Anti-plasmodial Property Of Moringa Oleifera Seed Extract On Swiss Mice

2.1.5 Molecular Cell Biology and Pathogenesis of Malaria
Plasmodium species have 14 chromosomes, one mitochondrion, and one apicoplast organelle similar to chloroplast but not photosynthetic (VanDooren and Striepen, 2013). All Apicomplexa including malaria parasites are characterized by a set of apical organelles called rhoptries, dense granules and micronemes. In Plasmodium, there are three invasive forms involving the apical organelles: sporozoite, merozoite, and ookinete (Bannister et al., 2000). The co-receptors on sporozoites that mediate invasion (Robson et al., 1995) bind specifically to the heparan sulfate proteoglycans (Frevert et al., 1993) on hepatocytes and Kupffer cells. CD81 and CD68 are receptors for falciparum invasion in hepatocytes (Cha et al., 2015). After penetrating space of Disse in the liver, sporozoites migrate via several hepatocytes and engage in a final invasion, with the formation of a parasitophorous vacuolar membrane (PVM) (Silvie et al., 2003). PVM is then ruptured by plasmodial enzymes and merozoite egress from the infected hepatocyte to access blood circulation (Cha et al., 2015).
Within the circulation, merozoites are rapidly and specifically enter RBCs, thus implying receptor-ligand interactions. Merozoite surface protein-1 (MSP-1) associated with the parasite membrane via a glycosylphosphatidylinositol (GPI) anchor does binds to the RBC surface proteins (Goel et al., 2003; Baldwin et al., 2015; Boston, 2016). Eight other merozoite surface-bound GPI-anchored proteins interact with RBC have been reviewed elsewhere (Cowman et al., 2012). After binding to RBC, the merozoite reorients itself using apical membrane antigen 1 (AMA-1) so that the apical end of the parasite will locate adjacent to the RBC membrane with a transient RBC deformation. The contents of apical organelles are going to be expelled as the parasite invades (Mitchell et al., 2004).
2.1.6 Diagnosis of Malaria
Malaria must be diagnosed early and accurately to end up with an effective management of patients. Broadly, one can classify diagnosis of malaria in to clinical and parasitological diagnoses. Clinical diagnosis is based on the patient's symptoms and on signs at physical examination (WHO, 2015; CDC, 2016). WHO recommends malaria should be suspected in any patient presenting with a history of fever or temperature >37.5 0C in the absence of other obvious causes (WHO, 2015). Nigerian FMoH advocates clinical diagnosis of malaria should be made in a patient who has fever or history of fever in the last 48 h and lives in malaria-endemic areas or has a history of travel within the last 30 days to malaria-endemic areas (FMoH, 2012).

All of suspected malaria should be confirmed with a parasitological diagnosis in all settings (WHO, 2015). Light microscopy and RDTs are routinely employed methods for parasitological diagnosis of malaria. In 2005, single-species RDTs were introduced in Ethiopia. Years after, multi-species RDTs are being supplied by FMoH to health posts (FMoH, 2012). PCR based method and serology tests are another parasitological diagnostic means (CDC, 2016). Recently developed rolling circle enhanced enzyme activity detection (REEAD) - and micromagnetic resonance reflaxometric (MMR) - test are also amenable to deployment in field conditions (Kumar and Renu, 2015).