Plasmodium chabaudi

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Plasmodium chabaudi
Scientific classification edit
Domain: Eukaryota
(unranked): Diaphoretickes
Clade: SAR
Infrakingdom: Alveolata
Phylum: Apicomplexa
Class: Aconoidasida
Order: Haemospororida
Family: Plasmodiidae
Genus: Plasmodium
Subgenus: Vinckeia
Species:
P. chabaudi
Binomial name
Plasmodium chabaudi
Landau, 1965
Subspecies

Plasmodium chabaudi is a parasite of the genus Plasmodium subgenus Vinckeia. As in all Plasmodium species, P. chabaudi has both vertebrate and insect hosts. The vertebrate hosts for this parasite are rodents.[1]

Taxonomy[edit]

This species was described in 1965 by Irène Landau.[2] It is named after the French parasitologist Alain Chabaud.

Subspecies[edit]

Two subspecies have been defined: P. chabaudi chabaudi and P. chabaudi adami.[3]

Genome[edit]

The nuclear genome is 18.8 megabases in size with a karyotype of 14 chromosomes. The G+C content is ~23%. A genome sequencing project is underway.

Distribution[edit]

P. chabaudi is found in Africa. It was first isolated from the blood of a shining thicket rat (Thamnomys rutilans) in the Central African Republic.[4]

Hosts[edit]

While it is difficult to study P. chabaudi in its natural host given the difficulty of taming the thicket rat, it has been studied extensively in laboratory mice, largely using the clone P. chabaudi chabaudi (AS). The pathology resembles that of human malaria in that animals are susceptible to parasite growth and pathology such as anemia, hypoglycemia, changes in body temperature, weight loss, and occasional death. The other cloned strains vary in growth rates and virulence.[5] One unique feature of this species is its prolonged course of infection. While it seems to persist for years in the thicket rat, P. chabaudi (AS) lasts up to three months in BALB/c or C57Bl/6 mice [6] P. falciparum has been observed to persist for up to a year,[7] and even in conditions of drought when there are no new infections.[8] Other species that are used to model human infection do not have this property. The other unique properties of this parasite are that it is synchronous, as first described for malaria by Galen, and that it prefers to infect normocytes, similar to P. falciparum, the most virulent human parasite, while several of the other rodent parasites have a preference for immature red blood cells, or reticulocytes, which they share with P. vivax.

In Anopheles stephensi the parasite synchronizes its circadian and diurnal rhythms with the host's.[9] Schneider et al., 2018 finds P. chabaudi is selected to take advantage of the cycles of feeding and lowered immunity of the mosquito.[9] They did not find any evidence for such a pattern in Mus musculus, testing for migration to peripheral vessels and finding none.[9] This parasite/mosquito synchronization is believed to hold for malaria parasites in general.[9]

Host resistance[edit]

Peak parasitaemia in Thamnomys rutilans – the natural host – is still unknown as of 2004. Landau 1965 and 66 did however find them to suffer to some severe degree, as did Ellerman 1940 in the sympatric and genetically close Grammomys surdaster. The peak is known to be 30% (109ml) for laboratory mice from many studies, including Jarra and Brown 1985. For specifically resistant breeds like C57Bl/6J Stevenson et al., 1982 finds the mortality is 5-20%, while for those known not to be resistant such as CBA/Ca and Dilute, Brown and non-Agouti (DBA), they find much higher mortalities.[10]

Lifecycle[edit]

There is usually a high female-to-male ratio in mature infections but this inhibits transmission at low densities due to lack of any male partner at the beginning of a new infection.[11][12][13] Therefore Reece et al., 2008 find P. chabaudi will bias toward a more even ratio at lower densities and when several clonal lineages are competing with each other in the same host.[11][12][13] This is believed to generalize beyond this species, to all Plasmodium.[11][12][13]

Therapeutic uses[edit]

P. chabaudi can reduce autoimmunity. Zinger et al., 2003 deliberately infected mice with the parasite and found reduced symptoms of autoimmunity.[14]

External links[edit]

References[edit]

  1. ^ Hoffman, Stephen P. (1996). Malaria Vaccine Development: A Multi-Immune Response Approach. American Society Microbiology. ISBN 978-1-55581-111-2.
  2. ^ Landau I (1965). "Description de Plasmodium chabaudi n. sp., parasite de rongeurs africains". C. R. Acad. Sci. 260: 3758–3761.
  3. ^ Carter, R.; Walliker, D. (1976). "Malaria parasites of rodents of the Congo (Brazzaville): Plasmodium chabaudi adami subsp. nov. and Plasmodium vinckei lentum Landau, Michel, Adam and Boulard, 1970". Annales de Parasitologie Humaine et Comparée. 51 (6): 637–646. doi:10.1051/parasite/1976516637. ISSN 0003-4150. PMID 800328. open access
  4. ^ Landau I, Killick-Kendrick R (1966). "Rodent plasmodia of the République Centrafricaine: the sporogony and tissue stages of Plasmodium chabaudi and P. berghei yoelii". Trans R Soc Trop Med Hyg. 60 (5): 633–49. doi:10.1016/0035-9203(66)90010-1. PMID 4163669.
  5. ^ Stephens R, Culleton RL, Lamb TJ (Feb 2012). "The contribution of Plasmodium chabaudi to our understanding of malaria". Trends Parasitol. 28 (2): 73–82. doi:10.1016/j.pt.2011.10.006. PMC 4040349. PMID 22100995.
  6. ^ Achtman AH, Stephens R, Cadman ET, Harrison V, Langhorne J (Sep 2007). "Malaria-specific antibody responses and parasite persistence after infection of mice with Plasmodium chabaudi chabaudi". Parasite Immunol. 29 (9): 435–44. doi:10.1111/j.1365-3024.2007.00960.x. PMID 17727567.
  7. ^ Collins WE, Jeffery GM (May 2002). "A retrospective examination of sporozoite-induced and trophozoite-induced infections with Plasmodium ovale: development of parasitologic and clinical immunity during primary infection". Am J Trop Med Hyg. 66 (5): 492–502. doi:10.4269/ajtmh.2002.66.492. PMID 12201582.
  8. ^ Characteristics (Oct 1998). "Plasmodium falciparum parasites that survive the lengthy dry season in eastern Sudan where malaria transmission is markedly seasonal. Babiker HA, Abdel-Muhsin AM, Ranford-Cartwright LC, Satti G, Walliker D". Am J Trop Med Hyg. 59 (4): 582–90. doi:10.4269/ajtmh.1998.59.582. PMID 9790434.
  9. ^ a b c d Westwood, Mary L.; O'Donnell, Aidan J.; de Bekker, Charissa; Lively, Curtis M.; Zuk, Marlene; Reece, Sarah E. (2019-03-18). "The evolutionary ecology of circadian rhythms in infection". Nature Ecology & Evolution. Nature Portfolio. 3 (4): 552–560. doi:10.1038/s41559-019-0831-4. ISSN 2397-334X.
  10. ^ Mackinnon, Margaret J.; Read, Andrew F. (2004-06-29). "Virulence in malaria: an evolutionary viewpoint". Philosophical Transactions of the Royal Society B. The Royal Society. 359 (1446): 965–986. doi:10.1098/rstb.2003.1414. ISSN 0962-8436.
  11. ^ a b c Bousema, Teun; Drakeley, Chris (2011). "Epidemiology". journal. American Society for Microbiology. 24 (2): 377–410. doi:10.1128/cmr.00051-10. ISSN 0893-8512. PMC 3122489. PMID 21482730. S2CID 27743505.
  12. ^ a b c Cornwallis, Charlie K.; Uller, Tobias (2010). "Towards an evolutionary ecology of sexual traits". Trends in Ecology & Evolution. Cell Press. 25 (3): 145–152. doi:10.1016/j.tree.2009.09.008. ISSN 0169-5347. PMID 19853321. S2CID 30059984.
  13. ^ a b c Bousema, Teun; Okell, Lucy; Felger, Ingrid; Drakeley, Chris (2014-10-20). "Asymptomatic". Nature Reviews Microbiology. Nature Portfolio. 12 (12): 833–840. doi:10.1038/nrmicro3364. ISSN 1740-1526. PMID 25329408. S2CID 20524090.
  14. ^ Shoenfeld, Yehuda (2004). "The idiotypic network in autoimmunity: antibodies that bind antibodies that bind antibodies". Nature. Nature Portfolio. 10 (1): 17–18. doi:10.1038/nm0104-17. ISSN 1078-8956.