It is the causative agent of Malaria. It is endemic in tropical and subtropical areas worldwide where mortality is mainly in children and pregnant women. In the USA malaria is seen in travellers returning from endemic areas and in recent immigrants from these areas.
Pathogenesis: Plasmodium goes through various stages of its life cycle. Female Anopheles mosquitoes serve as vectors. Gametocytes infect mosquitoes and multiply to form sporozoites which migrate to salivary glands of the infected mosquito. The sporozoites are injected into human blood during a mosquito bite. They reach the human liver to start the exoerythrocytic stage/schizogony of life cycle. Liver sporozoites will mature into schizonts , which rupture and release merozoites. They undergo an erythrocytic stage/ schizogony in their life cycle as well where merozoites infect RBCs, go through phases of immature trophozoite or ring form and then mature trophozoite, followed by schizonts which rupture to release merozoites. Some parasites will undergo a sexual cycle to form gametocytes.
The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host The number 1. Sporozoites infect liver cells The number 2 and mature into schizonts The number 3, which rupture and release merozoites The number 4. (Of note, in P. vivax and P. ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks, or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony The letter A), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony The letter B). Merozoites infect red blood cells The number 5. The ring stage trophozoites mature into schizonts, which rupture releasing merozoites The number 6. Some parasites differentiate into sexual erythrocytic stages (gametocytes) The number 7. Blood stage parasites are responsible for the clinical manifestations of the disease.
The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal The number 8. The parasites’ multiplication in the mosquito is known as the sporogonic cycle The letter C. While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes The number 9. The zygotes in turn become motile and elongated (ookinetes) The number 10 which invade the midgut wall of the mosquito where they develop into oocysts The number 11. The oocysts grow, rupture, and release sporozoites The number 12, which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle.
Interestingly, persons who are negative for the Duffy blood group have red blood cells that are resistant to infection by P. vivax. Persons who have sickle cell trait are relatively protected against P. falciparum malaria.
Clinical features: Malaria presents with flu-like symptoms initially such as fever, chills, sweats, headaches, muscle pains, jaundice, nausea and vomiting. Fever cycles every fourth day in P. malariae (quartan malaria) while it cycles every third day (tertian malaria) in P. falciparum, P ovale and P vivax. In severe malaria (primarily caused by Plasmodium falciparum which causes cerebral malaria) there will be confusion, coma, neurological focal signs, renal failure, severe anemia and respiratory difficulties. Cerebral malaria is commonly associated with hypoglycemia. Hemolysis leading to hemoglobinuria can cause renal shutdown with dark urine, a condition called 'blackwater fever” due to the dark color of the urine.
Diagnosis of Malaria: Blood smears stained with Giemsa show gametocytes and/or trophozoites and rarely, schizonts. Gametocytes of P.falciparum are crescent shaped or banana shaped while all other species are spherical. Rapid diagnostic tests (RDTs) using immunochromatography give results in 20 minutes or less. RDTs have to be confirmed with microscopy. PCR can be done for confirming the species. Indirect immunofluorescence and ELISA can be done for detecting antimalarial antibodies but they are more useful in diagnosing past infections.
Rings of P. falciparum in a thin blood smear.
Ring-form trophozoites of P. falciparum in a thin blood smear, exhibiting Maurer’s clefts.
Gametocyte of P. falciparum in a thin blood smear.
Ring-form trophozoites of P. vivax in a thin blood smear.
Trophozoite of P. vivax in a thin blood smear. Note the amoeboid appearance, Schüffner’s dots and enlarged infected RBCs.
Schizont of P. vivax in a thin blood smear.
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