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General Biology
Published in Ronald Fayer, Lihua Xiao, Cryptosporidium and Cryptosporidiosis, 2007
Sporozoites that excyst from oocysts are motile, approach a potential host-cell anterior (apical) end first, and actively invade the cell (Wetzel et al., 2005). They are characterized by the presence of secretory organelles that exocytose during the invasion process (Figure 1.3) (O’Hara et al., 2005). When the sporozoite initially contacts the host cell membrane, the single rhoptry extends to the attachment site, and the micronemes and dense granules move to the apical complex region (Huang et al., 2004). Sporozoites (and merozoites) of C. parvum express a 1300-kDa conserved apical complex glycoprotein called CSL that contains a ligand involved in attachment to intestinal epithelial cells during the infection process (Riggs et al., 1997; Langer and Riggs, 1999). Binding of CSL was found to be localized to a surface-exposed, conserved receptor on the microvillar surface of cells of epithelial origin, (Langer et al., 2001). Similar findings have been reported for additional mucin-like glycoproteins localized at the apical region (Cevallos et al., 2000) and for a thrombospondin-related adhesive protein crucial for invasion of host cells (Spano et al., 1998). The attached sporozoites, initially slender and crescent or boomerang shaped, become oval or spherical. Vacuoles form near the anterior end, possibly arising from the parasite, and cluster together, surrounding the parasite and forming a preparasitophorous vacuole (Figure 1.4) (Huang et al., 2004). This vacuolar area fuses with the host-cell membrane to form a host–parasite interface. Thin membrane-bound cytoplasmic extensions from the host cell microvilli surround the parasite, eventually containing it within a mature parasitophorous vacuole (Umemiya et al., 2005). Sporozoites within the parasitophorous vacuole are intracellular but are not directly in contact with the host-cell cytoplasm—they are extracytoplasmic. During formation of the parasitophorous vacuole, material appears to be released from the conoid at the anterior tip of the sporozoite, while a large membrane-bound electron-lucent vacuole forms within the anterior third of the sporozoite where the rhoptry and micronemes had been present (Figure 1.4). Also during this time, vacuole-like structures at the apical end of the sporozoite appear to be directly connected to the host-cell cytoplasm. Both an electron-dense band beneath this site and the parasitophorous vacuole keep the parasite intracellular but extracytoplasmic. The electron-dense band subsequently matures into a unique structure referred to as an attachment or feeder organelle. As this internalization process progresses, the sporozoite becomes spherical and is called a trophozoite (Figures 1.4, 1.5, 1.6, and 1.7). In cell culture, attachment and internalization was completed in 15 min (Lumb et al., 1988).
Mathematical model for the in-host malaria dynamics subject to malaria vaccines
Published in Letters in Biomathematics, 2018
Titus Okello Orwa, Rachel Waema Mbogo, Livingstone Serwadda Luboobi
Malaria is a mosquito-borne infectious disease caused by an intracellular protozoan parasite of the genus Plasmodium (Liehl et al., 2015; Risco-Castillo et al., 2015). Plasmodium falciparum is the deadliest (Derbyshire, Mota, & Clardy, 2011) and predominant malaria parasite in sub-Saharan African and was responsible for 99% of all malaria cases in 2016 (WHO, 2017b). While probing for blood, female Anopheles mosquito inoculates sporozoites into the human dermis. The deposited parasites rapidly migrate to the liver, where they invade the hepatocytes with the formation of protective parasitophorous vacuole (Bertolino & Bowen, 2015; Ishino, Yano, Chinzei, & Yuda, 2004; Mota et al., 2001). During this pre-erythrocytic stage, the sporozoites undergo rapid asexual reproduction (White et al., 2014; White, 2017), develop and differentiate asymptomatically into thousands of erythrocytic forms called merozoites (Sturm et al., 2006). The cyclical erythrocytic stage begins when infected hepatocytes burst open, releasing infective-merozoites into the blood stream (Haldar, Murphy, Milner, & Taylor, 2007). The released merozoites quickly invade susceptible red blood cells leading to the formation of infected red blood cells (IRB) cells. The waves of bursting erythrocytes and invasions of fresh erythrocytes by secondary merozoites produce malaria characteristic symptoms such as chills and headache (Derbyshire et al., 2011). Some merozoites develop into sexual forms called gametocytes that are later sucked up by feeding mosquitoes for sexual reproduction and development within the mosquito gut (sporogonic stage). If left untreated, malaria patients may develop severe symptoms and progress to coma or death.