Abstract
Plasmodium is the malaria parasite that completes the life cycle between two different hosts, such as human and Anopheles mosquito. These parasites go through several developmental stages like exo-erythrocytic stage that is absent in Plasmodium falciparum, so relapses do not occur. The drugs which contain three P’s like proguanil, primaquine, and pyrimethamine kill schizonts in the liver. Due to prolonged treatment of high dose of chloroquine, there may be serious side effects named as Bull’s eye maculopathy. Atovaquone is rapidly acting blood schizonticide that acts by collapsing the parasite’s membrane. Artemisinins are the fastest acting drugs against malaria. Mepacrine is an anti malarial drug which concentrates in collagen tissue. Infection by P. falciparum is the most lethal form of malaria, in this case agglutination of the infected RBC occurs and these agglutinised RBCs block the capillary vessels of the internal organs. Tafenoquine is a single dose medication for radical cure of P. vivax malaria. People with an enzyme problem G6PD deficiency can cause severe anaemia. At least two genes affecting red cells which are resistant to P. falciparum are autosomal gene for haemoglobin S (HbS) and the gene linked to sex G6PD variant gene. Anaemia is the main result due to malaria by haemolysis of infected and uninfected erythrocytes, dyserythropoiesis, splenomegaly and depletion of folate stores. Cerebral malaria is the most urgent complication that is manifested by confusion or coma by clusters of parasitized red blood cells to form large size cells of the capillary circulation which adhere to the vascular endothelium and block the circulation causing cerebral hypoxia and resulting to neurological symptoms and diagnosed cerebral malaria. Blackwater fever associated with falciparum malaria is mostly common with individuals that have taken antimalarial treatment irregularly or deficient in G6PD deficiency. Tropical splenomegaly is another symptom in falciparum malaria. HbAS was the genetic variant which associated with protection against malaria incidence and other variants such as alpha thalassemia, G6PD deficiency, polymormhism of genes encoding NOS2A and TNF, as well as protection against uncomplicated malaria. Key words: Malaria, pathogenicity of malaria, parasite of malaria.  
Highlights
The innumerable microscopic and macroscopic forms which after attacking the human body manifest different diseases are known as pathogens and their activity are known as pathogenicity
Microbiological research revealed that five different species of Plasmodium genus protozoas, namely, P. falciparum, P. vivax, P. ovale, P. knowlesi, and P. malariae have been identified as causes of malaria in human (Anne et al, 2013)
A survey was carried out in Ethiopian young subjects who were admitted in hospital; the results obtained from the respective disciplines showed that the subjects with P. falciparum malaria had a high level of lymphocytes, other WBCs (White Blood cells) were within range, but the hemolysis was greater in patients having P. falciparum type of malaria when compared to other malarial parasites attacks
Summary
Modern approach of treatment on destroyable pathogenicity of malaria parasite: A review article. Plasmodium is the malaria parasite that completes the life cycle between two different hosts, such as human and Anopheles mosquito. These parasites go through several developmental stages like exoerythrocytic stage that is absent in Plasmodium falciparum, so relapses do not occur. Blackwater fever associated with falciparum malaria is mostly common with individuals that have taken antimalarial treatment irregularly or deficient in G6PD deficiency. Tropical splenomegaly is another symptom in falciparum malaria.
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