Plasmodium vivax
Plasmodium vivax | ||||||||||||
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![]() Trophozoites of Plasmodium vivax in stained blood smear |
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Systematics | ||||||||||||
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Scientific name | ||||||||||||
Plasmodium vivax | ||||||||||||
( Grassi & Feletti , 1890) |
Plasmodium vivax is a unicellular parasite of the genus Plasmodium and a pathogen of malaria tertiana . Plasmodium vivax infectionsare common, and although the disease is generally considered to be relatively benign, the pathogen contributes significantly to morbidity with an estimated 132 to 391 million infections per year in the affected countries. Historically, P. vivax hascontributed significantly to mortality in Europe, presumably in combination with other factors, and even today the severity of the disease is easily underestimated. Like other malaria pathogens, Plasmodium vivax is transmittedby female Anopheles mosquitoes . The main distribution area today is in Asia and the Western Pacific, but the vivax malaria is also importantin Central and South America, while the parasite is relatively rare in Africa.
Discovery and Description
history
Malaria pathogens were first described by Alphonse Laveran in 1880 . Laveran assumed only one type of pathogen, which he called Oscillaria malariae ; It is believed that Laveran observed pathogens causing tropica malaria, tertiana malaria and quartana malaria in Algeria. Camillo Golgi was only able to differentiate these different disease courses and their pathogens a few years later . In 1890, after reviewing the literature, Grassi and Feletti proposed the name Haemamoeba vivax for the causative agent of Tertiana malaria . The term vivax refers to the lively amoeboid form of young trophozoites in the erythrocytes , a property that the other classic malaria pathogens do not show. In 1885 Marchiafava and Celli had already proposed the generic name Plasmodium . In 1954, the popular combination Plasmodium vivax was declared valid by the International Commission for Zoological Nomenclature .
morphology
As with all plasmodia, P. vivax occurs in different stages of development. Liver schizonts are often oval in shape, about 44 by 52 micrometers in size, and contain a large number of merozoites , each 0.8 to 1.2 micrometers in size. When the parasite multiplies in erythrocytes, multiple infections of a cell are not uncommon. In the course of the development of the trophozoites, the erythrocytes are normally significantly enlarged and show characteristic Schüffner stippling , which is not as prominent as in Plasmodium ovale . The trophozoites themselves show an amoeboid cytoplasm. Mature blood schizonts contain 8 to a maximum of 24, typically 16, merozoites.
- Forms of development in the stained blood smear
Immature gametocytes are microscopically easy to distinguish from the asexual forms because their cytoplasm is not amoeboid. Mature macrogametocytes fill the host cell completely; the cytoplasm is colored light blue with distributed dark pigment, the cell nucleus is relatively small. Mature microgametocytes show a blue-gray cytoplasm with a large nucleus.
Systematics
Traditionally, Plasmodium vivax is classified in the subgenus Plasmodium with many other plasmodia that infect primates . A species very closely related to P. vivax is P. simium , which was found in monkeys in Brazil. According to the gene sequences available so far, both species are practically identical, and it is assumed that P. simium arose from a host change of P. vivax from humans to monkeys.
Closely related but clearly distinguishable are a number of species of Plasmodium that infect various macaques in Asia , including P. cynomolgi and P. simiovale , but also Plasmodium knowlesi . It is believed that P. vivax originated from these plasmodia and passed from macaques to humans in Asia several 100,000 years ago. The closeness of P. vivax to P. knowlesi was also confirmed by analyzes of the completely sequenced genomes of both species, which showed an extensive syntany of the chromosomes . A rare malaria pathogen called “ P. vivax- like” in the literature looks microscopic like P. vivax , but is molecularly very similar to P. simiovale , possibly even identical to it.
Distribution and host animals
In principle, Plasmodium vivax can occur worldwide in temperate and tropical regions, especially in coastal areas, marshes and similar areas. For example, the parasite existed in Germany as a cause of marsh fever until the 20th century . Today the distribution is limited to tropical and subtropical countries. The greatest number of diseases originate in Southeast Asia and the Western Pacific. In Central and South America the absolute number of cases is lower, but P. vivax causes more than 70% of all malaria cases there. Infections with P. vivax are comparatively rare in Africa , as large parts of the local population are resistant to the parasite. P. vivax requires a host protein, the Duffy antigen , to penetrate the erythrocytes ; this antigen is absent in more than 90% of the population in West, Central and East Africa.
Humans are considered to be the only relevant reservoir host for Plasmodium vivax . Experimentally, chimpanzees and gibbons and a number of New World monkeys , but no macaques, could be infected. It is unclear whether monkeys infected with the very similar, presumably identical P. simium represent an epidemiologically relevant reservoir for human infections. Hosts for P. simium are the brown howler monkey and, rarely, the southern spider monkey ; the distribution area of P. simium is limited to forests in the coastal region in southern and southeastern Brazil. In the meantime P. vivax / P. simium also found in wild howler monkeys using PCR .
A large number of species in the genus Anopheles can transmit P. vivax ; this is also the cause of the large potential range of the parasite. Among other things, the species Anopheles atroparvus P. vivax, native to Europe, is a suitable vector for the parasite.
Life cycle
The life cycle of P. vivax is essentially the same as that of other plasmodia. The parasite shows an obligatory change of host . The sporozoites enter the human bloodstream through infected mosquitoes, migrate from there to the liver and penetrate hepatocytes , in which they reproduce asexually through schizogony . The incubation period of this liver phase is at least eight days. The liver schizonts each produce large numbers of merozoites, which are released and attack erythrocytes, usually those in the reticulocyte stage. Further asexual reproduction takes place in these cells. The generation time for the replication in the erythrocytes averages 48 hours or a little less. Since development is often synchronous, there is a massive release of new parasites at the end of each reproduction cycle, which is associated with a fever attack. The term malaria tertiana is derived from the periodicity of the fever attacks.
A few plasmodia develop in the erythrocytes into sex forms, the gametocytes. In contrast to the equally widespread malaria pathogen Plasmodium falciparum , gametocytes develop in P. vivax before the disease breaks out. This allows mosquitoes to spread the parasites even before the disease is recognized and treated. The microgametocytes and macrogametocytes can be ingested by mosquitoes with a blood meal and start a new development cycle in the insect's intestine. After the gametes fuse, new sporozoites are formed in the intestine, which migrate to the mosquito's salivary gland, from where they can be transferred to a new host. The development time in the mosquito is around 11 to 12 days at 25 ° C. P. vivax can complete its development in the mosquito even at 16 ° C.
Not all liver parasites are released into the bloodstream. There remain calm forms, called Hypnozoiten , in the liver, after weeks or months and recurrences can lead relapses mentioned. These recurrences contribute significantly to morbidity. The hypnozoites must be eliminated by treatment with primaquine .
Individual evidence
- ↑ a b R. N. Price, E. Tjitra, CA Guerra, S. Yeung, NJ White, NM Anstey: Vivax malaria: neglected and not benign. In: Am J Trop Med Hyg. 77 (6 Suppl), Dec 2007, pp. 79-87. PMID 18165478
- ↑ a b K. Mendis, BJ Sina, P. Marchesini, R. Carter: The neglected burden of Plasmodium vivax malaria. In: Am. J. Trop. Med. Hyg. 64 (1, 2) S, 2001, pp. 97-106. PMID 11425182
- ↑ a b O. E. Cornejo, AA Escalante: The origin and age of Plasmodium vivax. In: Trends Parasitol. 22 (12), Dec 2006, pp. 558-563. PMID 17035086
- ↑ JM Carlton, JH Adams, JC Silva, SL Bidwell, H. Lorenzi, E. Caler, J. Crabtree, SV Angiuoli, EF Merino, P. Amedeo, Q. Cheng, RM Coulson, BS Crabb, HA Del Portillo, K . Essien, TV Feldblyum, C. Fernandez-Becerra, PR Gilson, AH Gueye, X. Guo, S. Kang'a, TW Kooij, M. Korsinczky, EV Meyer, V. Nene, I. Paulsen, O. White, SA Ralph, Q. Ren, TJ Sargeant, SL Salzberg, CJ Stoeckert, SA Sullivan, MM Yamamoto, SL Hoffman, JR Wortman, MJ Gardner, MR Galinski, JW Barnwell, CM Fraser-Liggett: Comparative genomics of the neglected human malaria parasite Plasmodium vivax. In: Nature. 455 (7214), Oct 9, 2008, pp. 757-763. PMID 18843361
- ↑ SH Qari, YP Shi, IF Goldman, V. Udhayakumar, MP Alpers, WE Collins, AA Lal: Identification of Plasmodium vivax-like human malaria parasite. In: Lancet. 341 (8848), Mar 27, 1993, pp. 780-783. PMID 8095999
- ↑ W. Köhler, M. Köhler: Zentralblatt für Bakteriologie - 100 years ago: malaria in north-west Germany. In: Int J Med Microbiol. 298 (5-6), Jul 2008, pp. 339-343. PMID 17897879
- ^ R. Rosenberg: Plasmodium vivax in Africa: hidden in plain sight? In: Trends Parasitol. 23 (5), May 2007, pp. 193-196. Epub 2007 Mar 13. PMID 17360237
- ↑ LM Deane: Simian malaria in Brazil. In: Mem Inst Oswaldo Cruz. 87 Suppl 3, 1992, pp. 1-20. PMID 1343676
- ↑ AM Duarte, S. Malafronte Rdos, C. Cerutti Jr, I. Curado, BR de Paiva, AY Maeda, T. Yamasaki, ME Summa, V. Neves Ddo, SG de Oliveira, C. Gomes Ade: Natural Plasmodium infections in Brazilian wild monkeys: reservoirs for human infections? In: Acta Trop. 107 (2), Aug 2008, pp. 179-185. PMID 18620330
literature
- G. Robert Coatney, William E. Collins, McWilson Warren, Peter G. Contacos: The primate malarias. US National Institute of Allergy and Infectious Diseases, Bethesda 1971. Chapter 5, p. 43 ff .: Plasmodium vivax PDF