| Plasmodium falciparum |
|
| Blood smear of Plasmodium falciparum (gametocytes - sexual forms) |
| Scientific classification |
| Domain: |
Eukaryota |
| (unranked): |
SAR |
| (unranked): |
Alveolata |
| Phylum: |
Apicomplexa |
| Class: |
Aconoidasida |
| Order: |
Haemosporida |
| Family: |
Plasmodiidae |
| Genus: |
Plasmodium |
| Species: |
P. falciparum |
| Binomial name |
Plasmodium falciparum
(William H. Welch, 1897) |
| Synonyms[1] |
|
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 protozoan parasite, one of the species of Plasmodium that cause malaria in humans. It is transmitted by the female Anopheles mosquito. This species causes the disease's most dangerous form, malignant[2] or falciparum[3] malaria.[4] It has the highest complication rates and mortality. 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.
The 2015 World Health Organization report found 214 million cases of malaria worldwide. This resulted in an estimated 438,000 deaths.[5] Rates of infection decreased from 2000 to 2015 by 37%,[5] but increased from 2014's 198 million cases.[6] In sub-Saharan Africa, over 75% of cases were due to P. falciparum, whereas in most other malarial countries, other, less virulent plasmodial species predominate. Almost every malarial death is caused by P. falciparum.[7]
Of the six malarial parasites,[8] P. falciparum causes the most-often fatal and medically severe form of disease. Roughly 50% of all malarial infections are caused by P. falciparum.
Contents
- 1 History
- 2 Life cycle
- 2.1 In human
- 2.1.1 Liver stage or exo-erythrocytic schizogony
- 2.1.2 Blood stage or erythrocytic schizogony
- 2.1.2.1 Trophozoite
- 2.1.2.2 Schizont
- 2.1.2.3 Gametocyte
- 2.2 Incubation period
- 2.3 In mosquito
- 3 Pathogenesis
- 4 Structure
- 5 Influence on the human genome
- 6 Origin and evolution
- 7 Treatment
- 7.1 History
- 7.2 Uncomplicated malaria
- 7.3 Severe malaria
- 7.4 Vaccination
- 8 See also
- 9 References
- 10 Further reading
- 11 External links
History
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 Giovanni Maria Lancisi (1717) of malaria with the poisonous vapours of swamps. This species' name comes from the Latin falx, meaning "sickle" and parere meaning "to give birth".
Treatment
Attempts to make synthetic antimalarials began in 1891. Atabrine, developed in 1933, was used widely throughout the Pacific in World War II, but was 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. Chinese scientist Tu Youyou discovered artemisinin in the 1970s based on a medicine described in China in 340 CE. This 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.[10] A 2008 study highlighted the emergence of artemisinin-resistant strains of P.falciparum in Cambodia.[11] In February 2015, the WHO confirmed that P. falciparum resistant to artemisinin therapies were detected in five countries in Southeast Asia; Cambodia, the Lao People’s Democratic Republic, Myanmar, Thailand and Viet Nam.[12]
Life cycle
Humans are the intermediate hosts in which asexual reproduction occurs, and female anopheline mosquitos are the definitive hosts harbouring the sexual reproduction stage.
In human
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.
Infection in humans begins with the bite of an infected female Anopheles mosquito. There are about 460 species of Anopheles mosquito, but only 68 transmit malaria. Anopheles gambiae is one of the best malaria vectors since it is long-lived, prefers feeding on humans, and lives in areas near human habitation. A. gambiae is found in Africa.[13]
Plasmodium sporozoites released from the salivary glands of the mosquito enter the bloodstream during feeding. The mosquito saliva contains antihemostatic and anti-inflammatory enzymes that disrupt blood clotting and inhibit the pain reaction. Typically, each infected bite contains 5-200 sporozoites.[13] The immune system clears the sporozoites from the circulation within 30 minutes. But few escape and quickly invade liver cells (hepatocytes).[14]
Liver stage or exo-erythrocytic schizogony
Entering the hepatocytes, the parasite loses its apical complex and surface coat, and transforms into a trophozoite. Within the parasitophorous vacuole of the hepatocyte, it undergoes 13-14 rounds of mitosis and meiosis which produce a syncytial cell called schizont. This process is called schizogony. A schizont contains tens of thousands of nuclei. From the surface of schizont, tens of thousands of haploid (1n) daughter cells called merozoites emerge. The merozoites are eventually released into the bloodstream in parasite-filled vesicles called merosomes.[15]
Blood stage or erythrocytic schizogony
Merozoites are roughly 1.5 μm in length and 1 μm in diameter, and use the apicomplexan invasion organelles (apical complex, pellicle and surface coat) to recognize and enter the host erythrocyte (red blood cell). The parasite first binds 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 vesicle, to allow for its development inside the erythrocyte.[16] 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 has been shown to be dependent on the human host's own circadian rhythm.[17]
Within the erythrocyte, the parasite metabolism depends on the digestion of hemoglobin. The clinical symptoms of malaria such as fever, anemia, and neurological disorder are produced during the blood stage.[14]
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 on human cells. Sequestration in the brain causes cerebral malaria, a very severe form of the disease, which increases the victim's likelihood of death.
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 young trophozoite (or "ring" stage, because of its morphology on stained blood films) grows substantially before undergoing schizogony.[18]
Schizont
At the schizont stage, the parasite replicates its DNA multiple times and multiple mitotic divisions occur asynchronously.[19][20] Each schizont forms 16-18 merozoites.[18] 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.[16]
The duration of each blood stage 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.[21]
Gametocyte
Not all of the merozoites divide into schizonts; some differentiate into sexual forms, male and female gametocytes. These gametocytes take roughly 7–15 days to reach full maturity, through the process called gametocytogenesis. These gametocytes are taken up by a female Anopheles mosquito during a blood meal.[22]
Incubation period
The time of appearance of the symptoms from infection (called incubation period) in P. falciparum infection is 11 days, but may range from 11 to 14 days. Parasites can be detected from blood samples by the 10th day after infection (pre-patent period).[21]
In mosquito
Within the mosquito midgut, the female gamete maturation process entails slight morphological changes, as it becomes enlarged and spherical. While the male gametocyte undergoes a rapid nuclear division within 15 minutes, producing eight flagellated microgametes but the process called exflagellation.[23] The flagellated microgamate fertilizes the female macrogamete to produce a diploid cell called zygote. The zygote then develops into an ookinete. Ookinete is a motile cell and capable of invading other organs of the mosquito. It traverses the peritrophic membrane of the mosquito midgut and crosses the midgut epithelium. Once through the epithelium, the ookinete enters the basil lamina, and settles to an immotile oocyst. For several days, the oocyst undergoes 10 to 11 rounds of cell division to create a syncytial cell (sporoblast) containing thousands of nuclei. Meiosis takes place inside the sporoblast to produce over 3,000 haploid daughter cells called sporozoites on the surface of the mother cell.[24] Immature sporozoites break through the oocyst wall into the haemolymph. They migrate to the mosquito salivary glands where they undergo further development and become infective to humans.[14]
Pathogenesis
Main article: Malaria
The clinical symptoms of falciparum malaria are produced by the rupture of schizont and destruction of erythrocytes. Most of the patients experience fever (>92% of cases), chills (79%), headaches (70%), and diaphoresis (64%). Dizziness, malaise, myalgia, abdominal pain, nausea, vomiting, mild diarrhea, and dry cough are also generally associated. Tachycardia, jaundice, pallor, orthostatic hypotension, hepatomegaly, and splenomegaly are also diagnosed.[21]
P. falciparum works via sequestration, a distinctive property not shared by any other Plasmodium. The mature schizonts change the surface properties of infected erythrocytes, causing them to stick to blood vessel walls (cytoadherence). This leads to obstruction of the microcirculation and results in dysfunction of multiple organs, such as the brain in cerebral malaria.[25]
Complicated malaria occurs more commonly in children under age 5 and sometimes in pregnant women. Women become susceptible to severe complicated malaria if infected by P. falciparum during their first pregnancy even if they live in hyperendemic areas. Susceptibility to severe malaria is reduced in subsequent pregnancies due to increased antibody levels against variant surface antigens that appear on infected erythrocytes.[citation needed]
Structure
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.
The preferred method to diagnose malaria and identify the species of Plasmodium is by microscopic examination of a blood film. Each species has distinctive physical characteristics. 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 hosting more than one parasite (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.
Like most apicomplexans, malaria parasites harbor a plastid, an apicoplast, similar to plant chloroplasts, which they probably acquired by engulfing (or being invaded by) a eukaryotic alga and retaining the algal plastid as a distinctive organelle encased within four membranes. The apicoplast is an essential organelle, thought to be involved in the synthesis of lipids and several other compounds and provides an attractive drug target. During the asexual blood stage of infection, the essential function of the apicoplast is to produce the isoprenoid intermediate isopentenyl pyrophosphate.[26]
Genome
In 1995 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,[27] 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 was reported on 3 October 2002.[28] The roughly 24-megabase genome is extremely AT-rich (about 80%) and is organised into 14 chromosomes. Just over 5,300 genes were described. Many genes involved in antigenic variation are located in the subtelomeric regions of the chromosomes. These are divided into the var, rif, and stevor families. Within the genome, there exist 59 var, 149 rif, and 28 stevor genes, along with multiple pseudogenes and truncations. It is estimated that 551, or roughly 10%, of the predicted nuclear-encoded proteins are targeted to the apicoplast, while 4.7% of the proteome is targeted to the mitochondria.[28]
Influence on the human genome
Further information: Genetic resistance to malaria
The presence of the parasite in human populations caused selection in the human genome, as humans developed 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. The first and best case is sickle-cell anemia. Sickle-cell anemia is a deadly genetic disease. However, many African have sickle-cell trait (only half the gene or allele of haemoglobin S) and they are resistant to falciparum malaria. In sickle-cell trait, the red blood cell sticky knobs are altered inhibiting their binding with the merozites, therby preventing the symptoms of infection.
Origin and evolution
The closest relative of P. falciparum is P. reichenowi, a parasite of chimpanzees. These two species are not closely related to any other Plasmodium species. They were once thought to originate from a parasite of birds.[32] Later analyses instead suggest that the ability to parasitize mammals evolved only once within Plasmodium.[33] Mitochondrial, apicoplastic and nuclear DNA sequences suggest that P. falciparum originated from a Plasmodium lineage present in gorillas.[34][35][36] P. falciparum and P. reichenowi may both represent host switches from an ancestral line in gorillas; P. falciparum went on to infect humans, while P. reichenowi infect chimpanzees. [37]
Molecular clock analyses suggest P. falciparum is as old as the human lineage; diverging at the same time as those of humans and chimpanzees.[38] However, low levels of polymorphism within the P. falciparum genome are present.[39] This suggest that P. falciparum population recently underwent a great expansion.[40] Some evidence indicates that P. reichenowi was the ancestor of P. falciparum.[41]
Treatment
Main article: Antimalarial medication
History
See also: History of malaria
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 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.
Uncomplicated malaria
According to WHO guidelines 2010,[42] artemisinin-based combination therapies (ACTs) are the recommended first line antimalarial treatments for uncomplicated malaria caused by P. falciparum. WHO recommends combinations such as artemether/lumefantrine, artesunate/amodiaquine, artesunate/mefloquine, artesunate/sulfadoxine-pyrimethamine, and dihydroartemisinin/piperaquine.[42]
The choice of ACT is based on the level of resistance to the constituents in the combination. Artemisinin and its derivatives are not appropriate for monotherapy. As second-line antimalarial treatment, when initial treatment does not work, an alternative ACT known to be effective in the region is recommended, such as artesunate plus tetracycline or doxycycline or clindamycin, and quinine plus tetracycline or doxycycline or clindamycin. Any of these combinations is to be given for 7 days. For pregnant women, the recommended first-line treatment during the first trimester is quinine plus clindamycin for 7 days.[42] Artesunate plus clindamycin for 7 days is indicated if this treatment fails. For travellers returning to nonendemic countries, atovaquone/proguanil, artemether/lumefantrineany and quinine plus doxycycline or clindamycin are recommende.[42]
Severe malaria
For adults, intravenous (IV) or intramuscular (IM) artesunate is recommended.[42] Quinine is an acceptable alternative if parenteral artesunate is not available.[42]
For children, especially in the malaria-endemic areas of Africa, artesunate IV or IM, quinine (IV infusion or divided IM injection), and artemether IM are recommended.[42]
Parenteral antimalarials should be administered for a minimum of 24 hours, irrespective of the patient's ability to tolerate oral medication earlier.[42] Thereafter, complete treatment is recommended including complete course of ACT or quinine plus clindamycin or doxycycline.[42]
Vaccination
See also: Malaria vaccine
RTS,S is the only vaccine to have gone through clinical trials as an effective vaccine.
See also
- Malaria Atlas Project
- List of parasites (human)
- UCSC Malaria Genome Browser
References
- ^ Coatney GR, Collins WE, Warren M, Contacos PG (1971). "22 Plasmodium falciparum (Welch, 1897)". The primate malarias. Division of Parasitic Disease, CDC. p. 263.
- ^ 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. doi:10.1073/pnas.0907740106. PMC 2720412 . PMID 19666593.
- ^ 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. doi:10.7150/ijbs.7.1427. PMC 3221949 . PMID 22110393.
- ^ Perlmann, P; Troye-Blomberg, M (2000). "Malaria blood-stage infection and its control by the immune system". Folia biologica. 46 (6): 210–8. PMID 11140853.
- ^ a b "Malaria Fact sheet N°94". WHO. Retrieved 2 February 2016.
- ^ WHO (2014). World Malaria Report 2014. Geneva, Switzerland: World Health Organization. pp. 32–42. ISBN 978-92-4156483-0.
- ^ "World Malaria Report 2008" (PDF). World Health Organisation. 2008. p. 10. Retrieved 2009-08-17.
- ^ Fuehrer, Hans-Peter; Noedl, Harald (2014-02-01). "Recent Advances in Detection of Plasmodium ovale: Implications of Separation into the Two Species Plasmodium ovale wallikeri and Plasmodium ovale curtisi". Journal of Clinical Microbiology. 52 (2): 387–391. doi:10.1128/JCM.02760-13. ISSN 0095-1137. PMC 3911344 . PMID 24478466.
- ^ Trager, W; J B Jensen (1976-08-20). "Human malaria parasites in continuous culture". Science. 193 (4254): 673–5. Bibcode:1976Sci...193..673T. doi:10.1126/science.781840. PMID 781840.
- ^ 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. doi:10.1056/NEJMc0805011. PMID 19064625.
- ^ World Health Organization
- ^ a b "Malaria eModule - Transmission".
- ^ a b c Gerald, N.; Mahajan, B.; Kumar, S. (2011). "Mitosis in the Human Malaria Parasite Plasmodium falciparum". Eukaryotic Cell. 10 (4): 474–482. doi:10.1128/EC.00314-10. PMC 3127633 . PMID 21317311.
- ^ Sturm, A. (2006). "Manipulation of Host Hepatocytes by the Malaria Parasite for Delivery into Liver Sinusoids". Science. 313 (5791): 1287–1290. doi:10.1126/science.1129720.
- ^ a b Cowman, Alan F.; Crabb, Brendan S. (2006). "Invasion of Red Blood Cells by Malaria Parasites". Cell. 124 (4): 755–766. doi:10.1016/j.cell.2006.02.006. PMID 16497586.
- ^ "Malaria eModule - SYNCHRONICITY".
- ^ a b "Malaria eModule - ASEXUAL ERYTHROCYTIC STAGES".
- ^ Read, M.; Sherwin, T.; Holloway, S. P.; Gull, K.; Hyde, J. E. (1993). "Microtubular organization visualized by immunofluorescence microscopy during erythrocytic schizogony in Plasmodium falciparum and investigation of post-translational modifications of parasite tubulin". Parasitology. 106: 223–232. doi:10.1017/s0031182000075041.
- ^ Arnot, D. E.; Ronander, E.; Bengtsson, D. C. (2011). "The progression of the intra-erythrocytic cell cycle of Plasmodium falciparum and the role of the centriolar plaques in asynchronous mitotic division during schizogony". Int. J. Parasitol. 41: 71–80. doi:10.1016/j.ijpara.2010.07.012.
- ^ a b c Trampuz, Andrej; Jereb, Matjaz; Muzlovic, Igor; Prabhu, Rajesh M (2003). "Clinical review: Severe malaria". Critical Care. 7 (4): 315. doi:10.1186/cc2183. PMC 270697 . PMID 12930555.
- ^ Talman, Arthur M; Domarle, Olivier; McKenzie, F; Ariey, Frédéric; Robert, Vincent (2004). "Gametocytogenesis: the puberty of Plasmodium falciparum". Malaria Journal. 3 (1): 24. doi:10.1186/1475-2875-3-24. PMC 497046 . PMID 15253774.
- ^ Sinden, R. E.; Canning, E. U.; Bray, R. S.; Smalley, M. E. (1978). "Gametocyte and Gamete Development in Plasmodium falciparum". Proceedings of the Royal Society B: Biological Sciences. 201 (1145): 375–399. doi:10.1098/rspb.1978.0051.
- ^ Rungsiwongse, Jarasporn; Rosenberg, Ronald (1991). "The Number of Sporozoites Produced by Individual Malaria Oocysts". The American Journal of Tropical Medicine and Hygiene. 45 (5): 574–577. doi:10.4269/ajtmh.1991.45.574.
- ^ 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. doi:10.1016/j.actatropica.2003.10.004. PMID 14744557.
- ^ Yeh, Ellen; DeRisi, Joseph L. (2011-08-30). "Chemical Rescue of Malaria Parasites Lacking an Apicoplast Defines Organelle Function in Blood-Stage Plasmodium falciparum". PLOS Biol. 9 (8): e1001138. doi:10.1371/journal.pbio.1001138. ISSN 1545-7885. PMC 3166167 . PMID 21912516.
- ^ Wilson RJ; Denny PW; Preiser PR; et al. (August 1996). "Complete gene map of the plastid-like DNA of the malaria parasite Plasmodium falciparum". Journal of Molecular Biology. 261 (2): 155–72. doi:10.1006/jmbi.1996.0449. PMID 8757284.
- ^ a b 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". Nature. 419 (6906): 498–511. Bibcode:2002Natur.419..498G. doi:10.1038/nature01097. PMID 12368864.
- ^ 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. doi:10.1016/S0166-6851(01)00241-9. PMID 11356517.
- ^ 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. doi:10.1111/j.1439-0469.2006.00377.x.
- ^ 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. Bibcode:2010Natur.467..420L. doi:10.1038/nature09442. PMC 2997044 . PMID 20864995.
- ^ 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. Bibcode:2010PNAS..10710561D. doi:10.1073/pnas.1005435107. PMC 2890828 . PMID 20498054.
- ^ 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. 27 (5): 222–229. doi:10.1016/J.Pt.2011.01.006. PMC 3087880 . PMID 21354860.
- ^ 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. doi:10.1371/journal.ppat.1001283. PMC 3044689 . PMID 21383971.
- ^ 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. ISSN 0737-4038. PMID 7659017.
- ^ Hartl, DH (January 2004). "The origin of malaria: mixed messages from genetic diversity". Nature Reviews Microbiology. 2 (1): 15–22. doi:10.1038/nrmicro795. PMID 15035005.
- ^ 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. Bibcode:2003Sci...300..318J. doi:10.1126/science.1081449. PMID 12690197.
- ^ 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. Bibcode:2009PNAS..10614902R. doi:10.1073/pnas.0907740106. PMC 2720412 . PMID 19666593.
- ^ a b c d e f g h i 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
Further reading
- Colombian scientists develop computacional tool to detect the plasmodium falciparum (in spanish)
- Allison, A.C. (February 1954). "Protection Afforded by Sickle-cell Trait Against Subtertian Malarial Infection". Br Med J. 1 (4857): 290–4. doi:10.1136/bmj.1.4857.290. PMC 2093356 . PMID 13115700.
- Allison, AC (1964). "Polymorphism and Natural Selection in Human Populations". Cold Spring Harb. Symp. Quant. Biol. 29: 137–49. doi:10.1101/sqb.1964.029.01.018. PMID 14278460.
- 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. Bibcode:2008PNAS..105..991C. doi:10.1073/pnas.0711401105. PMC 2242681 . PMID 18192399.
- 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. doi:10.1016/j.trstmh.2003.10.001. PMID 15109555.
- Roberts, Larry S.; Janovy, John (2005). Foundations of Parasitology (7th ed.). McGraw-Hill Education (ISE Editions). ISBN 0-07-111271-5.
External links
- Malaria species info at CDC
- Web Atlas of Medical Parasitology
- Species profile at Encyclopedia of Life
- Taxonomy at UniProt
- Profile at Scientists Against Malaria
- Clinical Identification Case 1
- Clinical Identification Case 2
- Genome info at Wellcome Trust Sanger Institute
- PlasmoDB: The Plasmodium Genome Resource
- GeneDB Plasmodium falciparum gene info
- Genome
- UCSC Plasmodium Falciparum Browser
- Gene info at Kyoto University
|
Malaria
|
| Biology |
- Malaria
- Cerebral
- Blackwater fever
- Pregnancy-associated
- Plasmodium
- biology
- life cycle
- vivax
- falciparum
- ovale
- malariae
- knowlesi
- Anopheles mosquito
- Lifecycle
- Schizont
- Merozoite
- Hypnozoite
- Gametocyte
|
| Control and prevention |
- Public health
- DDT
- Mosquito net
- Malaria prophylaxis
- Mosquito control
- Sterile insect technique
- Genetic resistance
- Duffy antigen
- Sickle cell anaemia
- Thalassemia
- G6PDH deficiency
- Malaria vaccine
|
| Diagnosis and treatment |
- Diagnosis of malaria
- Malaria culture
- Blood film
- Malaria antigen detection tests
- Antimalarials
- Artemisinin
- Mefloquine
- Proguanil
|
| Society and malaria |
- Diseases of poverty
- Millennium Development Goals
- History of malaria
- Timeline
- Roman fever
- National Malaria Eradication Program
- World Malaria Day
- Epidemiology
- Malaria and the Caribbean
- Malaria Atlas Project
|
| Organisations |
- Roll Back Malaria Partnership
- Malaria Consortium
- Against Malaria Foundation
- Bill and Melinda Gates Foundation
- Imagine No Malaria
- Malaria No More
- Africa Fighting Malaria
- African Malaria Network Trust
- South African Malaria Initiative
- African Leaders Malaria Alliance
- Amazon Malaria Initiative
- The Global Fund to Fight AIDS, Tuberculosis and Malaria
- Medicines for Malaria Venture
|
|
Protozoan infection: Chromalveolate and Archaeplastida (A07, B50–B54,B58, 007, 084)
|
| Chromalveolate |
| Alveolate |
| Apicomplexa |
Conoidasida/
Coccidia |
- Coccidia: Cryptosporidium hominis/Cryptosporidium parvum
- Cystoisospora belli
- Cyclospora cayetanensis
- Toxoplasma gondii
|
| Aconoidasida |
- Plasmodium falciparum/vivax/ovale/malariae/knowlesi
|
|
| Ciliophora |
|
|
| Heterokont |
- Blastocystis
- Pythium insidiosum
|
|
| Archaeplastida |
- Algaemia: Prototheca wickerhamii
|
| Taxon identifiers |
- BioLib:: 133048
- EoL: 10408873
- NCBI: 5833
|
