Malaria is a mosquito-borne disease caused by five protozoa: Plasmodium

falciparum, P. vivax, P. malariae, P. ovale, and most recently implicated P.knowlesi.

Infection with P. falciparum is being accounted for more than 90% of the world’s
malaria mortality and therefore remains an important threat to public health on a
global scale.[1][2] The World Health Organization (WHO) World Malaria report
2019 estimates 228 million cases of malaria worldwide, causing 405 000 deaths in
the year 2018, many under the age of 5. Malaria is endemic in more than 90
countries, affecting approximately 40% of the world’s population.[2] There is a
significant number of cases of imported malaria and local transmission following
importation occurring in non-malarial countries, including North America and
Europe.[3] Malaria is associated with travelers to the endemic areas, and
increasing numbers of imported malaria necessitate an understanding of
frequently non-specific symptoms, difficulties related to the malarial diagnosis,
and treatment possibilities.[2]

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Etiology
Five species of genus Plasmodium are known to cause malaria in humans. The
vector for Plasmodium spp. is a female Anopheles mosquito that inoculates
sporozoites contained in her salivary glands into the puncture wound when
feeding.[3] Sporozoites enter peripheral bloodstream and are uptaken by
hepatocytes, where they undergo an asexual pre-erythrocytic liver-stage as liver
schizonts lasting up to 2 weeks before the onset of the blood stage.[3][4] As they
replicate within hepatocytes, they form motile merozoites that are subsequently
released into the bloodstream, where they invade red blood cells (RBC). The
process continues through serial cycles of asexual replication of merozoites that
go through ring, trophozoite, and schizont stages before forming and releasing
new invasive daughter merozoites that consequently infect new RBC, therefore
causing a rise in parasite numbers.[3][5] P. falciparum produces high levels of
blood-stage parasites and is known to modify the surface of the infected RBC,
creating an adhesive phenotype, e.g. (sticky cell) causing RBC sequestration inside
small and middle-sized vessels, removing the parasite from the circulation for
nearly half of the asexual cycle.[6] Sequestration leads to splenic parasite
clearance avoidance, host cell endothelial damage, and microvascular
obstruction.[5][6] A small fraction of intra-erythrocytic parasites switch to sexual
development, producing morphologically distinct male and female gametocytes
that reach the host's dermis and are ingested by a mosquito, rendering it
infectious to humans.[3][4][5] After in