposplenism and insufficient activity of the reticuloendothelial (RE) system; such subjects are not protected from malaria 

Alpha and beta thalassemias and certain red blood cell membrane abnormalities (such as ovalocytosis) may provide some degree of protection against malaria. 

There is excellent epidemiological evidence that glucose-6-phosphate dehydrogenase (G6PD) deficiency can also provide a certain degree of protection.