Protozoa - Plasmodium Life Cycle

Plasmodium Life Cycle

Because Plasmodium falciparum is a significant cause of malarial deaths, and is the most prevalent form in sub-Saharan Africa, we'll use its morphology in our diagram.

Overview

See generalized Apicomplexa Life Cycle

One round of merogony in the human liver, followed by several rounds of merogony in RBCs.
Then, gametogony begins in RBC, and finishes in mosquito.

IN HUMAN HOST:

Asexual Reproduction

1. A female Anopheles mosquito bites a human host and transmits sporozoites in its saliva.

Exo-erythrocytic Phase (liver)

2. Sporozoites infect liver cells within a few hours of the bite. – Invasion is aided by apical complex – Sporozoites develop into hepatic schizonts, which contain tens of thousands of merozoites (this processes is often called "exoerythrocytic shizogony," which is a type of merogony). – **P. vivax and P. ovale sporozoites can stay dormant in liver as hypozoites, may reactivate later and enter blood as merozoites.** 3. The infected hepatocytes rupture, and the schizonts release the merozoites into the bloodstream – The merozoites are released in vesicles, which later release the merozoites in the pulmonary capillaries; the vesicles protect the parasite from the host immune system.

Erythrocytic Phase

4. Merozoites infect RBC.

Be aware that different species of Plasmodia target RBC of different developmental stages.

5. Merozoites become trophozoites (the immature stage is called the ring stage). – Trophozoites break down hemoglobin to access amino acid nutrients; the process produces malaria pigment hemozoin. Thus, the yellow/brown and black granules are indicative of blood-stage parasite form. 6. Some trophozoites become erythrocytic schizonts (via multiple rounds of nuclear division w/out cytokinesis). – Schizonts give rise to new generations of merozoites (erythrocytic schizogony, a form of merogony). In late stage schizonts, aka, segmenters, you can see the individual merozoites. – RBCs rupture and release the merozoites, which infect other RBCs. Parasitemia occurs, and clinical symptoms are caused by antigens and waste products of ruptured cell. – Every time the parasites break free and invade new RBC, fever occurs, which explains the cyclical timing of symptoms. – Erythrocytic cycle duration varies by species: P. falciparum, P. vivax, and P. ovale = 48 hours P. malariae = 72 hours P. knowlesi = 24 hours – Note that RBCs infected by P. falciparum trophozoites and schizont stick to capillary endothelial cells, so they aren’t found in peripheral circulation like other Plasmodium spp. 7. Some parasites bypass additional rounds of merogony and enter the sexual reproduction pathway to produce gametocytes, which circulate in the blood extracellularly (and are nonpathogenic). 8. Gametocytes are ingested by a mosquito during a blood meal. The remainder of the life cycle takes place within the mosquito.

IN MOSQUITO:

Note that the mosquito is not harmed by the parasite, as the human host is.

1. Mosquito ingests gametocytes from human during blood meal. 2. Gametocytes go through sporogonic cycle, give rise to gametes (gametogenesis), which fuse to produce zygotes. 3. Zygotes become motile and elongate, are now called ookinetes. 4. Ookinetes invade the mosquito midgut wall, develop into oocytes on its external surface. 5. Oocytes go through sporogony (asexual reproduction) to produce thousands of haploid sporozoites. 6. The oocytes rupture and release the sporozoites, which migrate to the mosquito's salivary glands. 7. The sporozoites are transferred to human host during a blood meal.

Protozoa - Plasmodium Life Cycle

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