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Plasmodium vivax From Wikipedia, the free encyclopedia

Jump to: navigation, search Plasmodium vivax Mature P. vivax trophozoite

Scientific classification Kingdom: Phylum: Class: Order: Family: Genus: Species:

Protista Apicomplexa Aconoidasida Haemosporida Plasmodiidae Plasmodium P. vivax

Binomial name Plasmodium vivax Grassi & Feletti 1890

Plasmodium vivax is a protozoal parasite and a human pathogen. The most frequent and widely distributed cause of recurring (tertian) malaria, P. vivax is one of four species of malarial parasite that commonly infect humans. It is less virulent than Plasmodium falciparum, the deadliest of the four, and seldom fatal. P. vivax is carried by the female Anopheles mosquito, since it is the only sex of the species that bites.

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1 Health o 1.1 Epidemiology o 1.2 Treatment o 1.3 Eradication Efforts in Korea 2 Biology o 2.1 Life Cycle  2.1.1 Human Infection  2.1.2 Liver Stage

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2.1.3 Erythrocytic Cycle 2.1.4 Sexual Stage 2.1.5 Mosquito Stage 3 Laboratory Considerations 4 See also 5 References

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6 External links

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[edit] Health [edit] Epidemiology P. vivax is found mainly in Asia, Latin America, and in some parts of Africa. P. vivax can cause death due to splenomegaly (a pathologically enlarged spleen), but more often it causes debilitating – but non-fatal – symptoms.[1]

[edit] Treatment Chloroquine remains the treatment of choice for vivax malaria, 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.[2] 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;[3] mefloquine is a good alternative and in some countries is more readily available.[4] Atovaquone-proguanil is an effective alternative in patients unable to tolerate chloroquine.[5] Quinine may be used to treat vivax malaria but is associated with inferior outcomes. Thirty-two to 100% of patients will relapse following successful treatment of P. vivax infection if a radical cure (eradication of liver stages) is not given.[6][7][8] Eradication of the liver stages is achieved by giving primaquine, after checking the patients G6PD status to reduce the risk of haemolysis.[9] Recently, this point has taken particular importance for the increased incidence of vivax malaria among travelers.[10]

[edit] Eradication Efforts in Korea 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 a unique opportunity to work together on an important health problem that affects both countries.[11][12]

[edit] Biology P. vivax can reproduce both asexually and sexually, depending on its life cycle stage. Asexual forms: • •

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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 corpuslce becomes distended and larger than normal. There are about sixteen merozoites.

Sexual forms: Gametocytes: Round. The gametocytes of P. vivax are commonly found in the peripheral blood at about the end of the first week of parasitemia.

[edit] Life Cycle The incubation period for the 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. [edit] Human Infection The infection of Plasmodium vivax takes place in human when an infected female anopheles mosquito sucks blood from a healthy person. During feeding, mosquito injects saliva to prevent clotting of blood and along with the saliva, thousands of Sporozoites are inoculated into human blood and reproduce asexually giving rise to thousands of merozoites(Plasmodium daughter cells) in the circulatory system including liver. [edit] 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 variable from one hypnozoite to another and the factors that will eventually trigger growth are not known; this explains how a single infection can be responsible for a series of waves of parasitaemia or "relapses".[13] Different strains of P. vivax have their own characteristic relapse pattern and timing.[14] [edit] Erythrocytic Cycle

[15]

P. vivax preferentially penetrates young red blood cells (reticulocytes). 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 (Fya and Fyb) as receptors to penetrate red blood cells. These antigens do not occur in the majority of humans in West Africa [phenotype Fy (a-b-)]. As a result P. vivax does not occur in West Africa.[16] The parasitised red blood cell is up to twice as large as a normal red cell and Schüffner's stippling (also known as Schüffner's dots or Schüffner's granules) is seen on the infected cell's surface, the spotted appearance of which varies 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. [edit] Sexual Stage The sexual stage includes following processes by which P. vivax reproduces sexually: i) Transfer to mosquito ii) Gametogenesis a) Microgametes b) Macrogametes

iii) Fertilization iv) Ookinite v) Oocyst vi) Sporogony [edit] Mosquito Stage

[edit] Laboratory Considerations P. vivax and P. ovale that has been sitting in EDTA for more than half-an-hour 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

half-an-hour of the blood being drawn and must certainly be made within an hour of the blood being drawn.

[edit] See also List of parasites (human)

[edit] References 1. ^ "Biology: Malaria Parasites". Malaria publisher=CDC. 2004-04-23. http://www.cdc.gov/malaria/biology/parasites/index.htm. Retrieved on 2008-0930. 2. ^ Lee KS, Kim TH, Kim ES, et al. (01 Feb 2009). "Chloroquine-resistant Plasmodium vivax in the Republic of Korea". Am J Trop Med Hyg 80 (2): 215– 217. PMID 19190216. http://www.ajtmh.org/cgi/content/abstract/80/2/215. 3. ^ Pukrittayakamee S, et al. (2000). "Therapeutic responses to different antimalarial drugs in vivax malaria". Antimicrob Agents Chemother 44 (6): 1680– 5. doi:10.1128/AAC.44.6.1680-1685.2000. PMID 10817728. 4. ^ Maguire JD, Krisin, Marwoto H, Richie TL, Fryauff DJ, Baird JK (2006). "Mefloquine is highly efficacious against chloroquine-resistant Plasmodium vivax malaria and Plasmodium falciparum malaria in Papua, Indonesia". Clin Infect Dis 42 (8): 1067–72. doi:10.1086/501357. 5. ^ Looareesuwan S, Wilairatana P, Glanarongran R, et al. (1999). "Atovaquone and proguanil hydrochloride followed by primaquine for treatment of Plasmodium vivax malaria in Thailand". Trans. R. Soc. Trop. Med. Hyg. 93 (6): 637–40. doi:10.1016/S0035-9203(99)90079-2. PMID 10717754. 6. ^ Wiselogle FY (1943). J.W. Edwards(ed.). ed. A survey of antimalarial drugs, 1941–1945 (2 vols.). Ann Arbor, Michigan. 7. ^ Alving AS, Hankey DD, Coatney GR, et al. (1953). "Korean vivax malaria. II. Curative treatment with pamaquine and primaquine". Am J Trop Med Hyg 6: 9706. 8. ^ Adak T, Sharma VP, Orlov VS (1998). "Studies on the Plasmodium vivax relapse pattern in Delhi, India". Am J Trop Med Hyg 59: 1759. 9. ^ Baird JK, Hoffman SL (November 2004). "Primaquine therapy for malaria". Clin. Infect. Dis. 39 (9): 1336–45. doi:10.1086/424663. PMID 15494911. http://www.journals.uchicago.edu/cgi-bin/resolve?CID33149. 10. ^ Saleri N, Gulletta M, Matteelli A, et al. (2006). "Acute respiratory distress syndrome in Plasmodium vivax malaria in traveler returning from Venezuela". J Travel Med 13 (2): 112–3. doi:10.1111/j.1708-8305.2006.00024.x. PMID 16553597. http://www.blackwellsynergy.com/openurl?genre=article&sid=nlm:pubmed&issn=11951982&date=2006&volume=13&issue=2&spage=112. 11. ^ http://www.koreatimes.co.kr/www/news/opinon/2008/05/160_24386.html For Re-Eradication of Malaria in Korea, Korea Times 05-19-2008

12. ^ http://www.feer.com/international-relations/2008/july/Korean-War-AgainstMalaria The Korean War Against Malaria, Far Eastern Economic Review 07-092008 13. ^ "1.4". http://www.impactmalaria.com/FR/EPS/Formations_et_cours_internationaux/Formation_de_la_Live rpool_School_LSTMH/cours_liverpool/Unit_1/1_4.html. Retrieved on 2008-0930. 14. ^ "1.4.1". http://www.impactmalaria.com/FR/EPS/Formations_et_cours_internationaux/Formation_de_la_Live rpool_School_LSTMH/cours_liverpool/Unit_1/1_4_1.html. Retrieved on 200809-30. 15. ^ Bozdech Z, Llinás M, Pulliam BL, Wong ED, Zhu J, DeRisi JL (October 2003). "The transcriptome of the intraerythrocytic developmental cycle of Plasmodium falciparum". PLoS Biol. 1 (1): E5. doi:10.1371/journal.pbio.0000005. PMID 12929205. PMC: 176545. http://biology.plosjournals.org/perlserv/?request=getdocument&doi=10.1371/journal.pbio.0000005. 16. ^ Van den Enden J. "Illustrated Lecture Notes on Tropical Medicine". Illustrated Lecture Notes on Tropical Medicine. http://content-e.itg.be/contente/pub_ITG/Illustrated_lecture_notes_on_Tropical_Medicine_1169817124568/ind ex.htm. Retrieved on 2008-09-30.

[edit] External links •

Malaria Atlas Project

[hide] v•d•e

Infectious diseases - Parasitic disease: protozoan infection: unicellular bikont (A06-A07, B50-B64)

Alveolate

Coccidia: Cryptosporidium hominis/Cryptosporidium parvum (Cryptosporidiosis) · Conoidasida/ Isospora belli (Isosporiasis) · Coccidia Cyclospora cayetanensis (Cyclosporiasis) · Toxoplasma Apicomplexa gondii (Toxoplasmosis)

Chromalveolate

Plasmodium falciparum/vivax/ovale/malariae Aconoidasida (Malaria, Blackwater fever) Babesia (Babesiosis) CiliophoraBalantidium coli (Balantidiasis) HeterokontBlastocystis (Blastocystosis) T. brucei (African Trypanosomiasistrypanosomiasis) · T. cruzi (Chagas disease)

Trypanosomatida Discicristata Excavata

Schizopyrenida

Leishmania major/L. mexicana/L. aethiopica/L. tropica (Cutaneous leishmaniasis) · L. Leishmaniasisbraziliensis (Mucocutaneous leishmaniasis) · L. donovani/infantum (Visceral leishmaniasis) Naegleria fowleri (Primary amoebic meningoencephalitis)

DiplomonadidaGiardia lamblia (Giardiasis) Trichozoa Trichomonadida

Trichomonas vaginalis (Trichomoniasis) · Dientamoeba fragilis (Dientamoebiasis)

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