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__NOTOC__
{{About1|Plasmodium}}
'''For patient information click [[{{PAGENAME}} (patient information)|here]]'''
'''For patient information click [[{{PAGENAME}} (patient information)|here]]'''
{{Malaria}}
{{Malaria}}
{{CMG}}
{{Infobox_Disease
| Name          = Malaria
| ICD10          = {{ICD10|B|50||b|50}}
| ICD9          = {{ICD9|084}}
| Image          = Plasmodium.jpg
| Caption        = ''Plasmodium falciparum'' ring-forms and gametocytes in human blood.
| DiseasesDB    = 7728
| MedlinePlus    = 000621
|MIM          = 248310
| eMedicineSubj  = med
| eMedicineTopic = 1385
| eMedicine_mult = {{eMedicine2|emerg|305}} {{eMedicine2|ped|1357}}
| MeshName      = Malaria
| MeshNumber    = C03.752.250.552 |
}}
==[[Malaria overview|Overview]]==
==[[Malaria historical perspective|Historical perspective]]==
==[[Malaria epidemiology and demographics|Epidemiology & Demographics]]==
==[[Malaria history and symptoms|History & Symptoms]]==
Symptoms of malaria include [[fever]], [[shivering]], [[arthralgia]] (joint pain), [[vomiting]], [[anemia]] caused by [[hemolysis]], [[hemoglobinuria]], and [[convulsion]]s. There may be the feeling of tingling in the skin, particularly with malaria caused by ''P. falciparum''. The classical symptom of malaria is cyclical occurrence of sudden coldness followed by rigor and then fever and sweating lasting four to six hours, occurring every two days in ''P. vivax'' and ''P. ovale'' infections, while every three for ''P. malariae''.<ref name=RBMarmenia>[http://www.malaria.am/eng/pathogenesis.php Malaria life cycle & pathogenesis]. Malaria in Armenia. Accessed October 31, 2006.</ref> ''P. falciparum'' can have recurrent fever every 36-48 hours or a less pronounced and almost continuous fever.  For reasons that are poorly understood, but which may be related to high [[intracranial pressure]], children with malaria frequently exhibit [[abnormal posturing]], a sign indicating severe brain damage.<ref name="Idro ">{{cite journal | last =Idro  | first =R | authorlink = | coauthors =Otieno G, White S, Kahindi A, Fegan G, Ogutu B, Mithwani S, Maitland K, Neville BG, Newton CR | title = Decorticate, decerebrate and opisthotonic posturing and seizures in Kenyan children with cerebral malaria| journal =Malaria Journal | volume =4 | issue =57 | pages = | publisher = | date = | url =http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16336645 | doi = | id =PMID 16336645 | accessdate =2007-01-21 }} </ref>  Malaria has been found to cause cognitive impairments, especially in children. It causes widespread [[anemia]] during a period of rapid brain development and also direct brain damage.  This neurologic damage results from cerebral malaria to which children are more vulnerable.<ref>Boivin, M.J., "[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12394524&dopt=Citation Effects of early cerebral malaria on cognitive ability in Senegalese children]," ''Journal of Developmental and Behavioral Pediatrics'' 23, no. 5 (October 2002): 353&ndash;64. Holding, P.A. and Snow, R.W., "[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11425179&dopt=Citation Impact of Plasmodium falciparum malaria on performance and learning: review of the evidence]," ''American Journal of Tropical Medicine and Hygiene'' 64, suppl. nos. 1&ndash;2 (January&ndash;February 2001): 68&ndash;75.</ref>
Severe malaria is almost exclusively caused by ''P. falciparum'' infection and usually arises 6-14 days after infection.<ref name=Trampuz>{{cite journal | author = Trampuz A, Jereb M, Muzlovic I, Prabhu R | title = Clinical review: Severe malaria. | url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=12930555 | journal = Crit Care | volume = 7 | issue = 4 | pages = 315-23 | year = 2003 | id = PMID 12930555}}</ref> Consequences of severe malaria include [[coma]] and death if untreated&mdash;young children and pregnant women are especially vulnerable. [[Splenomegaly]] (enlarged spleen), severe [[headache]], cerebral [[ischemia]], [[hepatomegaly]] (enlarged liver), [[hypoglycemia]], and hemoglobinuria with [[renal failure]] may occur. Renal failure may cause [[blackwater fever]], where hemoglobin from lysed red blood cells leaks into the urine. Severe malaria can progress extremely rapidly and cause death within hours or days.<ref name=Trampuz/> In the most severe cases of the disease fatality rates can exceed 20%, even with intensive care and treatment.<ref>{{cite journal | author = Kain K, Harrington M, Tennyson S, Keystone J | title = Imported malaria: prospective analysis of problems in diagnosis and management. | journal = Clin Infect Dis | volume = 27 | issue = 1 | pages = 142-9 | year = 1998 | id = PMID 9675468}}</ref> In endemic areas, treatment is often less satisfactory and the overall fatality rate for all cases of malaria can be as high as one in ten.<ref>{{cite journal | author = Mockenhaupt F, Ehrhardt S, Burkhardt J, Bosomtwe S, Laryea S, Anemana S, Otchwemah R, Cramer J, Dietz E, Gellert S, Bienzle U | title = Manifestation and outcome of severe malaria in children in northern Ghana. | journal = Am J Trop Med Hyg | volume = 71 | issue = 2 | pages = 167-72 | year = 2004 | id = PMID 15306705}}</ref> Over the longer term, developmental impairments have been documented in children who have suffered episodes of severe malaria.<ref name="carter2005">{{cite journal | author=Carter JA, Ross AJ, Neville BG, Obiero E, Katana K, Mung'ala-Odera V, Lees JA, Newton CR | title=Developmental impairments following severe falciparum malaria in children | journal=Trop Med Int Health | year=2005 | volume=10 | pages=3-10  | id=PMID 15655008}}</ref>
Chronic malaria is seen in both ''P. vivax'' and ''P. ovale'', but not in ''P. falciparum''. Here, the disease can relapse months or years after exposure, due to the presence of latent parasites in the liver. Describing a case of malaria as cured by observing the disappearance of parasites from the bloodstream can therefore be deceptive. The longest incubation period reported for a ''P. vivax'' infection is 30 years.<ref name=Trampuz/> Approximately one in five of ''P. vivax'' malaria cases in temperate areas involve overwintering by hypnozoites (i.e., relapses begin the year after the mosquito bite).<ref>{{cite journal | author = Adak T, Sharma V, Orlov V | title = Studies on the Plasmodium vivax relapse pattern in Delhi, India. | journal = Am J Trop Med Hyg | volume = 59 | issue = 1 | pages = 175-9 | year = 1998 | id = PMID 9684649}}</ref>
==[[Malaria causes|Causes of Malaria]]==
==[[Malaria pathophysiology|Pathophysiology]]==
[[Image:MalariacycleBig.jpg|thumb|right|400px|The life cycle of malaria parasites in the human body. The various stages in this process are discussed in the text.]]
Malaria in humans develops via two phases: an exoerythrocytic (hepatic) and an erythrocytic phase. When an infected mosquito pierces a person's skin to take a blood meal, [[sporozoite]]s in the mosquito's saliva enter the bloodstream and migrate to the [[liver]]. Within 30 minutes of being introduced into the human host, they infect [[hepatocyte]]s, multiplying asexually and asymptomatically for a period of 6&ndash;15 days. Once in the liver these organisms differentiate to yield thousands of [[merozoite]]s which, following rupture of their host cells, escape into the blood and infect [[red blood cell]]s, thus beginning the erythrocytic stage of the life cycle.<ref>[http://www.sma.org/pdfs/objecttypes/smj/91C48D32-BCD4-FF25-565C69314AF7EB48/1196.pdf Bledsoe, G. H. (December 2005) "Malaria primer for clinicians in the United States"  ''Southern Medical Journal'' 98(12): pp. 1197-204, (PMID: 16440920)];</ref> The parasite escapes from the liver undetected by wrapping itself in the cell membrane of the infected host liver cell.<ref name="sturm2006">{{cite journal | author=Sturm A,
Amino R, van de Sand C, Regen T, Retzlaff S, Rennenberg A, Krueger A, Pollok JM, Menard R, Heussler VT | title=Manipulation of host hepatocytes by the malaria parasite for delivery into liver sinusoids | journal=Science | year=2006 | volume=313 | pages=1287-1490  | id=PMID 16888102}}</ref>
 
Within the red blood cells the parasites multiply further, again asexually, periodically breaking out of their hosts to invade fresh red blood cells. Several such amplification cycles occur. Thus, classical descriptions of waves of fever arise from simultaneous waves of merozoites escaping and infecting red blood cells.
Some ''P. vivax'' and ''P. ovale'' sporozoites do not immediately develop into exoerythrocytic-phase merozoites, but instead produce hypnozoites that remain dormant for periods ranging from several months (6&ndash;12 months is typical) to as long as three years. After a period of dormancy, they reactivate and produce merozoites. Hypnozoites are responsible for long incubation and late relapses in these two species of malaria.<ref>{{cite journal | author = Cogswell F | title = The hypnozoite and relapse in primate malaria. | url=http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=358221&blobtype=pdf | journal = Clin Microbiol Rev | volume = 5 | issue = 1 | pages = 26-35 | year = 1992 | id = PMID 1735093}}</ref>


The parasite is relatively protected from attack by the body's [[immune system]] because for most of its human life cycle it resides within the liver and blood cells and is relatively invisible to immune surveillance.  However, circulating infected blood cells are destroyed in the [[spleen]]. To avoid this fate, the ''P. falciparum'' parasite displays adhesive [[protein]]s on the surface of the infected blood cells, causing the blood cells to stick to the walls of small blood vessels, thereby sequestering the parasite from passage through the general circulation and the spleen.<ref name=Chen>{{cite journal | author = Chen Q, Schlichtherle M, Wahlgren M | title = Molecular aspects of severe malaria. | url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=10885986 | journal = Clin Microbiol Rev | volume = 13 | issue = 3 | pages = 439-50 | year = 2000 | id = PMID 10885986}}</ref>  This "stickiness"  is the main factor giving rise to [[hemorrhage|hemorrhagic]] complications of malaria. [[High endothelial venules]] (the smallest branches of the circulatory system) can be blocked by the attachment of masses of these infected red blood cells. The blockage of these vessels causes symptoms such as in placental and cerebral malaria. In cerebral malaria the sequestrated red blood cells can breach the [[blood-brain barrier|blood brain barrier]] possibly leading to coma.<ref>{{cite journal | author = Adams S, Brown H, Turner G | title = Breaking down the blood-brain barrier: signaling a path to cerebral malaria? | journal = Trends Parasitol | volume = 18 | issue = 8 | pages = 360-6 | year = 2002 | id = PMID 12377286}}</ref>
{{CMG}}; {{AE}}{{USAMA}}


Although the red blood cell surface adhesive proteins (called PfEMP1, for ''Plasmodium falciparum'' erythrocyte membrane protein 1) are exposed to the immune system they do not serve as good immune targets because of their extreme diversity; there are at least 60 variations of the protein within a single parasite and perhaps limitless versions within parasite populations.<ref name=Chen/>  Like a thief changing disguises or a spy with multiple passports, the parasite switches between a broad repertoire of PfEMP1 surface proteins, thus staying one step ahead of the pursuing immune system. 
== [[Malaria overview|Overview]] ==


Some merozoites turn into male and female [[gametocyte]]s. If a mosquito pierces the skin of an infected person, it potentially picks up gametocytes within the blood. Fertilization and sexual recombination of the parasite occurs in the mosquito's gut, thereby defining the mosquito as the [[definitive host]] of the disease. New sporozoites develop and travel to the mosquito's salivary gland, completing the cycle. Pregnant women are especially attractive to the mosquitoes,<ref>{{cite journal | author = Lindsay S, Ansell J, Selman C, Cox V, Hamilton K, Walraven G | title = Effect of pregnancy on exposure to malaria mosquitoes. | journal = Lancet | volume = 355 | issue = 9219 | pages = 1972 | year = 2000 | id = PMID 10859048}}</ref> and malaria in pregnant women is an important cause of [[stillbirth]]s, infant mortality and low birth weight.<ref>{{cite journal | author = van Geertruyden J, Thomas F, Erhart A, D'Alessandro U | title = The contribution of malaria in pregnancy to perinatal mortality. | url=http://www.ajtmh.org/cgi/content/full/71/2_suppl/35 | journal = Am J Trop Med Hyg | volume = 71 | issue = 2 Suppl | pages = 35-40 | year = 2004 | id = PMID 15331817}}</ref>
== [[Malaria historical perspective|Historical Perspective]] ==


==Evolutionary pressure of malaria on human genes==
== [[Malaria classification|Classification]]==
{{further|[[Evolution]], [[Natural selection]]}}
Malaria is thought to have been the greatest [[selection|selective pressure]] on the [[human genome]] in recent history.<ref name=Kwiatkowski_2005>{{cite journal | author=Kwiatkowski, DP | title=How Malaria Has Affected the Human Genome and What Human Genetics Can Teach Us about Malaria| journal=Am J Hum Genet | year=2005 | volume=77 | pages=171-92 |url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16001361 |id=PMID 16001361}}</ref> This is due to the high levels of [[death|mortality]] and [[morbidity]] caused by malaria, especially the ''[[Plasmodium falciparum|P. falciparum]]'' species.


===Sickle-cell disease===
== [[Malaria pathophysiology|Pathophysiology]] ==
[[Image:Sickle cell distribution.jpg|thumb|right|Distribution of the sickle cell trait.]]
[[Image:Malaria distribution.jpg|thumb|right|Distribution of Malaria.]]
The best-studied influence of the malaria parasite upon the human genome is the blood disease, [[sickle-cell disease]]. In sickle-cell disease, there is a mutation in the ''HBB'' gene, which encodes the beta globin subunit of [[haemoglobin]]. The normal allele encodes a [[glutamate]] at position six of the beta globin protein, while the sickle-cell allele encodes a [[valine]]. This change from a hydrophilic to a hydrophobic amino acid encourages binding between haemoglobin molecules, with polymerization of haemoglobin deforming red blood cells into a "sickle" shape. Such deformed cells are cleared rapidly from the blood, mainly in the spleen, for destruction and recycling.


In the merozoite stage of its life cycle the malaria parasite lives inside red blood cells, and its metabolism changes the internal chemistry of the red blood cell. Infected cells normally survive until the parasite reproduces, but if the red cell contains a mixture of sickle and normal haemoglobin, it is likely to become deformed and be destroyed before the daughter parasites emerge.  Thus, individuals [[heterozygous]] for the mutated allele, known as sickle-cell trait, may have a low and usually unimportant level of [[anaemia]], but also have a greatly reduced chance of serious malaria infection. This is a classic example of [[heterozygote advantage]].
== [[Malaria causes|Causes]] ==


Individuals [[homozygous]] for the mutation have full sickle-cell disease and in traditional societies rarely live beyond adolescence. However, in populations where malaria is [[Endemic (epidemiology)|endemic]], the [[gene frequencies|frequency]] of sickle-cell genes is around 10%. The existence of four [[haplotype]]s of sickle-type hemoglobin suggests that this mutation has emerged independently at least four times in malaria-endemic areas, further demonstrating its evolutionary advantage in such affected regions. There are also other mutations of the HBB gene that produce haemoglobin molecules capable of conferring similar resistance to malaria infection. These mutations produce haemoglobin types HbE and HbC which are common in Southeast Asia and Western Africa, respectively.
== [[Malaria differential diagnosis|Differentiating Malaria from other Diseases]]==


===Thalassaemias===
== [[Malaria epidemiology and demographics|Epidemiology and Demographics]] ==
Another well documented set of mutations found in the human genome associated with malaria are those involved in causing blood disorders known as [[thalassaemias]]. Studies in Sardinia and Papua New Guinea have found that the [[gene frequency]] of [[Thalassemia#Beta (β) thalassemias|β-thalassaemias]] is related to the level of malarial endemicity in a given population. A study on more than 500 children in Liberia found that those with β-thalassaemia had a 50% decreased chance of getting clinical malaria. Similar studies have found links between gene frequency and malaria endemicity in the α+ form of α-thalassaemia. Presumably these genes have also been [[natural selection|selected]] in the course of human evolution.


===Duffy antigens===
== [[Malaria risk factors|Risk Factors]]==
The [[Duffy antigen]]s are [[antigens]] expressed on red blood cells and other cells in the body acting as a [[chemokine]] receptor. The expression of Duffy antigens on blood cells is encoded by Fy genes (Fya, Fyb, Fyc etc.). ''[[Plasmodium vivax]]'' malaria uses the Duffy antigen to enter blood cells. However, it is possible to express no Duffy antigen on red blood cells (Fy-/Fy-). This [[genotype]] confers complete resistance to ''P. vivax'' infection. The genotype is very rare in European, Asian and American populations, but is found in almost all of the indigenous population of West and Central Africa.<ref>{{cite journal |author=Carter R, Mendis KN |title=Evolutionary and historical aspects of the burden of malaria |url=http://cmr.asm.org/cgi/content/full/15/4/564?view=long&pmid=12364370#RBC%20Duffy%20Negativity |journal=Clin. Microbiol. Rev. |volume=15 |issue=4 |pages=564-94 |year=2002 |pmid=12364370}}</ref> This is thought to be due to very high exposure to ''P. vivax'' in Africa in the last few thousand years.


===G6PD===
== [[Malaria screening|Screening]]==
[[Glucose-6-phosphate dehydrogenase]] (G6PD) is an [[enzyme]] which normally protects from the effects of [[oxidative stress]] in red blood cells. However, a genetic deficiency in this enzyme results in increased protection against severe malaria.


===HLA and interleukin-4===
== [[Malaria natural history, complications, and prognosis|Natural History, Complications and Prognosis]]==
[[Human leukocyte antigen|HLA-B53]] is associated with low risk of severe malaria. This [[Major histocompatibility complex|MHC class I]] molecule presents [[liver]] stage and [[sporozoite]] [[antigens]] to [[T-Cells]]. Interleukin-4, encoded by IL4, is produced by activated T cells and promotes proliferation and differentiation of antibody-producing B cells. A study of the Fulani of Burkina Faso, who have both fewer malaria attacks and higher levels of antimalarial antibodies than do neighboring ethnic groups, found that the IL4-524 T allele was associated with elevated antibody levels against malaria antigens, which raises the possibility that this might
be a factor in increased resistance to malaria.<ref>{{cite journal |author=Verra F, Luoni G, Calissano C, Troye-Blomberg M, Perlmann P, Perlmann H, Arcà B, Sirima B, Konaté A, Coluzzi M, Kwiatkowski D, Modiano D |title=IL4-589C/T polymorphism and IgE levels in severe malaria |journal=Acta Trop. |volume=90 |issue=2 |pages=205-9 |year=2004 |pmid=15177147}}</ref>


== Diagnosis ==
== Diagnosis ==
==[[Malaria laboratory tests|Lab Tests]]==
[[Malaria history and symptoms|History and Symptoms]] | [[Malaria physical examination|Physical Examination]] | [[Malaria laboratory findings|Laboratory Findings]] | [[Malaria xray|X rays]] | [[Malaria ultrasound|Ultrasound]] | [[Malaria ct scan|CT scan]] | [[Malaria mri|MRI]]


== Treatment ==
== Treatment ==


==[[Malaria medical therapy|Medical Therapy]]==
[[Malaria medical therapy|Medical Therapy]] | [[Malaria prevention|Prevention]] | [[Malaria cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Malaria future or investigational therapies|Future or Investigational Therapies]]


==[[Malaria primary prevention|Primary Prevention]]==
== Case Studies ==
==References==
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==<font color=#FFFFFF>External links</font>==
[[Malaria case study one|Case #1]]
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'''General information'''
* [http://www7.nationalgeographic.com/ngm/0707/index.html National Geographic July 2007 Issue on Malaria]
* [http://www.who.int/malaria/ WHO site on malaria]
** [http://www.who.int/malaria/docs/TreatmentGuidelines2006.pdf 2006 WHO Guidelines for the Treatment of Malaria]
* {{McGrawHillAnimation|microbiology|Malaria}}
* [http://ocw.jhsph.edu/courses/malariology/lectureNotes.cfm Johns Hopkins Malariology Open Courseware]
** [http://www.rollbackmalaria.org/wmr2005/ World Malaria Report 2005]
* [http://www.malariacontrol.net/ www.malariacontrol.net] distributed computing project for the fight against malaria
* [http://www.cdc.gov/malaria/ United States Centers for Disease Control - ''Malaria''] information pages
* [http://www.doctorswithoutborders.org/news/malaria/index.cfm Doctors Without Borders/Medecins Sans Frontieres - ''Malaria''] information pages
* [http://www.eldis.org/go/topics/resource-guides/health/malaria HRC/Eldis Health Resource Guide - ''Malaria''] research and resources on health in developing countries
* [http://www.nlm.nih.gov/medlineplus/malaria.html Medline Plus - ''Malaria'']
* [http://www.vega.org.uk/video/programme/87 Interview with Dr Andrew Speilman, Harvard malaria specialist]
* [http://www.malariaconsortium.org/ Malaria Consortium website]
* [http://www.globalhealthfacts.org/topic.jsp?i=20 GlobalHealthFacts.org] Malaria Cases and Deaths by Country
* [http://www.xs4all.nl/~ottoknot/werk/Malaria.html Survey article: History of malaria around the North Sea]
* [http://www.driveagainstmalaria.org DriveAgainstMalaria.org], "World's longest journey to fight the biggest killer of children"
* [http://ocw.jhsph.edu/courses/malariology/ Malaria on JHSPH OpenCourseWare]
* [http://www.malaria.org/ Malaria Foundation International]
* [http://www.map.ox.ac.uk Malaria Atlas Project]
* [http://www.unitaid.eu UNITAID, International Facility for the Purchase of Drugs] ([[UNITAID|Wikipedia Article]])
'''Vaccine and other research'''
* [http://news.bbc.co.uk/2/hi/health/3742876.stm BBC - ''Hopes of Malaria Vaccine by 2010''] 15 October 2004
* [http://news.bbc.co.uk/1/hi/health/4419835.stm BBC - ''Science shows how malaria hides''] 8 April 2005
* [http://www.malariasite.com/malaria/History.htm History of discoveries in malaria]
* [http://www.who.int/tdr/diseases/malaria/default.htm Malaria. The UNICEF-UNDP-World Bank-WHO Special Programme for Research and Training in Tropical Diseases]
* [http://www.malariavaccine.org Malaria Vaccine Initiative]
* [http://stevenlehrer.com/explorers/chapter_6-5.htm Story of the discovery of the vector of the malarial parasite]
* [http://www.wellcome.ac.uk/en/malaria/ Wellcome Trust against Malaria]
* [http://blogs.cgdev.org/vaccine/ "Vaccines for Development" - Blog on vaccine research and production for developing countries]
* [http://www.mmv.org/index.php Medicines for Malaria Venture]
* [http://www.allmosquitos.com/deseases/mosquito-transmitted-human-diseases/malaria.html Malaria and Mosquitos - questions and answers]
'''Mosquito Netting as Prevention'''
* [http://www.hisnets.org Hisnets] - Fighting Malaria: One Net At A Time
* [http://www.unicef.org/media/media_23447.html Call for Increased Production of Long-Lasting Insecticidal Nets as Part of the U.N. Millenium Campaign]
* [http://www.gmin.org/m3s1.html Providing everyone with a LLIN in Sahn Malen, a small village in Sierra Leone]
'''DDT'''
* [http://www.who.int/malaria/ddtandmalariavectorcontrol.html DDT and malaria vector control]
* [http://www.who.int/malaria/stockholmconventiononpops.html WHO Position on DDT Use]
* [http://info-pollution.com/ddtban.htm The DDT Ban Myth]
'''Animations, images and photos'''
* [http://news.bbc.co.uk/2/shared/spl/hi/picture_gallery/05/world_burden_of_malaria/html/1.stm Burden of Malaria], BBC pictures relating to malaria in northern Uganda
* [http://www.sumanasinc.com/scienceinfocus/sif_malaria.html Malaria: Cooperation among Parasite, Vector, and Host (Animation)]
*[http://www.malariafreefuture.org/blog/ Malaria Blog from the Johns Hopkins Bloomberg School of Public Health Center for Communications Programs]
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Latest revision as of 22:37, 29 July 2020

This page is about clinical aspects of the disease.  For microbiologic aspects of the causative organism(s), see Plasmodium.

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