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Plasmodium falciparum


Plasmodium falciparum

Plasmodium falciparum
Blood smear of Plasmodium falciparum (gametocytes - sexual forms)
Scientific classification
Domain: Eukarya
Kingdom: Chromalveolata
Phylum: Apicomplexa
Class: Aconoidasida
Order: Haemosporida
Family: Plasmodiidae
Genus: Plasmodium
Species: P. falciparum
Binomial name
Plasmodium falciparum
(William H. Welch, 1897)

Oscillaria malariae Laveran, 1881
Plasmodium malariae Marchiafava and Celli, 1885
Laverania malariae Feletti and Grassi, 1890
Ematozoo falciforme Antolisei and Angelini, 1890
Haemamoeba immaculata Grassi, 1891
Haemamoeba laverani Labbe, 1894
Haematozoon falciforme Thayer and Hewetson, 1895
Haematozoon falciparum Welch, 1897
Haemosporidium sedecimanae Lewkowicz, 1897
Haemosporidium undecimanae Lewkowicz, 1897
Haemosporidium vigesimotertianae Lewkowicz, 1897

Plasmodium falciparum is a

  • Colombian scientists develop computacional tool to detect the plasmodium falciparum (in spanish)
  • Allison AC (February 1954). "Protection Afforded by Sickle-cell Trait Against Subtertian Malarial Infection". Br Med J 1 (4857): 290–4.  
  • Allison AC (1964). "Polymorphism and Natural Selection in Human Populations". Cold Spring Harb. Symp. Quant. Biol. 29: 137–49.  
  • Cholera R; Brittain NJ; Gillrie MR; et al. (January 2008). "Impaired cytoadherence of Plasmodium falciparum-infected erythrocytes containing sickle hemoglobin". Proc. Natl. Acad. Sci. U.S.A. 105 (3): 991–6.  
  • Mockenhaupt FP; Ehrhardt S; Otchwemah R; et al. (May 2004). "Limited influence of haemoglobin variants on Plasmodium falciparum msp1 and msp2 alleles in symptomatic malaria". Trans. R. Soc. Trop. Med. Hyg. 98 (5): 302–10.   Category:CS1 maint: Explicit use of et al.)
  • Janovy, John; Roberts, Larry S. (2005). Foundations of Parasitology (7th ed.). McGraw-Hill Education (ISE Editions).  


  • Gardner, MJ; Hall, N; Fung, E; White, O; Berriman, M; Hyman, RW; Carlton, JM; Pain, A; Nelson, KE (2002). "Genome sequence of the human malaria parasite Plasmodium falciparum". Nature 419 (6906): 498–511.  
  • PlasmoDB: The Plasmodium Genome Resource
  • GeneDB Plasmodium falciparum
  • Genome
  • UCSC Plasmodium Falciparum Browser

Plasmodium falciparum genome data

  • Low power H & E
  • High power H & E
  • High power H & E
  • Membrane stain
  • Membrane stain
  • Low power H & E
  • High power H & E
  • Gross pathology
  • Low power H & E
  • Smear preparation
  • Smear preparation
  • Gross pathology
  • Low power H & E stain
  • High power H & E stain showing parasite adherence to the vessel walls

Pathology due to Plasmodium falciparum

  • Case 1
  • Case 2
  • Case 3
  • Case 4

Case histories

  • Blood forms
  • Blood forms
  • Blood forms
  • Blood forms
  • Multiple blood forms
  • Female gametocyte
  • Female gametocyte

Blood slides

  • Malaria Atlas Project

Spatial distribution

  • Introductory
  • Overview
  • Malaria biology
  • Life cycle cartoon


Sources and further reading

  1. ^ Coatney GR, Collins WE, Warren M, Contacos PG (1971). "22 Plasmodium falciparum (Welch, 1897)". The primate malarias. Division of Parasitic Disease, CDC. p. 263. 
  2. ^ Rich, S. M.; Leendertz, F. H.; Xu, G.; Lebreton, M.; Djoko, C. F.; Aminake, M. N.; Takang, E. E.; Diffo, J. L. D.; Pike, B. L.; Rosenthal, B. M.; Formenty, P.; Boesch, C.; Ayala, F. J.; Wolfe, N. D. (2009). "The origin of malignant malaria". Proceedings of the National Academy of Sciences 106 (35): 14902–14907.  
  3. ^ Perkins, D. J.; Were, T.; Davenport, G. C.; Kempaiah, P.; Hittner, J. B.; Ong'Echa, J. M. (2011). "Severe malarial anemia: Innate immunity and pathogenesis". International journal of biological sciences 7 (9): 1427–1442.  
  4. ^ Perlmann, P; Troye-Blomberg, M (2000). "Malaria blood-stage infection and its control by the immune system". Folia biologica 46 (6): 210–8.  
  5. ^ "Factsheet on the World Malaria Report 2014". World Health Orgnization. 2014. Retrieved 2 February 2015. 
  6. ^ WHO (2014). World Malaria Report 2014. Geneva, Switzerland: World Health Organization. pp. 32–42.  
  7. ^ "World Malaria Report 2008" (PDF). World Health Organisation. 2008. p. 10. Retrieved 2009-08-17. 
  8. ^
  9. ^ Biodiversity of the Malaria in the World, Sylvie Manguin et al. Editorial John Libbey, 2008. p. 23
  10. ^ Dondorp AM, Pongponratn E, White NJ (February 2004). "Reduced microcirculatory flow in severe falciparum malaria: pathophysiology and electron-microscopic pathology". Acta Trop. 89 (3): 309–17.  
  11. ^ Wilson RJ; Denny PW; Preiser PR; et al. (August 1996). "Complete gene map of the plastid-like DNA of the malaria parasite Plasmodium falciparum".  
  12. ^ Gardner MJ; Hall N; Fung E; Berriman, Matthew; Hyman, Richard W.; Carlton, Jane M.; Pain, Arnab; Nelson, Karen E.; Bowman, Sharen; Paulsen, Ian T.; James, Keith; Eisen, Jonathan A.; Rutherford, Kim; Salzberg, Steven L.; Craig, Alister; Kyes, Sue; Chan, Man-Suen; Nene, Vishvanath; Shallom, Shamira J.; Suh, Bernard; Peterson, Jeremy; Angiuoli, Sam; Pertea, Mihaela; Allen, Jonathan; Selengut, Jeremy; Haft, Daniel; Mather, Michael W.; Vaidya, Akhil B.; et al. (October 2002). "Genome sequence of the human malaria parasite Plasmodium falciparum".  
  13. ^ (Allison, 1954).
  14. ^ a b c Roberts and Janovy Jr., 2005
  15. ^ a b Cholera, R., Brittain, N., Gillrie, M. et al. (2007)
  16. ^ Mockenhaupt, 2004
  17. ^ Allison 1964
  18. ^ Mbogo CM; Mwangangi JM; Nzovu J; et al. (June 2003). "Spatial and temporal heterogeneity of Anopheles mosquitoes and Plasmodium falciparum transmission along the Kenyan coast". Am. J. Trop. Med. Hyg. 68 (6): 734–42.  
  19. ^ Rathore, D; Wahl AM, Sullivan M, McCutchan TF (2001-04-25). "A phylogenetic comparison of gene trees constructed from plastid, mitochondrial and genomic DNA of Plasmodium species". Molecular and Biochemical Parasitology 114 (1): 89–94.  
  20. ^ Yotoko, KSC; C Elisei (November 2006). "Malaria parasites (Apicomplexa, Haematozoea) and their relationships with their hosts: is there an evolutionary cost for the specialization?". Journal of Zoological Systematics and Evolutionary Research 44 (4): 265–73.  
  21. ^ Liu, W; Y Li, GH Learn, RS Rudicell, JD Robertson, BF Keele, JN Ndjango, CM Sanz, DB Morgan, S Locatelli, MK Gonder, PJ Kranzusch, PD Walsh, E Delaporte, E Mpoudi-Ngole, AV Georgiev, MN Muller, GM Shaw, M Peeters, PM Sharp, JC Rayner, BH Hahn (2010). "Origin of the human malaria parasite Plasmodium falciparum in gorillas". Nature 467 (7314): 420–5.  
  22. ^ Duval, L; M Fourment, E Nerrienet, D Rousset, SA Sadeuh, SM Goodman, NV Andriaholinirina, M Randrianarivelojosia, RE Paul, V Robert, FJ Ayala, F Ariey (2010). "African apes as reservoirs of Plasmodium falciparum and the origin and diversification of the Laverania subgenus". Proceedings of the National Academy of Sciences of the United States of America 107 (23): 10561–6.  
  23. ^ Rayner, J; WM Liu, M Peeters, PM Sharp, BH Hahn (2011). "A plethora of Plasmodium species in wild apes: a source of human infection?". Trends in Parasitology 467 (5): 222–229.  
  24. ^ Prugnolle, F; P Durand, B Ollomo, L Duval, F Ariey, C Arnathau, JP Gonzalez, E Leroy, F Renaud (2011). Manchester, Marianne, ed. "A Fresh Look at the Origin of Plasmodium falciparum, the Most Malignant Malaria Agent". PLOS Pathogens 7 (2): e1001283.  
  25. ^ Escalante, AA; E Barrio, FJ Ayala (1995). "Evolutionary origin of human and primate malarias: evidence from the circumsporozoite protein gene". Molecular Biology and Evolution 12 (4): 616–26.  
  26. ^ Hartl, DH (January 2004). "The origin of malaria: mixed messages from genetic diversity". Nature Reviews Microbiology 2 (1): 15–22.  
  27. ^ Joy, DA; Feng X, Mu J, Furuya T, Chotivanich K, Krettli AU, Ho M, Wang A, White NJ, Suh E, Beerli P, Su XZ. (2003-04-11). "Early origin and recent expansion of Plasmodium falciparum". Science 300 (5617): 318–21.  
  28. ^ Rich SM, Leendertz FH, Xu G, Lebreton M, Djoko CF, Aminake MN, Takang EE, Diffo JL, Pike BL, Rosenthal BM, Formenty P, Boesch C, Ayala FJ, Wolfe ND; Leendertz; Xu; Lebreton; Djoko; Aminake; Takang; Diffo; Pike; Rosenthal; Formenty; Boesch; Ayala; Wolfe (2009). "The origin of malignant malaria". Proc Natl Acad Sci USA 106 (35): 14902–7.  
  29. ^ Buckling AG, Taylor LH, Carlton JM, Read AF (April 1997). "Adaptive changes in Plasmodium transmission strategies following chloroquine chemotherapy". Proc. Biol. Sci. 264 (1381): 553–9.  
  30. ^ Paul, REL; Arley, F; Robert, V (2003). "The evolutionary ecology of Plasmodium". Ecology Letters 6: 866–880.  
  31. ^ a b c d e f g h i j k l m n o p q r s t u v Guidelines for the treatment of malaria, second edition Authors: WHO. Number of pages: 194. Publication date: 2010. Languages: English. ISBN 978-92-4-154792-5
  32. ^ Babalwa Zani; et al. (2014). "Dihydroartemisinin-piperaquine for treating uncomplicated Plasmodium falciparum malaria". Cochrane Database of Systematic Reviews 1.  
  33. ^ Trager, W; J B Jensen (1976-08-20). "Human malaria parasites in continuous culture". Science 193 (4254): 673–5.  
  34. ^ Noedl H, Se Y, Schaecher K, Smith BL, Socheat D, Fukuda MM (December 2008). "Evidence of artemisinin-resistant malaria in western Cambodia". N. Engl. J. Med. 359 (24): 2619–20.  
  35. ^ World Health Organization


See also

Although an antimalarial vaccine is urgently needed, infected individuals never develop a sterilizing (complete) immunity, making the prospects for such a vaccine dim. The parasites live inside cells, where they are largely hidden from the immune response. Infection has a profound effect on the immune system including immune suppression. Dendritic cells suffer a maturation defect following interaction with infected erythrocytes and become unable to induce protective liver-stage immunity. Infected erythrocytes directly adhere to and activate peripheral blood B cells from nonimmune donors. The var gene products, a group of highly expressed surface antigens, bind the Fab and Fc fragments of human immunoglobulins in a fashion similar to protein A to Staphylococcus aureus, which may offer some protection to the parasite from the human immune system. Despite the poor prospects for a fully protective vaccine, it may be possible to develop a vaccine that would reduce the severity of malaria for children living in endemic areas.


Attempts to make synthetic antimalarials began in 1891. Atabrine, developed in 1933, was used widely throughout the Pacific in World War II, but was deeply unpopular because of the yellowing of the skin it caused. In the late 1930s, the Germans developed chloroquine, which went into use in the North African campaigns. Mao Zedong encouraged Chinese scientists to find new antimalarials after seeing the casualties in the Vietnam War. Artemisinin was discovered in the 1970s based on a medicine described in China in the year 340. This new drug became known to Western scientists in the late 1980s and early 1990s and is now a standard treatment. In 1976, P. falciparum was successfully cultured in vitro for the first time, which facilitated the development of new drugs substantially.[33] A 2008 study highlighted the emergence of artemisinin-resistant strains of P.falciparum in Cambodia.[34] In February 2015, the WHO confirmed that P.falciparum malaria parasites resistant to artemisinin therapies were detected in five countries in Southeast Asia; Cambodia, the Lao People’s Democratic Republic, Myanmar, Thailand and Viet Nam.[35]

History of falciparum malaria treatment

  • rectal artesunate
  • quinine IM
  • artesunate IM
  • artemether IM

If complete treatment of severe malaria is not possible, patients should be given prereferral treatment and referred immediately to an appropriate facility for further treatment. The following are options for prereferral treatment:[31]

  • an ACT
  • artesunate plus clindamycin or doxycycline
  • quinine plus clindamycin or doxycycline

Parenteral antimalarials should be administered for a minimum of 24 hours in the treatment of severe malaria, irrespective of the patient's ability to tolerate oral medication earlier.[31] Thereafter, complete treatment is recommended by giving a complete course of any of the following:[31]

  • artesunate IV or IM,
  • quinine (IV infusion or divided IM injection),
  • artemether IM - should be used only if none of the alternatives is available, as its absorption may be erratic.[31]

For children, especially in the malaria-endemic areas of Africa, any the following antimalarial medicines is recommended:[31]

For adults, intravenous (IV) or intramuscular (IM) artesunate is recommended.[31] Quinine is an acceptable alternative if parenteral artesunate is not available.[31]

In severe falciparum malaria, rapid clinical assessment is recommended and confirmation of the diagnosis be made, followed by administration of full doses of parenteral antimalarial treatment without delay with whichever effective antimalarial is first available.[31]

For travellers returning to nonendemic countries, any of the following is recommended:[31]

In infants and young children, the recommended first-line treatment is ACTs, with attention to accurate dosing and ensuring the administered dose is retained.[31]

For pregnant women, the recommended first-line treatment during the first trimester is quinine plus clindamycin for 7 days.[31] Artesunate plus clindamycin for 7 days is indicated if this treatment fails.[31] Still, an ACT is indicated only if this is the only treatment immediately available, or if treatment with 7-day quinine plus clindamycin fails or if there is uncertainty of compliance with a 7-day treatment.[31] In second and third trimesters, the recommended treatment is an ACT known to be effective in the country/region or artesunate plus clindamycin for 7 days, or quinine plus clindamycin for 7 days.[31] Lactating women should receive standard antimalarial treatment (including ACTs) except for dapsone, primaquine and tetracyclines.

In Africa, the overall treatment failure was less for dihydroartemisinin-piperaquine when compared to artemether-lumefantrine, and both drugs had PCR-adjusted failure rates of less than 5%. However, in Asian countries, dihydroartemisinin-piperaquine was found to be better tolerated, but as effective as artesunate plus mefloquine.[32]

Any of these combinations are to be given for 7 days.[31]

  • Artesunate plus tetracycline or doxycycline or clindamycin.[31]
  • Quinine plus tetracycline or doxycycline or clindamycin[31]

The choice of ACT in a country or region will be based on the level of resistance to the constituents in the combination.[31] Artemisinin and its derivatives should not be used as monotherapy in uncomplicated falciparum malaria.[31] As second-line antimalarial treatment, when initial treatment does not work or stops working, an alternative ACT known to be effective in the region is recommended, such as:

According to WHO guidelines 2010,[31] artemisinin-based combination therapies (ACTs) are the recommended first line antimalarial treatments for uncomplicated malaria caused by P. falciparum.[31] The following ACTs are recommended by the WHO:[31]

Uncomplicated P. falciparum malaria


During the erythrocyte stage, some P. falciparum merozoites develop into male and female gametocytes. Gametocyte production likely has an adaptive basis: it increases when conditions for asexual reproduction of the parasite worsen (e.g. upon exposure to immunological stress and/or antimalarial chemotherapy).[29] During the mosquito blood meal, male and female haploid gametocytes are ingested. These gametocytes quickly mature into gametes that fuse to form a diploid zygote (ookinete) that then encysts in the mosquito gut to form an oocyst where meiosis rapidly ensues.[30] Because fusion of gametes, zygote formation and meiosis must occur in the mosquito gut for the parasite to complete its life cycle, P. falciparum is an obligate sexual organism. While P. falciparum is a sexual organism, it is often self-fertilizing. Its population structure appears to predominantly reflect inbreeding.

Like most endosymbiotic theory). The apicoplast is an essential organelle, thought to be involved in the synthesis of lipids and several other compounds, and it provides an attractive target for antimalarial drug development, in particular in light of the emergence of parasites resistant to chloroquine and other existing antimalarial agents.

More recently, P. falciparum has evolved in response to human interventions. Most strains of malaria can be treated with chloroquine, but P. falciparum has developed resistance to this treatment. A combination of quinine and tetracycline has also been used, but some strains of P. falciparum have grown resistant to this treatment, as well. Different strains of P. falciparum have grown resistant to different treatments. Often, the resistance of the strain depends on where it was contracted. Many cases of malaria that come from parts of the Caribbean and west of the Panama Canal, as well as the Middle East and Egypt, can often be treated with chloroquine, since they have not yet developed resistance. Nearly all cases contracted in Africa, India, and Southeast Asia have grown resistant to this medication, and cases in Thailand and Cambodia have shown resistance to nearly all treatments. Often, the strain grows resistant to the treatment in areas where the use is not as tightly regulated.

Molecular clock analyses suggest P. falciparum is as old as the human line; the two species diverged at the same time as humans and chimpanzees.[25] However, low levels of polymorphism within the P. falciparum genome suggest a much more recent origin.[26] It may be that this discrepancy exists because P. falciparum is old, but its population recently underwent a great expansion.[27] Some evidence still indicates that P. reichenowi was the ancestor of P. falciparum.[28] The timing of this event is unclear at present, but it may have occurred about 10,000 years ago.

A third species that appears to related to these two has been discovered: P. gaboni. This putative species is (as of 2009) known only from two DNA sequences and awaits a full species description before it can be regarded as valid.

According to this theory, P. falciparum and P. reichenowi may both represent host switches from an ancestral line that infected primarily gorillas; P. falciparum went on to infect primarily humans, while P. reichenowi specialized in chimpanzees. The ongoing debate over the evolutionary origin of P. falciparum will likely be the focus of continuing genetic study.[24]

New evidence based on analysis of more than 1,100 mitochondrial, apicoplastic, and nuclear DNA sequences has suggested that P. falciparum may in fact have speciated from a lineage present in gorillas.[21][22][23]

The closest relative of P. falciparum is Plasmodium reichenowi, a parasite of chimpanzees. P. falciparum and P. reichenowi are not closely related to the other Plasmodium species that parasitize humans, or indeed mammals in general. These two species arguably originated from a parasite of birds.[19] More recent analyses do not support this, however, instead suggesting that the ability to parasitize mammals evolved only once within the genus Plasmodium.[20]

Origins and evolution

Known vectors

Many may wonder why natural selection has not phased out sickle-cell anemia. Individuals with sickle-cell trait are greatly desired in areas where malarial infections are endemic. Malaria kills between 1 and 2 million people per year. It is the leading cause of death among children in tropical regions. Individuals with sickle-cell deformities are able to fight Plasmodium parasite infections and do not become victims of malarial demise. Therefore, individuals expressing the genes and individuals carrying genes are selected to remain within the population.[17] It is no surprise that the incidence of sickle-cell anemia matches that of endemic regions for malarial infections.

Individuals with sickle-cell anemia may also experience greatly reduced symptoms of malaria because P. falciparum trophozoites cannot bind to hemoglobin to form sticky knobs. Without knob-binding complexes, which is an exclusive feature of P. falciparum, red blood cells do not stick to endothelial walls of blood vessels, and infected individuals do not experience symptoms such as cerebral malaria.[15]

These individuals have reduced attachment when compared to red blood cells with the normally functioning hemoglobin because of differing protein interactions. In normal circumstances, merozoites enter red blood cells through two PfEMP-1 protein-dependent interactions. These interactions promote the malaria inflammatory response associated with symptoms of chills and fever. When these proteins are impaired, as in sickle-cell cases, parasites cannot undergo cytoadherance interactions and cannot infect the cells; therefore, sickle-cell-anemic individuals and individuals carrying the sickle-cell trait have lower parasite loads and shorter time for symptoms than individuals expressing normal red blood cells.[16]

Individuals with sickle-cell trait and sickle-cell anemia are privileged because they have altered sticky knobs. The merozoites of each parasite species that causes malaria invade the red blood cell in three stages: contact, attachment, and endocytosis.[15] Individuals suffering from sickle-cell anemia have deformed red blood cells that interfere with the attachment phase, and P. falciparum and the other forms of malaria have trouble with endocytosis.

P. falciparum trophozoites develop sticky knobs in red blood cells, which then adhere to endothelial cells in blood vessels, thus evading clearance in the spleen. The acquired adhesive nature of the red blood cells may cause cerebral malaria when sequestered cells prevent oxygenation of the brain. Symptoms of cerebral malaria include impaired consciousness, convulsions, neurological disorder, and coma. Additional complications from P. falciparum-induced malaria include advanced immunosuppression.[14]

Of the six malarial parasites, P. falciparum causes the most fatal and medically severe form. Malaria is prevalent in tropical countries with an incidence of 300 million per year and a mortality of 1 to 2 million per year. Roughly 50% of all malarial infections are caused by P. falciparum.[14] Upon infection by a bite from an infected Anopheles mosquito, sporozoites devastate the human body by first infecting the liver. While in the liver, sporozoites undergo asexual development and merozoites are released into the bloodstream. The trophozoites further develop and reproduce by invading red blood cells. During the reproduction cycle, P. falciparum produces up to 40,000 merozoites in one day. Other blood sporozoans, such as P. vivax, P. ovale, and P. malariae, that infect humans and cause malaria do not have such a productive cycle for invasion. The process of bursting red blood cells does not have any symptoms, but destruction of the cells does cause anemia, since the bone marrow cannot compensate for the damage. When red blood cells rupture, hemozoin wastes cause cytokine release, chills, and then fever.[14]

Individuals with sickle-cell anemia or sickle-cell trait do have reduced parasitemia when compared to wild-type individuals for the hemoglobin protein in red blood cells. These genetic deviations of hemoglobin from normal states provide protection against the deadly parasite that causes malaria.[13]

P. falciparum and sickle-cell anemia

The presence of the parasite in human populations caused selection in the human genome in a multitude of ways, as humans have been forced to develop resistance to the disease. Beet, a doctor working in Southern Rhodesia (now Zimbabwe) in 1948, first suggested that sickle-cell disease could offer some protection from malaria. This suggestion was reiterated by J. B. S. Haldane in 1949, who suggested that thalassaemia could provide similar protection. This hypothesis has since been confirmed and has been extended to hemoglobin C and hemoglobin E, abnormalities in ankyrin and spectrin (ovalocytosis, elliptocytosis), in glucose-6-phosphate dehydrogenase deficiency and pyruvate kinase deficiency, loss of the Gerbich antigen (glycophorin C) and the Duffy antigen on the erythrocytes, thalassemias and variations in the major histocompatibility complex classes 1 and 2 and CD32 and CD36.

Influence of P. falciparum on the human genome

In 1995, a consortium, the Malaria Genome Project, was set up to sequence the genome of P. falciparum. The genome of its mitochondrion was reported in 1995, that of the nonphotosynthetic plastid known as the apicoplast in 1996,[11] and the sequence of the first nuclear chromosome (chromosome 2) in 1998. The sequence of chromosome 3 was reported in 1999, and the entire genome on 3 October 2002.[12] Annotated genome data can now be fully analyzed at several database resources including the UCSC Malaria Genome Browser, PlasmoDB and GeneDB. The roughly 24-megabase genome is extremely AT-rich (about 80%) and is organised into 14 chromosomes. Just over 5,300 genes were described.

The P. falciparum genome

Among medical professionals, the preferred method to diagnose malaria and determine which species of Plasmodium is causing the infection is by examination of a blood film under microscope in a laboratory. Each species has distinctive physical characteristics that are apparent under a microscope. In P. falciparum, only early (ring-form) trophozoites and gametocytes are seen in the peripheral blood. It is unusual to see mature trophozoites or schizonts in peripheral blood smears, as these are usually sequestered in the tissues. The parasitised erythrocytes are not enlarged, and it is common to see cells with more than one parasite within them (multiply parasitised erythrocytes). On occasion, faint, comma-shaped, red dots called "Maurer's dots" are seen on the red cell surface. The comma-shaped dots can also appear as pear-shaped blotches.

Blood smear from a P. falciparum culture (K1 strain - asexual forms) - several red blood cells have ring stages inside them. Close to the center is a schizont and on the left a trophozoite.

Microscopic appearance

P. falciparum causes severe malaria via sequestration, a distinctive property not shared by any other human malaria. Within the 48-hour asexual blood stage cycle, the mature forms change the surface properties of infected red blood cells, causing them to stick to blood vessels (a process called cytoadherence). This leads to obstruction of the microcirculation and results in dysfunction of multiple organs, typically the brain in cerebral malaria.[10]


The lifecycle of all Plasmodium species is complex. Infection in humans begins with the bite of an infected female Anopheles mosquito. Sporozoites released from the salivary glands of the mosquito enter the bloodstream during feeding, quickly invading liver cells (hepatocytes). Sporozoites are cleared from the circulation within 30 minutes. During the next 14 days in the case of P. falciparum, the liver-stage parasites differentiate and undergo asexual multiplication, resulting in tens of thousands of merozoites that burst from the hepatocyte. Individual merozoites invade red blood cells (erythrocytes) and undergo an additional round of multiplication, producing 12-16 merozoites within a schizont. The length of this erythrocytic stage of the parasite lifecycle depends on the parasite species: an irregular cycle for P. falciparum, 48 hours for P. vivax and P. ovale, and 72 hours for P. malariae.[9] The clinical manifestations of malaria, fever, and chills are associated with the synchronous rupture of the infected erythrocytes. The released merozoites go on to invade additional erythrocytes. Not all of the merozoites divide into schizonts; some differentiate into sexual forms, male and female gametocytes. These gametocytes are taken up by a female Anopheles mosquito during a blood meal. Within the mosquito midgut, the male gametocyte undergoes a rapid nuclear division, producing eight flagellated microgametes that fertilize the female macrogamete. The resulting ookinete traverses the mosquito gut wall and encysts on the exterior of the gut wall as an oocyst. Soon, the oocyst ruptures, releasing hundreds of sporozoites into the mosquito body cavity, where they eventually migrate to the mosquito salivary glands.

Seasonal temperature suitability for transmission of P. falciparum. The Z(T) normalized index of temperature suitability for P. falciparum displayed by week across an average year.

Plasmodium life cycle

While no effective vaccines are known for any of the six or more species that cause human malaria, drugs have been employed for centuries. In 1640, Huan del Vego first employed the tincture of the cinchona bark for treating malaria; the native Indians of Peru and Ecuador had been using it even earlier for treating fevers. Thompson (1650) introduced this "Jesuits' bark" to England. Its first recorded use there was by Dr John Metford of Northampton in 1656. Morton (1696) presented the first detailed description of the clinical picture of malaria and of its treatment with cinchona. Gize (1816) studied the extraction of crystalline quinine from the cinchona bark, and Pelletier and Caventou (1820) in France extracted pure quinine alkaloids, which they named quinine and cinchonine.

Around the world, malaria is the most significant parasitic disease of humans, and claims the lives of more children worldwide than any other infectious disease. Since 1900, the area of the world exposed to malaria has been halved, yet two billion more people are presently exposed. Morbidity, as well as mortality, is substantial. Infection rates in children in endemic areas are on the order of 50%. Chronic infection has been shown to reduce school scores by up to 15%. Reduction in the incidence of malaria coincides with increased economic output.[8]

Malaria is caused by an infection with protozoa of the genus Plasmodium. The name malaria, from the Italian mala aria, meaning "bad air", comes from the linkage suggested by Laveran on November 6, 1880, at a military hospital in Constantine, Algeria, when he discovered a microgametocyte exflagellating. Patrick Manson (1894) hypothesised that mosquitoes could transmit malaria. This hypothesis was experimentally confirmed independently by Giovanni Battista Grassi and Ronald Ross in 1898. Grassi (1900) proposed an exerythrocytic stage in the lifecycle, later confirmed by Shortt, Garnham, Covell, and Shute (1948), who found Plasmodium vivax in the human liver.



  • Background 1
  • Plasmodium life cycle 2
  • Pathogenesis 3
  • Microscopic appearance 4
  • The P. falciparum genome 5
  • Influence of P. falciparum on the human genome 6
    • P. falciparum and sickle-cell anemia 6.1
  • Known vectors 7
  • Origins and evolution 8
  • Treatment 9
    • Uncomplicated P. falciparum malaria 9.1
    • History of falciparum malaria treatment 9.2
  • Vaccination 10
  • See also 11
  • References 12
  • Sources and further reading 13
    • Overview 13.1
    • Spatial distribution 13.2
    • Blood slides 13.3
    • Case histories 13.4
    • Pathology due to Plasmodium falciparum 13.5
    • Plasmodium falciparum genome data 13.6
    • Other 13.7

[7].P. falciparum, whereas in most other countries with malaria transmission, other, less virulent plasmodial species predominate. Almost every malarial death is caused by P. falciparum It is much more prevalent in sub-Saharan Africa than in many other regions of the world; in most African countries, over 75% of cases were due to [6][5]

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