Paper I — 2025 March (Supplementary (SAY)) (2019 Scheme) — Q15
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Paper I
2025 March (Supplementary (SAY)) (2019 Scheme) · 100 marks · 180 min
Question
Describe the life cycle of plasmodium falciparum
Q153 marksShort Answers
Answer
Life cycle of Plasmodium falciparum — a two-host life cycle, with asexual (schizogonic) development in humans and sexual development in the female Anopheles mosquito.
In the human host (asexual cycle):
Sporozoites are injected into the human bloodstream during the bite of an infected female Anopheles mosquito.
Pre-erythrocytic (exo-erythrocytic) schizogony — sporozoites travel to the liver, invade hepatocytes, and multiply asexually to form a tissue schizont, which ruptures to release thousands of merozoites into the bloodstream (this stage takes approximately 5–7 days for P. falciparum; notably, P. falciparum does not form persistent hypnozoites in the liver, unlike P. vivax/P. ovale, so it does not cause true relapse).
Erythrocytic schizogony — released merozoites invade red blood cells, developing sequentially through ring stage → trophozoite → schizont; the schizont ruptures the RBC, releasing new merozoites that invade further erythrocytes, perpetuating the cycle. This erythrocytic cycle takes approximately 48 hours in P. falciparum, correlating with the classical (though often irregular in falciparum) fever periodicity.
A proportion of merozoites differentiate into sexual forms — male and female gametocytes — which circulate in peripheral blood (notably, P. falciparum gametocytes are characteristically crescent/banana-shaped, distinguishing them from other Plasmodium species) but do not develop further unless taken up by a mosquito.
In the mosquito host (sexual cycle, sporogony):
A female Anopheles mosquito ingests gametocytes during a blood meal from an infected human.
In the mosquito midgut, male and female gametocytes mature into gametes; fertilization produces a zygote, which develops into a motile ookinete.
The ookinete penetrates the midgut wall and develops into an oocyst.
The oocyst undergoes sporogony, producing numerous sporozoites, which migrate to the mosquito’s salivary glands.
Sporozoites are then injected into a new human host during the mosquito’s next blood meal, completing the cycle.
Clinical correlation: the erythrocytic schizogony stage is responsible for all clinical manifestations of malaria (fever coinciding with synchronized schizont rupture); P. falciparum’s propensity to infect erythrocytes of all ages (unlike P. vivax, which prefers reticulocytes) contributes to its ability to cause very high parasitaemia and severe/malignant disease, including cerebral malaria due to sequestration of parasitized RBCs in cerebral microvasculature.
