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Plasmodium vivax
From Wikipedia, the free encyclopedia
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.
Contents
[hide]
• 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
2.1.3 Erythrocytic Cycle
2.1.4 Sexual Stage
2.1.5 Mosquito Stage
• 3 Laboratory Considerations
• 4 See also
• 5 References
• 6 External links
[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]
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:
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.
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.
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.
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]
[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.
The sexual stage includes following processes by which P. vivax reproduces sexually: i)
Transfer to mosquito ii) Gametogenesis
a) Microgametes
b) Macrogametes
[edit] References
1. ^ "Biology: Malaria Parasites". Malaria publisher=CDC. 2004-04-23.
http://www.cdc.gov/malaria/biology/parasites/index.htm. Retrieved on 2008-09-
30.
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.blackwell-
synergy.com/openurl?genre=article&sid=nlm:pubmed&issn=1195-
1982&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-Against-
Malaria The Korean War Against Malaria, Far Eastern Economic Review 07-09-
2008
13. ^ "1.4". http://www.impact-
malaria.com/FR/EPS/Formations_et_cours_internationaux/Formation_de_la_Live
rpool_School_LSTMH/cours_liverpool/Unit_1/1_4.html. Retrieved on 2008-09-
30.
14. ^ "1.4.1". http://www.impact-
malaria.com/FR/EPS/Formations_et_cours_internationaux/Formation_de_la_Live
rpool_School_LSTMH/cours_liverpool/Unit_1/1_4_1.html. Retrieved on 2008-
09-30.
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=get-
document&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/content-
e/pub_ITG/Illustrated_lecture_notes_on_Tropical_Medicine_1169817124568/ind
ex.htm. Retrieved on 2008-09-30.
Coccidia: Cryptosporidium
hominis/Cryptosporidium
parvum (Cryptosporidiosis) ·
Conoidasida/
Isospora belli (Isosporiasis) ·
Coccidia
Cyclospora cayetanensis
(Cyclosporiasis) · Toxoplasma
Apicomplexa
gondii (Toxoplasmosis)
Alveolate
Chromalveolate
Plasmodium
falciparum/vivax/ovale/malariae
Aconoidasida
(Malaria, Blackwater fever)
Babesia (Babesiosis)
HeterokontBlastocystis (Blastocystosis)
T. brucei (African
Trypanosomiasistrypanosomiasis) · T.
cruzi (Chagas disease)
Leishmania major/L.
mexicana/L.
aethiopica/L. tropica
Trypanosomatida (Cutaneous
leishmaniasis) · L.
Discicristata
Leishmaniasisbraziliensis
(Mucocutaneous
Excavata leishmaniasis) · L.
donovani/infantum
(Visceral
leishmaniasis)
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