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The hemoglobin of parasitized erythrocytes is a readily available source of nitrogen for the parasites, and the presence of large amounts of hematin in infected erythrocytes (2) suggests that the malaria parasite has the ability to break down hemoglobin during the coume of its metabolism.
PCR is most useful for confirming the species of malarial parasite after the diagnosis has been established by either smear microscopy or RDT. Serology detects antibodies against malaria parasites, using either indirect immunofluorescence (IFA) or enzyme-linked immunosorbent assay (ELISA).
Due to this, malaria causes biochemical abnormalities such as high bilirubin, elevated aspartate aminotransferase16, elevated alanine aminotransferase (ALT), and high creatinine, which increase the risk of disease complications17.
Life cycle of the malarial parasite. gametocytes are taken up with the blood meal, develop into gametes and combine sexually to form the zygote in the mosquito midgut. The zygote matures into a motile ookinete, which forces its way to the external wall of the midgut, where it forms an oocyst.
The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites .
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Amphotericin B deoxycholate and liposomal amphotericin B have been in use for the treatment of VL in the presence of concomitant illnesses or risk factors such as age extremes. Amphotericin B deoxycholate is highly toxic and has to be administered by slow intravenous infusion over 4 to 6 h, requiring hospitalization.
L (1) For the routine therapy of acute attacks of malaria, chloroquine (SN 7618) is the drug of choice.

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