Plasmodium vivax

Plasmodium vivax is a protozoal parasite and a human pathogen. This parasite is the most frequent and widely distributed cause of recurring malaria.[2] Although it is less virulent than Plasmodium falciparum, the deadliest of the five human malaria parasites, P. vivax malaria infections can lead to severe disease and death, often due to splenomegaly (a pathologically enlarged spleen).[3][4] P. vivax is carried by the female Anopheles mosquito; the males do not bite.[5]

Plasmodium vivax
Mature P. vivax trophozoite
Scientific classification
(unranked): Diaphoretickes
Clade: TSAR
Clade: SAR
Infrakingdom: Alveolata
Phylum: Apicomplexa
Class: Aconoidasida
Order: Haemospororida
Family: Plasmodiidae
Genus: Plasmodium
P. vivax
Binomial name
Plasmodium vivax
(Grassi & Feletti, 1890)
  • Haemamoeba vivax Grassi and Feletti, 1890
  • Plasmodium malariae tertianae Celli and Sanfelice, 1891
  • Haemamoeba laverani var. tertiana Labbe, 1894(?)
  • Haemosporidium tertianae Lewkowicz, 1897
  • Plasmodium camarense Ziemann, 1915



Plasmodium vivax is found mainly in Asia, Latin America, and in some parts of Africa.[6][7] P. vivax is believed to have originated in Asia, but latest studies have shown that wild chimpanzees and gorillas throughout central Africa are endemically infected with parasites that are closely related to human P. vivax. These findings indicate that human P. vivax is of African origin[8]. Plasmodium vivax accounts for 65% of malaria cases in Asia and South America.[9] Unlike Plasmodium falciparum, Plasmodium vivax is capable of undergoing sporogonic development[10] in the mosquito at lower temperatures.[11] It has been estimated that 2.5 billion people are at risk of infection with this organism.[12]

Although the Americas contribute 22% of the global area at risk, high endemic areas are generally sparsely populated and the region contributes only 6% to the total population at risk. In Africa, the widespread lack of the Duffy antigen in the population has ensured that stable transmission is constrained to Madagascar and parts of the Horn of Africa. It contributes 3.5% of global population at risk. Central Asia is responsible for 82% of global population at risk with high endemic areas coinciding with dense populations particularly in India and Myanmar. South East Asia has areas of high endemicity in Indonesia and Papua New Guinea and overall contributes 9% of global population at risk.[13]

P. vivax is carried by at least 71 mosquito species. Many vivax vectors live happily in temperate climates—as far north as Finland. Some prefer to bite outdoors or during the daytime, hampering the effectiveness of indoor insecticide and bed nets. Several key vector species have yet to be grown in the lab for closer study, and insecticide resistance is unquantified.[9]

Clinical presentation

Pathogenesis results from rupture of infected red blood cells, leading to fever. Infected red blood cells may also stick to each other and to walls of capillaries. Vessels plug up and deprive tissues of oxygen. Infection may also cause the spleen to enlarge. [14]

Unlike P. falciparum, P. vivax can populate the bloodstream with sexual-stage parasitesthe form picked up by mosquitoes on their way to the next victimeven before a patient shows symptoms. Consequently, prompt treatment of symptomatic patients doesn't necessarily help stop an outbreak, as it does with falciparum malaria, in which fevers occur as sexual stages develop. Even when symptoms appear, because they are usually not immediately fatal, the parasite continues to multiply.[9]

Plasmodium vivax can cause a more unusual form of malaria with atypical symptoms. It has been known to debut with hiccups,[15] loss of taste, lack of fever, pain while swallowing, cough and urinary discomfort.[16]

The parasite can go dormant in the liver for days to years, causing no symptoms and remaining undetectable in blood tests. They form what are called hypnozoites, a small stage that nestles inside an individual liver cell. This name derives from “sleeping organisms”.[17] The hypnozoites allow the parasite to survive in more temperate zones, where mosquitoes bite only part of the year.[9]

A single infectious bite can trigger six or more relapses a year, leaving sufferers more vulnerable to other diseases. Other infectious diseases, including falciparum malaria, appear to trigger relapses.[9]

Serious complications

Serious complications for malaria are dormant liver stage parasites, organ failures such as acute kidney failure. More complications of malaria can also be impairment of consciousness, neurological abnormalities, hypoglycemia and low blood pressures caused by cardiovascular collapse, clinical jaundice and or other vital organ dysfunctions and coagulation defects. The most serious complication ultimately being death.[18]


The main way to prevent malaria is through vector control. There are mostly three main forms that the vector can be controlled: (1) insecticide-treated mosquito nets, (2) indoor residual spraying and (3) antimalarial drugs. Long-lasting insecticidal nets (LLNs) are the preferred method of control because it is the most cost effective. The WHO is currently strategizing how to ensure that the net is properly maintained to protect people at risk. The second option is indoor residual spraying and has been proven effective if at least 80% of the homes are sprayed. However, such method is only effective for 3-6months. A drawback to these two methods, unfortunately, is that mosquito resistance against these insecticides has risen. National malaria control efforts are undergoing rapid changes to ensure the people are given the most effective method of vector control. Lastly, antimalarial drugs can also be used to prevent infection from developing into a clinical disease. However, there has also been an increase resistance to antimalarial medicine.[19]

In 2015 the World Health Organization (WHO) drew up a plan to address vivax malaria,[20] as part of their Global Technical Strategy for Malaria.


P. vivax and P. ovale that has been sitting in EDTA for more than 30 minutes before the blood film is made will look very similar in appearance to P. malariae, which is an important reason to warn the laboratory immediately when the blood sample is drawn so they can process the sample as soon as it arrives. Blood films are preferably made within 30 minutes of the blood draw and must certainly be made within an hour of the blood being drawn. Diagnosis can be done with the strip fast test of antibodies.


Chloroquine remains the treatment of choice for vivax malaria,[21] except in Indonesia's Irian Jaya (Western New Guinea) region and the geographically contiguous Papua New Guinea, where chloroquine resistance is common (up to 20% resistance). Chloroquine resistance is an increasing problem in other parts of the world, such as Korea[22] and India.

When chloroquine resistance is common or when chloroquine is contraindicated, then artesunate is the drug of choice, except in the U.S., where it is not approved for use.[23] Where an artemisinin-based combination therapy has been adopted as the first-line treatment for P. falciparum malaria, it may also be used for P. vivax malaria in combination with primaquine for radical cure.[21] An exception is artesunate plus sulfadoxine-pyrimethamine (AS+SP), which is not effective against P. vivax in many places.[21] Mefloquine is a good alternative and in some countries is more readily available.[24] Atovaquone-proguanil is an effective alternative in patients unable to tolerate chloroquine.[25] Quinine may be used to treat vivax malaria but is associated with inferior outcomes.

32100% of patients will relapse following successful treatment of P. vivax infection if a radical cure (eradication of liver stages) is not given.[26][27]

Eradication of the liver stages is achieved by giving primaquine. Patients with glucose-6-phosphate dehydrogenase deficiency risk haemolysis.[28] G6PD is an enzyme important for blood chemistry. No field-ready test is available.[9] Recently, this point has taken particular importance for the increased incidence of vivax malaria among travelers.[29] At least a 14-day course of primaquine is required for the radical treatment of P. vivax.[21]


In 2013 a Phase IIb trial was completed that studied a single-dose alternative drug named tafenoquine.[30] It is an 8-aminoquinoline, of the same family as primaquine,[31] developed by researchers at the Walter Reed Army Institute of Research in the 1970s and tested in safety trials. It languished, however, until the push for malaria elimination sparked new interest in primaquine alternatives.[9]

Among patients who received a 600-mg dose, 91% were relapse-free after 6 months. Among patients who received primaquine, 24% relapsed within 6 months. "The data are absolutely spectacular," Wells says. Ideally, he says, researchers will be able to combine the safety data from the Army's earlier trials with the new study in a submission to the U.S. Food and Drug Administration for approval. Like primaquine, tafenoquine causes hemolysis in people who are G6PD deficient.[9]

In 2013 researchers produced cultured human "microlivers" that supported liver stages of both P. falciparum and P. vivax and may have also created hypnozoites.[9]


Mass-treating populations with a primaquine can kill the hypnozoites, exempting those with G6PD deficiency. However, the standard regimen requires a daily pill for 14 days across an asymptomatic population.


P. vivax is the only indigenous malaria parasite on the Korean peninsula. In the years following the Korean War (1950–53), malaria-eradication campaigns successfully reduced the number of new cases of the disease in North Korea and South Korea. In 1979, World Health Organization declared the Korean peninsula vivax malaria-free, but the disease unexpectedly re-emerged in the late 1990s and still persists today. Several factors contributed to the re-emergence of the disease, including reduced emphasis on malaria control after 1979, floods and famine in North Korea, emergence of drug resistance and possibly global warming. Most cases are identified along the Korean Demilitarized Zone. As such, vivax malaria offers the two Koreas an opportunity to work together on an important health problem that affects both countries.[32][33]

Drug Targets

Given that drugs that target the various life stages of the parasite can sometimes have undesirable side effects, it is desirable to come up with drug molecules targeting specific proteins/enzymes that are essential for the parasite´s survival or that can compromise the fitness of the organism. Enzymes in the Purine salvage pathway had been favorite targets to this end. However, given the high degree of conservation in purine metabolism across the parasite and its host, there could be potential cross-reactivity making it difficult to design selective drugs against the parasite. To overcome this, recent efforts have focused on deducing the function of orphan hypothetical proteins whose functions have been unknown. Though, a lot of the hypothetical proteins have role in secondary metabolism, targeting them will be beneficial from two perspectives, i.e., specificity and reducing the virulence of the pathogen with no or minimal undesirable cross-reactivities.


Life cycle

Like all malaria parasites, P. vivax has a complex life cycle. It infects a definitive insect host, where sexual reproduction occurs, and an intermediate vertebrate host, where asexual amplification occurs. In P. vivax, the definitive hosts are Anopheles mosquitoes (also known as the vector), while humans are the intermediate asexual hosts. During its life cycle, P. vivax assumes many different physical forms.

Asexual forms:

  • Sporozoite: Transfers infection from mosquito to human
  • Immature trophozoites (Ring or signet-ring shaped), about 1/3 of the diameter of a RBC.
  • Mature trophozoites: Very irregular and delicate (described as amoeboid); many pseudopodial processes seen. Presence of fine grains of brown pigment (malarial pigment) or hematin probably derived from the haemoglobin of the infected red blood cell.
  • Schizonts (also called meronts): As large as a normal red cell; thus the parasitized corpuscle becomes distended and larger than normal. There are about sixteen merozoites.

Sexual forms:

  • Gametocytes: Round. P. vivax gametocytes are commonly found in human peripheral blood at about the end of the first week of parasitemia.
  • Gametes: Formed from gametocytes in mosquitoes.
  • Zygote: Formed from combination of gametes
  • Oocyst: Contains zygote, develops into sporozoites

Human infection

P. vivax human infection occurs when an infected mosquito feeds on a human. During feeding, the mosquito injects saliva to prevent blood clotting (along with sporozoites), thousands of sporozoites are inoculated into human blood; within a half-hour the sporozoites reach the liver. There they enter hepatic cells, transform into the trophozoite form and feed on hepatic cells, and reproduce asexually. This process gives rise to thousands of merozoites (plasmodium daughter cells) in the circulatory system and the liver.

The incubation period of human infection usually ranges from ten to seventeen days and sometimes up to a year. Persistent liver stages allow relapse up to five years after elimination of red blood cell stages and clinical cure.

Liver stage

The P. vivax sporozoite enters a hepatocyte and begins its exoerythrocytic schizogony stage. This is characterized by multiple rounds of nuclear division without cellular segmentation. After a certain number of nuclear divisions, the parasite cell will segment and merozoites are formed.

There are situations where some of the sporozoites do not immediately start to grow and divide after entering the hepatocyte, but remain in a dormant, hypnozoite stage for weeks or months. The duration of latency is thought to be variable from one hypnozoite to another and the factors that will eventually trigger growth are not known; this might explain how a single infection can be responsible for a series of waves of parasitaemia or "relapses".[34] It has been assumed that different strains of P. vivax have their own characteristic relapse pattern and timing. However, such recurrent parasitaemia is probably being over-attributed to hypnozoite activation.[35] One newly recognized, non-hypnozoite, possible contributing source to recurrent peripheral P. vivax parasitaemia is erythrocytic forms in bone marrow.[36]

Erythrocytic cycle

P. vivax preferentially penetrates young red blood cells (reticulocytes), unlike Plasmodium falciparum which can invade erythrocytes. In order to achieve this, merozoites have two proteins at their apical pole (PvRBP-1 and PvRBP-2). The parasite uses the Duffy blood group antigens (Fy6) to penetrate red blood cells. This antigen does not occur in the majority of humans in West Africa [phenotype Fy (a-b-)]. As a result, P. vivax occurs less frequently in West Africa.[37]

The parasitised red blood cell is up to twice as large as a normal red cell and Schüffner's dots (also known as Schüffner's stippling or Schüffner's granules) are seen on the infected cell's surface. Schüffner's dots have a spotted appearance, varying in color from light pink, to red, to red-yellow, as coloured with Romanovsky stains. The parasite within it is often wildly irregular in shape (described as "amoeboid"). Schizonts of P. vivax have up to twenty merozoites within them. It is rare to see cells with more than one parasite within them. Merozoites will only attach to immature blood cell (reticulocytes) and therefore it is unusual to see more than 3% of all circulating erythrocytes parasitised.

Mosquito stage

Parasite life cycle in mosquitoes includes all stages of sexual reproduction:

  1. Infection and Gametogenesis
    • Microgametes
    • Macrogametes
  2. Fertilization
  3. Ookinite
  4. Oocyst
  5. Sporogony
Mosquito Infection and Gamete Formation

When a female Anopheles mosquito bites an infected person, gametocytes and other stages of the parasite are transferred to the mosquito stomach. Gametocytes ultimately develop into gametes, a process known as gametogony.

Microgametocytes become very active, and their nuclei undergo fission (i.e. amitosis) to each give 6-8 daughter nuclei, which becomes arranged at the periphery. The cytoplasm develops long thin flagella like projections, then a nucleus enter into each one of these extensions. These cytoplasmic extensions later break off as mature male gametes (microgametes). This process of formation of flagella-like microgametes or male gametes is known as exflagellation. Macrogametocytes show very little change. They develop a cone of reception at one side and becomes mature as macrogametocytes (female gametes).


Male gametes move actively in the stomach of mosquitoes in search of female gametes. Male gametes then enter into female gametes through the cone of reception. The complete fusion of 2 gametes results in the formation of zygote. Here, fusion of 2 dissimilar gametes occurs, known as anisogamy.

The zygote remains inactive for sometime but it soon elongates, becomes vermiform (worm-like) and motile. It is now known as ookinete. The pointed ends of ookinete penetrate the stomach wall and come to lie below its outer epithelial layer. Here the zygote becomes spherical and develops a cyst wall around itself. The cyst wall is derived partly from the stomach tissues and partly produced by the zygote itself. At this stage, the zygote is known as an oocyst. The oocyst absorbs nourishment and grows in size. Oocysts protrude from the surface of stomach, giving it a blistered appearance. In a highly infected mosquito, as many as 1000 oocysts may be seen.


The oocyst nucleus divides repeatedly to form large number of daughter nuclei. At the same time, the cytoplasm develops large vacuoles and forms numerous cytoplasmic masses. These cytoplasmic masses then elongate and a daughter nuclei migrates into each mass. The resulting sickle-shaped bodies are known as sporozoites. This phase of asexual multiplication is known as sporogony and is completed in about 10–21 days. The oocyst then bursts and sporozoites are released into the body cavity of mosquito. Sporozoites eventually reach the salivary glands of mosquito via its hemolymph. The mosquito now becomes infectious. Salivary glands of a single infected mosquito may contain as many as 200,000 sporozoites. When the mosquito bites a healthy person, thousands of sporozoites are infected into the blood along with the saliva and the cycle starts again.


P. vivax can be divided into two clades one that appears to have origins in the Old World and a second that originated in the New World.[38] The distinction can be made on the basis of the structure of the A and S forms of the rRNA. A rearrangement of these genes appears to have occurred in the New World strains. It appears that a gene conversion occurred in an Old World strain and this strain gave rise to the New World strains. The timing of this event has yet to be established.

At present both types of P. vivax circulate in the Americas. The monkey parasite - Plasmodium simium - is related to the Old World strains rather than to the New World strains.

A specific name - Plasmodium collinsi - has been proposed for the New World strains but this suggestion has not been accepted to date.


It has been suggested that P. vivax has horizontally acquired genetic material from humans. [39]

Plasmodium vivax is not known to have a particular gram stain (negative vs. positive) and may appear as either.

Therapeutic use

P. vivax was used between 1917 and the 1940s for malariotherapy, that is, to create very high fevers to combat certain diseases such as tertiary syphilis. In 1917, the inventor of this technique, Julius Wagner-Jauregg, received the Nobel Prize in Physiology or Medicine for his discoveries. However, the technique was dangerous, killing about 15% of patients, so it is no longer in use.[40]

See also


  1. Coatney GR, Collins WE, Warren M, Contacos PG (1971). "5 Plasmodium vivax (Grassi and Feletti, 1890)". The primate malarias. Division of Parasitic Disease, CDC. p. 43.
  2. White NJ (January 2008). "Plasmodium knowlesi: the fifth human malaria parasite". Clinical Infectious Diseases. 46 (2): 172–3. doi:10.1086/524889. PMID 18171246.
  3. Baird JK (November 2007). "Neglect of Plasmodium vivax malaria". Trends in Parasitology. 23 (11): 533–9. doi:10.1016/ PMID 17933585.
  4. Anstey NM, Douglas NM, Poespoprodjo JR, Price RN (2012). Plasmodium vivax: clinical spectrum, risk factors and pathogenesis. Advances in Parasitology. 80. pp. 151–201. doi:10.1016/b978-0-12-397900-1.00003-7. ISBN 9780123979001. PMID 23199488.
  5. Crompton PD, Moebius J, Portugal S, Waisberg M, Hart G, Garver LS, Miller LH, Barillas-Mury C, Pierce SK (2014). "Malaria immunity in man and mosquito: insights into unsolved mysteries of a deadly infectious disease". Annual Review of Immunology. 32 (1): 157–87. doi:10.1146/annurev-immunol-032713-120220. PMC 4075043. PMID 24655294.
  6. "Biology: Malaria Parasites". Malaria. CDC. 2004-04-23. Archived from the original on 2008-10-13. Retrieved 2008-09-30.
  7. Lindsay SW, Hutchinson RA (2006). "Malaria and deaths in the English marshesAuthors' reply". Lancet. 368 (9542): 1152. doi:10.1016/S0140-6736(06)69467-1.
  8. Liu, Weimin; Li, Yingying; Shaw, Katharina S.; Learn, Gerald H.; Plenderleith, Lindsey J.; Malenke, Jordan A.; Sundararaman, Sesh A.; Ramirez, Miguel A.; Crystal, Patricia A. (2014-02-21). "African origin of the malaria parasite Plasmodium vivax". Nature Communications. 5: 3346. Bibcode:2014NatCo...5.3346L. doi:10.1038/ncomms4346. ISSN 2041-1723. PMC 4089193. PMID 24557500.
  9. Vogel G (November 2013). "The forgotten malaria". Science. 342 (6159): 684–7. doi:10.1126/science.342.6159.684. PMID 24202156.
  10. "sporogonic". The Free Dictionary.
  11. Gething PW, Van Boeckel TP, Smith DL, Guerra CA, Patil AP, Snow RW, Hay SI (May 2011). "Modelling the global constraints of temperature on transmission of Plasmodium falciparum and P. vivax". Parasites & Vectors. 4: 92. doi:10.1186/1756-3305-4-92. PMC 3115897. PMID 21615906.
  12. Gething PW, Elyazar IR, Moyes CL, Smith DL, Battle KE, Guerra CA, Patil AP, Tatem AJ, Howes RE, Myers MF, George DB, Horby P, Wertheim HF, Price RN, Müeller I, Baird JK, Hay SI (2012). "A long neglected world malaria map: Plasmodium vivax endemicity in 2010". PLoS Neglected Tropical Diseases. 6 (9): e1814. doi:10.1371/journal.pntd.0001814. PMC 3435256. PMID 22970336.
  13. Battle KE, Gething PW, Elyazar IR, Moyes CL, Sinka ME, Howes RE, Guerra CA, Price RN, Baird KJ, Hay SI (2012). The global public health significance of Plasmodium vivax. Public Health Resources. Advances in Parasitology. 80. pp. 1–111. doi:10.1016/b978-0-12-397900-1.00001-3. ISBN 9780123979001. PMID 23199486.
  14. Guadarrama-Conzuelo, F; Saad Manzanera, A D (2019-09-01). "Singultus as an Unusual Debut of Plasmodium vivax Malaria". Cureus. 11 (9). doi:10.7759/cureus.5548.
  15. Mohapatra, M. K.; Padhiary, K. N.; Mishra, D. P.; Sethy, G. (June 2002). "Atypical manifestations of Plasmodium vivax malaria". Indian Journal of Malariology. 39 (1–2): 18–25. ISSN 0367-8326. PMID 14686106.
  16. Markus MB (2011). "Malaria: origin of the term "hypnozoite"". Journal of the History of Biology. 44 (4): 781–6. doi:10.1007/s10739-010-9239-3. PMID 20665090.
  17. Control of Communicable Diseases Manual, 20th edition
  18. "Malaria Fact Sheet". World Health Organization. Retrieved 20 October 2016.
  19. "Control And Elimination Of Plasmodium Vivax Malaria" (PDF). World Health Organization. 2015. Retrieved 28 December 2016.
  20. 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
  21. Lee KS, Kim TH, Kim ES, Lim HS, Yeom JS, Jun G, Park JW (February 2009). "Short report: chloroquine-resistant Plasmodium vivax in the Republic of Korea". The American Journal of Tropical Medicine and Hygiene. 80 (2): 215–7. doi:10.4269/ajtmh.2009.80.215. PMID 19190216.
  22. Pukrittayakamee S, Chantra A, Simpson JA, Vanijanonta S, Clemens R, Looareesuwan S, White NJ (June 2000). "Therapeutic responses to different antimalarial drugs in vivax malaria". Antimicrobial Agents and Chemotherapy. 44 (6): 1680–5. doi:10.1128/AAC.44.6.1680-1685.2000. PMC 89932. PMID 10817728.
  23. Maguire JD, Marwoto H, Richie TL, Fryauff DJ, Baird JK (April 2006). "Mefloquine is highly efficacious against chloroquine-resistant Plasmodium vivax malaria and Plasmodium falciparum malaria in Papua, Indonesia". Clinical Infectious Diseases. 42 (8): 1067–72. doi:10.1086/501357. PMID 16575721.
  24. Looareesuwan S, Wilairatana P, Glanarongran R, Indravijit KA, Supeeranontha L, Chinnapha S, Scott TR, Chulay JD (1999). "Atovaquone and proguanil hydrochloride followed by primaquine for treatment of Plasmodium vivax malaria in Thailand". Transactions of the Royal Society of Tropical Medicine and Hygiene. 93 (6): 637–40. doi:10.1016/S0035-9203(99)90079-2. PMID 10717754.
  25. Wiselogle FY (1943). J.W. Edwards (ed.). A survey of antimalarial drugs, 19411945 (2 vols.). Ann Arbor, Michigan.
  26. Alving AS, Hankey DD, Coatney GR, Jones R, Coker WG, Garrison PL, Donovan WN (November 1953). "Korean vivax malaria. II. Curative treatment with pamaquine and primaquine". The American Journal of Tropical Medicine and Hygiene. 2 (6): 970–6. doi:10.4269/ajtmh.1953.2.970. PMID 13104805.
    Adak T, Sharma VP, Orlov VS (July 1998). "Studies on the Plasmodium vivax relapse pattern in Delhi, India". The American Journal of Tropical Medicine and Hygiene. 59 (1): 175–9. doi:10.4269/ajtmh.1998.59.175. PMID 9684649.
  27. Baird JK, Hoffman SL (November 2004). "Primaquine therapy for malaria". Clinical Infectious Diseases. 39 (9): 1336–45. doi:10.1086/424663. PMID 15494911.
  28. Saleri N, Gulletta M, Matteelli A, Caligaris S, Tomasoni LR, Antonini B, Perandin F, Castelli F (2006). "Acute respiratory distress syndrome in Plasmodium vivax malaria in traveler returning from Venezuela". Journal of Travel Medicine. 13 (2): 112–3. doi:10.1111/j.1708-8305.2006.00024.x. PMID 16553597.
  29. Llanos-Cuentas A, Lacerda MV, Rueangweerayut R, Krudsood S, Gupta SK, Kochar SK, Arthur P, Chuenchom N, Möhrle JJ, Duparc S, Ugwuegbulam C, Kleim JP, Carter N, Green JA, Kellam L (March 2014). "Tafenoquine plus chloroquine for the treatment and relapse prevention of Plasmodium vivax malaria (DETECTIVE): a multicentre, double-blind, randomised, phase 2b dose-selection study". Lancet. 383 (9922): 1049–58. doi:10.1016/S0140-6736(13)62568-4. PMID 24360369.
  30. "Tafenoquine". MMV. Retrieved 2014-02-17.
  31. For Re-Eradication of Malaria in Korea, Korea Times 05-19-2008
  32. The Korean War Against Malaria, Far Eastern Economic Review 07-09-2008
  33. White NJ (December 2016). "Why Do Some Primate Malarias Relapse?". Trends in Parasitology. 32 (12): 918–920. doi:10.1016/ PMC 5134685. PMID 27743866.
  34. Markus MB (March 2018). "Biological Concepts in Recurrent Plasmodium vivax Malaria". Parasitology. 145 (13): 1765–1771. doi:10.1017/S003118201800032X. PMID 29564998.
  35. Markus, MB (July 2017). "Malaria Eradication and the Hidden Parasite Reservoir". Trends in Parasitology. 33 (7): 492–495. doi:10.1016/ PMID 28366603.
  36. Van den Enden J. "Illustrated Lecture Notes on Tropical Medicine". Archived from the original on 2015-11-23. Retrieved 2015-11-01.
  37. Li J, Collins WE, Wirtz RA, Rathore D, Lal A, McCutchan TF (2001). "Geographic subdivision of the range of the malaria parasite Plasmodium vivax". Emerging Infectious Diseases. 7 (1): 35–42. doi:10.3201/eid0701.010105. PMC 2631686. PMID 11266292.
  38. Bar, Daniel; Bar, Daniel (2011). "Evidence of Massive Horizontal Gene Transfer Between Humans and Plasmodium vivax : Nature Precedings". Nature Precedings. doi:10.1038/npre.2011.5690.1. Retrieved 2014-02-17.
  39. Vogel G (November 2013). "Malaria as lifesaving therapy". Science. 342 (6159): 686. doi:10.1126/science.342.6159.686. PMID 24202157.
This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.