Editing Plasmodium falciparum (section)

====Blood stage or erythrocytic schizogony====
[[Merozoites]] use the [[apicomplexan]] invasion organelles ([[apical complex]], pellicle, and surface coat) to recognize and enter the host erythrocyte ([[red blood cell]]). The merozoites first bind to the erythrocyte in a random orientation. It then reorients such that the apical complex is in proximity to the erythrocyte membrane. The parasite forms a parasitophorous vacuole, to allow for its development inside the [[erythrocyte]].<ref name=cowman>{{cite journal|last1=Cowman|first1=Alan F.|last2=Crabb|first2=Brendan S.|title=Invasion of Red Blood Cells by Malaria Parasites|journal=Cell|date=2006|volume=124|issue=4|pages=755–766|doi=10.1016/j.cell.2006.02.006|pmid=16497586|s2cid=14972823|doi-access=free}}</ref> This infection cycle occurs in a highly synchronous fashion, with roughly all of the parasites throughout the blood in the same stage of development. This precise clocking mechanism is dependent on the human host's own [[circadian rhythm]].<ref name="1.5.2">{{cite web  | title = Malaria eModule – SYNCHRONICITY  | url = http://www.impact-malaria.com/FR/EPS/Formations_et_cours_internationaux/Formation_de_la_Liverpool_School_LSTMH/cours_liverpool/Unit_1/1_5_2.html  | access-date = 2017-06-04  | archive-date = 2007-12-22  | archive-url = https://web.archive.org/web/20071222211547/http://www.impact-malaria.com/FR/EPS/Formations_et_cours_internationaux/Formation_de_la_Liverpool_School_LSTMH/cours_liverpool/Unit_1/1_5_2.html  | url-status = dead  }}</ref>

Within the erythrocyte, the parasite metabolism depends on the digestion of [[haemoglobin]]. The clinical symptoms of malaria such as fever, anemia, and neurological disorder are produced during the blood stage.<ref name="gerald"/>

The parasite can also alter the morphology of the erythrocyte, causing knobs on the erythrocyte membrane. Infected erythrocytes are often sequestered in various human tissues or organs, such as the heart, liver, and brain. This is caused by parasite-derived cell surface proteins being present on the erythrocyte membrane, and it is these proteins that bind to receptors in human cells. Sequestration in the brain causes cerebral malaria, a very severe form of the disease, which increases the victim's likelihood of death.<ref>{{Cite journal|last1=Jensen|first1=Anja Ramstedt|last2=Adams|first2=Yvonne|last3=Hviid|first3=Lars|date=2020|title=Cerebral Plasmodium falciparum malaria: The role of PfEMP1 in its pathogenesis and immunity, and PfEMP1-based vaccines to prevent it|journal=Immunological Reviews|volume=293|issue=1|pages=230–252|doi=10.1111/imr.12807|pmc=6972667|pmid=31562653}}</ref>

=====Trophozoite=====
After invading the erythrocyte, the parasite loses its specific invasion organelles (apical complex and surface coat) and de-differentiates into a round trophozoite located within a parasitophorous vacuole. The trophozoite feeds on the haemoglobin of the erythrocyte, digesting its proteins and converting (by [[biocrystallization]]) the remaining heme into insoluble and chemically inert β-hematin [[crystals]] called haemozoin.<ref>{{cite journal |last1=Pagola |first1=Silvina |last2=Stephens |first2=Peter W. |last3=Bohle |first3=D. Scott |last4=Kosar |first4=Andrew D. |last5=Madsen |first5=Sara K. |title=The structure of malaria pigment β-haematin |journal=Nature |date=March 2000 |volume=404 |issue=6775 |pages=307–310 |doi=10.1038/35005132 |bibcode=2000Natur.404..307P|pmid=10749217|s2cid=4420567}}</ref><ref>{{cite journal |last1=Hempelmann |first1=Ernst |title=Hemozoin Biocrystallization in ''Plasmodium falciparum'' and the antimalarial activity of crystallization inhibitors |journal=Parasitology Research |date=1 March 2007 |volume=100 |issue=4 |pages=671–676 |doi=10.1007/s00436-006-0313-x |language=en |issn=1432-1955 |s2cid=30446678 |pmid=17111179}}</ref> The young trophozoite (or "ring" stage, because of its morphology on stained blood films) grows substantially before undergoing multiplication.<ref name="1.5">{{cite web | title = Malaria eModule – ASEXUAL ERYTHROCYTIC STAGES | url = http://www.impact-malaria.com/FR/EPS/Formations_et_cours_internationaux/Formation_de_la_Liverpool_School_LSTMH/cours_liverpool/Unit_1/1_5.html | access-date = 2017-06-04 | archive-date = 2007-12-22 | archive-url = https://web.archive.org/web/20071222163324/http://www.impact-malaria.com/FR/EPS/Formations_et_cours_internationaux/Formation_de_la_Liverpool_School_LSTMH/cours_liverpool/Unit_1/1_5.html | url-status = dead }}</ref>

=====Schizont=====
At the schizont stage, the parasite replicates its DNA multiple times and multiple mitotic divisions occur asynchronously.<ref>{{cite journal | last1 = Read | first1 = M. | last2 = Sherwin | first2 = T. | last3 = Holloway | first3 = S. P. | last4 = Gull | first4 = K. | last5 = Hyde | first5 = J. E. | year = 1993 | title = Microtubular organization visualized by immunofluorescence microscopy during erythrocytic schizogony in ''Plasmodium falciparum'' and investigation of post-translational modifications of parasite tubulin | journal = Parasitology | volume = 106 | issue = 3| pages = 223–232 | doi=10.1017/s0031182000075041| pmid = 8488059 | s2cid = 24655319 }}</ref><ref>{{cite journal |last1=Arnot |first1=David E. |last2=Ronander |first2=Elena |last3=Bengtsson |first3=Dominique C. |title=The progression of the intra-erythrocytic cell cycle of ''Plasmodium falciparum'' and the role of the centriolar plaques in asynchronous mitotic division during schizogony |journal=International Journal for Parasitology |date=January 2011 |volume=41 |issue=1 |pages=71–80 |doi=10.1016/j.ijpara.2010.07.012 |pmid = 20816844 }}</ref> Cell division and multiplication in the erythrocyte is called erythrocytic schizogony. Each schizont forms 16-18 merozoites.<ref name="1.5"/> The red blood cells are ruptured by the merozoites. The liberated merozoites invade fresh erythrocytes. A free merozoite is in the bloodstream for roughly 60 seconds before it enters another erythrocyte.<ref name=cowman/>

The duration of one complete erythrocytic schizogony is approximately 48 hours. This gives rise to the characteristic clinical manifestations of falciparum malaria, such as fever and chills, corresponding to the synchronous rupture of the infected erythrocytes.<ref name=trampuz03>{{cite journal|last1=Trampuz|first1=Andrej|last2=Jereb|first2=Matjaz|last3=Muzlovic|first3=Igor|last4=Prabhu|first4=Rajesh M|title=Clinical review: Severe malaria|journal=Critical Care|date=2003|volume=7|issue=4|pages=315–23|doi=10.1186/cc2183|pmid=12930555|pmc=270697 |doi-access=free }}</ref>

=====Gametocyte=====
Some merozoites differentiate into sexual forms, male and female [[gametocyte]]s. These gametocytes take roughly 7–15 days to reach full maturity, through the process called gametocytogenesis. These are then taken up by a female ''Anopheles'' mosquito during a blood meal.<ref>{{cite journal|last1=Talman|first1=Arthur M|last2=Domarle|first2=Olivier|last3=McKenzie|first3=F|last4=Ariey|first4=Frédéric|last5=Robert|first5=Vincent|title=Gametocytogenesis: the puberty of ''Plasmodium falciparum''|journal=Malaria Journal|date=2004|volume=3|issue=1|pages=24|doi=10.1186/1475-2875-3-24|pmid=15253774|pmc=497046 |doi-access=free }}</ref>