Plasmodium
Summary
Plasmodium is a genus of protozoan parasites transmitted by female Anopheles mosquitoes that cause malaria. The major species affecting humans are P. falciparum, P. vivax, P. ovale, P. malariae, and P. knowlesi, each with distinct clinical patterns and complications. P. falciparum is the most lethal species, causing severe complications like cerebral malaria and blackwater fever.
Detail
Plasmodium species have a complex life cycle involving both mosquito (definitive host, sexual stage) and human (intermediate host, asexual stage) hosts. Infection begins when an infected female Anopheles mosquito injects sporozoites, which travel to the liver and invade hepatocytes (exo-erythrocytic schizogony). P. vivax and P. ovale can form dormant hypnozoites in the liver, causing relapses months to years later. Merozoites released from the liver invade RBCs, undergoing asexual replication (erythrocytic schizogony), causing RBC rupture and the classic cyclic fevers—every 48 hours (tertian) for P. vivax/ovale/falciparum, every 72 hours (quartan) for P. malariae. Some merozoites differentiate into gametocytes, which are taken up by mosquitoes to continue the sexual cycle (sporogony) in the mosquito gut, producing sporozoites that migrate to salivary glands.
Clinical features include cyclical fever, chills, rigors, headache, myalgias, splenomegaly, and hemolytic anemia. P. falciparum causes the most severe disease due to its ability to sequester in microvasculature (cytoadherence via PfEMP1 protein), leading to cerebral malaria, acute respiratory distress syndrome, renal failure (blackwater fever), and high parasitemia. Diagnosis is via thick and thin blood smears (Giemsa stain)—thick for detection, thin for species identification and parasitemia quantification. Key morphologic findings: P. falciparum shows banana-shaped gametocytes and multiple ring forms per RBC with no enlargement of infected RBCs; P. vivax/ovale show enlarged RBCs with Schüffner's stippling.
Treatment depends on species and resistance patterns: chloroquine for sensitive strains; artemisinin-based combination therapy (ACT) for P. falciparum in resistant areas; primaquine is added for P. vivax/ovale to eradicate hypnozoites (must screen for G6PD deficiency first due to hemolysis risk). Sickle cell trait, G6PD deficiency, and Duffy-antigen negativity (protective against P. vivax) are classic protective genetic factors tested on boards.
Sources
- First Aid for the USMLE Step 1
- CDC DPDx Malaria Parasite Overview
- Harrison's Principles of Internal Medicine
- Sherris Medical Microbiology
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