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The Vector-host Plasmodium Life Cycle; A Brief Overview Of The Malaria-causing Parasite.

Review of malaria parasite life cycle

Date : 06/04/2021

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Uploaded by : Bethany
Uploaded on : 06/04/2021
Subject : Biology

Malaria is a febrile vector-borne disease caused by five species of the Plasmodium protozoan parasite P. falciparum, P. malariae, P. ovale, P. vivax and P. knowlesi. The female Anopheles mosquito is responsible for transmitting the Plasmodium parasite only the females of this genus feast on human blood meals, as this nutrient-rich resource is required for mosquito egg growth. Existing in the sporozoite form of the parasite within the mosquito salivary glands, Plasmodium is injected by the mosquito vector to the human host during a blood meal. Here, the sporozoites migrate from the intradermal injection site to the blood capillaries, whereby they are transported via the blood stream to the liver target organ. If not engulfed and destroyed by blood phagocytes, the sporozoites enter the paraenchymal hepatocytes (human liver cells) where they undertake asexual pre-erythrocytic schizogeny. This is a growth stage where the parasite progresses from its sporozoite form to a schizont, and eventually reaches maturity to the merozoite stage within the liver cell. During this stage of infection, the malaria patient is asymptomatic and may be unaware they have contracted the infectious disease. The merozoites exit hepatocytes via a mechanism not well established, although parasite-induced hepatocyte rupture is not postulated to occur. Instead, liver-membrane-bound merozoites are hypothesized to bud off from the host organ. Transported via the blood, hepatic vesicles of merozoites travel via the vena cava, through the right side of the heart and exit to the pulmonary artery, whereby the membrane-bound vesicle disintegrates and merozoites are liberated into the pulmonary microvasculature. To avoid destruction by circulating phagocytic cells, the free merozoites invade erythrocytes (red blood cells), secreting predatory enzymes to encourage engulfing entry into their target red cell. Once securely within the erythrocyte, merozoites undergo morphological transformation and growth into the trophozoite form, digesting intracellular red cell components of haemoglobin and proteins for the production of anabolic amino acids and haem groups for parasite respiration electron transport chains. Elongation and segmentation during parasite growth is erythrocytic schizogeny - consecutive rounds of asexual reproduction which ultimately result in schizont formation containing mature merozoites descended from the intermediate trophozoite form. These schizonts rupture (this is the characteristic symptomatic stage of malaria the patient experiences), with merozoites released from the infected erythrocyte. This stage perpetuates as further red cells are targeted for invasion and phagocyte evasion, thus the parasite multiplies many times. During the blood stage of infection, some merozoites undergo sexual reproduction after multiple rounds of intraerythrocytic multiplication. This is gametogenesis, in which male microgametocytes are formed via exflagellation, and female macrogametocytes are formed also. When another Anopheles mosquito withdraws a blood meal from the malaria infected human, these gametocytes are taken up by the disease vector and arrive in the mosquito midgut. If they survive the vector immune defences, the female macrogametocyte is fertilized by the male microgametocyte within the mosquito stomach, resulting in the formation of an ookinete zygote. The ookinete becomes embedded within the Anopheles mosquito gut wall, with maturity of the oocyst spore phase forming sporozoites. The oocyst eventually ruptures and the mature sporozoites migrate via the mosquito anatomy to the saliva glands, waiting for another cycle of infection to a new human host upon another blood meal.

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