False-colored electron micrograph of a Plasmodium sp. sporozoite.
Scientific classification
(unranked): SAR
Superphylum: Alveolata
Phylum: Apicomplexa
Class: Aconoidasida
Order: Haemosporida
Family: Plasmodiidae
Genus: Plasmodium
Marchiafava & Celli, 1885

about 200

Plasmodium, commonly known as the malaria parasite, is a large malaria, a deadly disease widespread in the tropics.

The parasite always has two hosts in its life cycle: a Dipteran insect host and a vertebrate host. Sexual reproduction always occurs in the insect definitive host (also known as the disease vector).

The life-cycle is very complex, involving a sequence of different stages both in the vector and the vertebrate host. These stages include sporozoites, which are injected by the insect vector into the vertebrate host's blood; latent hypnozoites, which may rest undetected in the liver for up to 30 years; merosomes and merozoites, which infect the red cells (erythrocytes) of the blood; trophozoites, which grow in the red cells, and schizonts, which divide in red blood cells. Schizonts produce merozoites, which leave to infect more red cells. The sexual forms, gametocytes, are taken up by other insect hosts during feeding. Gametocytes develop into gametes in the insect midgut, and then fertilize each other to form motile zygotes, which escape the gut. Zygotes grow into new sporozoites, which move to the insect's salivary glands. Sporozoites are injected into vertebrate hosts during insect feeding, thus completing the cycle of infection.

The genus Plasmodium was first described in 1885. It now contains about 200 species divided into several subgenera; as of 2006 the taxonomy was shifting, and species from other genera are likely to be added to Plasmodium. At least ten species infect humans; other species infect other animals, including birds, reptiles and rodents, while 29 species infect non-human primates. The parasite is thought to have originated from Dinoflagellates, photosynthetic protozoa.

The most common forms of human malaria are caused by Plasmodium falciparum, P. vivax, P. knowlesi, and P. malariae. P. falciparum, common in sub-Saharan Africa, and P. knowlesi, common in Southeast Asia, are especially dangerous.


  • Taxonomy and host range 1
  • Life cycle 2
  • Evolution 3
  • Molecular biology 4
  • Taxonomy 5
    • Subgenera 5.1
    • Species infecting humans 5.2
    • Infections in primates 5.3
    • Infections in non-primate mammals 5.4
    • Infections in birds 5.5
    • Infections in reptiles 5.6
    • Species reclassified into other genera 5.7
  • References 6
  • Further reading 7
    • Identification 7.1
    • Biology 7.2
    • History 7.3
  • External links 8

Taxonomy and host range






Life cycle



The development from the hepatic stages to the erythrocytic stages has been obscure. In 2006[3] it was shown that the parasite buds off the hepatocytes in merosomes containing hundreds or thousands of merozoites. These merosomes have been subsequently shown[4] to lodge in the pulmonary capillaries and to disintegrate there slowly over 48–72 hours releasing merozoites. Erythrocyte invasion is enhanced when blood flow is slow and the cells are tightly packed: both of these conditions are found in the alveolar capillaries.


In the mosquito's midgut, the gametocytes develop into gametes and fertilize each other, forming a zygote. After a brief period of inactivity, zygotes transform into a motile form called ookinetes. The ookinetes penetrate and escape the midgut, then embed themselves onto the exterior of the gut membrane and transform into oocysts. The nuclei of oocysts divide many times to produce large numbers of tiny elongated sporozoites. These sporozoites migrate to the salivary glands of the mosquito where they are injected into the blood of the next host the mosquito bites. The sporozoites move to the liver where they repeat the cycle.

The pattern of alternation of sexual and asexual reproduction is common in parasitic species. The evolutionary advantages of this type of life cycle were recognised by Mendel. Under favourable conditions, asexual reproduction is superior to sexual as the parent is well adapted to its environment and its descendents share all its genes. Transferring to a new host or in times of stress, sexual reproduction is generally superior as it shuffles the genes of two parents, producing a variety of individuals, some of which will be better adapted to the new environment.



The life cycle of Plasmodium is best understood in terms of its evolution.

The Apicomplexa—the phylum to which Plasmodium belongs—are thought to have originated within the opaque bodies this ability would most likely rapidly be lost.

It is thought that Plasmodium evolved from a parasite spread by the fecal-oral route which infected the intestinal wall. At some point this parasite evolved the ability to infect the liver. This pattern is seen in the genus Cryptosporidium, to which Plasmodium is distantly related. At some later point this ancestor developed the ability to infect blood cells and to survive and infect mosquitoes. Plasmodium subsequently evolved a mechanism to invade the salivary glands of mosquitoes, allowing for transmission from mosquito to host. Once mosquito transmission was firmly established, the previous fecal-oral route was lost within the Plasmodium genus.[5]

The survivorship and relative fitness of mosquitoes are not adversely affected by Plasmodium infection which indicates the importance of vector fitness in shaping the evolution of Plasmodium.[6] Plasmodium has evolved the capability to manipulate mosquito feeding behavior. Mosquitoes harboring Plasmodium have a higher propensity to bite than uninfected mosquitoes. This tendency has facilitated the spread of Plasmodium to the various hosts.[7]


Leukocytes, hepatocytes and most spleen cells actively phagocytose particulate matter, making entry into the cell easier for the parasite. The mechanism of entry of Plasmodium species into erythrocytes is still very unclear, taking as it does less than 30 seconds. It is not yet known if this mechanism evolved before mosquitoes became the main vectors for transmission of Plasmodium.

Plasmodium evolved about 130 million years ago. This period coincided with the rapid spread of the angiosperms (flowering plants). This expansion in the angiosperms is thought to be due to at least one genomic duplication event. It seems probable that the increase in the number of flowers led to an increase in the number of mosquitoes and their contact with vertebrates.

Environmental factors play a considerable role in the evolution of Plasmodium and the transmission of malaria. The genetic information of Plasmodium falciparum has signaled a recent expansion that coincides with the agricultural revolution It is likely that the development of extensive agriculture increased mosquito population densities by giving rise to more breeding sites, which may have triggered the evolution and expansion of Plasmodium falciparum.[8]


There are over one hundred species of mosquito-transmitted Plasmodium. The phylogeny of these malarial parasites suggests that the Plasmodium of mammalian hosts forms a well-defined clade strongly associated with the specialization to the Anopheles mosquito vector. This was a major evolutionary transition that allowed Plasmodium to exploit humans and other mammals.[9]

P. falciparum, the most lethal malaria parasite of humans, evolved from a "nearly identical" parasite of western gorillas, not from chimpanzees, bonobos or ancient human populations.[10]

The high mortality and morbidity caused by malaria—especially that caused by P. falciparum —has placed the greatest selective pressure on the human genome in recent history. Several genetic factors provide some resistance to Plasmodium infection, including sickle cell trait, thalassaemia traits, glucose-6-phosphate dehydrogenase deficiency, and the absence of Duffy antigens on red blood cells.[11] [12]

Although there are therapeutic medications to treat malaria, Plasmodium has accumulated increasing drug resistance over time. A recent examination has shown that even artemisinin, one of the most powerful anti-malarial drugs, has been experiencing decreased efficacy due to the development of resistance.[13]

Molecular biology

Plasmodium is a nucleus, but with unusual features

All the species examined to date have 14

  • Malaria Atlas Project
  • "Plasmodium". NCBI Taxonomy Browser. 5820. 

External links



  • Baldacci P, Ménard R (October 2004). "The elusive malaria sporozoite in the mammalian host". Mol. Microbiol. 54 (2): 298–306.  
  • Bledsoe GH (December 2005). "Malaria primer for clinicians in the United States" (PDF). South. Med. J. 98 (12): 1197–204; quiz 1205, 1230.  
  • Shortt HE (1951). "Life-cycle of the mammalian malaria parasite". Br. Med. Bull. 8 (1): 7–9.  




Further reading

  4. ^ Baer K, Klotz C, Kappe SH, Schnieder T, Frevert U (November 2007). merozoites into the pulmonary microvasculature"Plasmodium yoelii"Release of hepatic . PLoS Pathog. 3 (11): e171.  
  5. ^ Ghosh, A.K; Devenport, M; Jethwaney, D. "Malaria parasite invasion of the mosquito salivary glands requires interaction between the Plasmoidum TRAP and the Anopheles saglin proteins". PLoS Pathog. 5(1):e1000265. 
  6. ^ Ferguson, HM; Mackinnon, MJ; Chan, BH; Read, AF. (2003). "Mosquito mortality and the evolution of malaria virulence". Evolution 57 (12): 2792–804.  
  7. ^ Koella, J.C.; Sørensen, F.L.; Anderson, R.A. (1998). "The malaria parasite, Plasmodium falciparum, increases the frequency of multiple feeding of its mosquito vector, Anopheles gambiae". Proc Biol Sci 265 (1398): 763–8.  
  8. ^ Hume, J.C.; Lyons, E.J.; Day, K.P. (2003). "Human migration, mosquitoes and the evolution of Plasmodium falciparum". Trends Parasitol 19 (3): 144–9.  
  9. ^ Martinsen ES, Perkins SL, Schall JJ. (2008). "A three-genome phylogeny of malaria parasites (Plasmodium and closely related genera): evolution of life-history traits and host switches". Molecular Phylogenetic Evolution 47 (1): 261–273.  
  10. ^ Weimin Liu, Yingying Li, Gerald H. Learn, Rebecca S. Rudicell, Joel D. Robertson, Brandon F. Keele, Jean-Bosco N. Ndjango, Crickette M. Sanz, David B. Morgan, Sabrina Locatelli, Mary K. Gonder, Philip J. Kranzusch, Peter D. Walsh, Eric Delaporte, Eitel Mpoudi-Ngole, Alexander V. Georgiev, Martin N. Muller, George M. Shaw, Martine Peeters, Paul M. Sharp, Julian C. Rayner & Beatrice H. Hahn (23 September 2010). "Origin of the human malaria parasite Plasmodium falciparum in gorillas". Nature 467 (7314): 420–425.  
  13. ^ Ashley, E.A.; Dhorda, M.; Fairhurst, R.M.; et al. (2014). "Spread of artemisinin resistance in Plasmodium falciparum malaria". N Engl J Med 371 (5): 411–23.  
  14. ^ vanDooren, G; Striepen, B (2013). "The Algal Past and Parasite Present of Apicoplast". Annual Reviews of Microbiology 67: 271–289.  
  15. ^ Perkins SL, Schall JJ (October 2002). 0972:AMPOMP2.0.CO;2 "A molecular phylogeny of malarial parasites recovered from cytochrome b gene sequences"]. J. Parasitol. 88 (5): 972–8.  
  20. ^ Garnham 1966
  26. ^ Collins WE, Sullivan JS, Nace D, Williams T, Williams A, Barnwell JW (February 2008). to monkeys"Plasmodium vivax"Observations on the sporozoite transmission of . J. Parasitol. 94 (1): 287–8.  
  27. ^ Collins WE, Richardson BB, Morris CL, Sullivan JS, Galland GG (July 1998). monkeys and mosquitoes for transmission-blocking vaccine trials"Aotus in Plasmodium vivax"Salvador II strain of . Am. J. Trop. Med. Hyg. 59 (1): 29–34.  
  28. ^ Collins WE, Sullivan JS, Nace D, et al. (April 2002). 0295:EIOAFW2.0.CO;2 "Experimental infection of Anopheles farauti with different species of Plasmodium"]. J. Parasitol. 88 (2): 295–8.  
  30. ^ Tan CH, Vythilingam I, Matusop A, Chan ST, Singh B (2008). "Plasmodium knowlesi in Kapit, Sarawak, Malaysian Borneo in relation to the transmission of zoonotic simian malaria parasite Anopheles latens"Bionomics of . Malar. J. 7: 52.  
  37. ^ Clark, Nicholas; Clegg, Sonya; Lima, Marcos (2014). "A review of global diversity in avian haemosporidians (Plasmodium and Haemoproteus: Haemosporida): new insights from molecular data". International Journal for Parasitology 44 (5): 329–338.  
  43. ^ Murata K, Nii R, Sasaki E, et al. (February 2008). ) at a Japanese zoo"Crossoptilon crossoptilon infection in a captive white eared-pheasant (Plasmodium (Bennettinia) juxtanucleare". J. Vet. Med. Sci. 70 (2): 203–5.  
  46. ^ Valkiũnas G, Iezhova TA (August 2001). 0930:ACOTBP2.0.CO;2 "A comparison of the blood parasites in three subspecies of the yellow wagtail Motacilla flava"]. J. Parasitol. 87 (4): 930–4.  
  54. ^ Telford SR, Telford SR (April 2003). 0362:RAROPP2.0.CO;2 "Rediscovery and redescription of Plasmodium pifanoi and description of two additional Plasmodium parasites of Venezuelan lizards"]. J. Parasitol. 89 (2): 362–8.  


Species reclassified into other genera


Species in the subgenera Asiamoeba, Carinamoeba, Lacertaemoba, Paraplasmodium and Sauramoeba infect reptiles.[49]

Over 3000 species of lizard, including the Carolina anole (Anolis carolinensis), carry some 90 kinds of malaria.

Infections in reptiles

Species in five Plasmodium subgenera infect birdsBennettinia, Giovannolaia, Haemamoeba, Huffia and Novyella.[36] Giovannolaia appears to be a polyphyletic group and may be sudivided in the future.[19] DNA evidence is in 2014 helping to improve understanding of the diversity of Plasmodium species that infect birds.[37]

Many bird species, from raptors to passerines like the red-whiskered bulbul (Pycnonotus jocosus), can carry malaria.

Infections in birds



Many non-primate mammals, such as mouse-deer (Tragulus kanchil) can carry malaria parasites.

Infections in non-primate mammals



Species of Plasmodium infect many primates across the world, such as the brown lemur, Eulemur fulvus, of Madagascar.

Infections in primates

Taxonomy in parasitology before DNA based methods was always problematic, and revisions are continuing, leaving many obsolete names for Plasmodium species that infect humans.[25]

Plasmodium shortii and Plasmodium osmaniae are now considered junior synonyms of Plasmodium inui

P. ovale can be transmitted to chimpanzees. P. ovale has an unusual distribution, being found in Africa, the Philippines and New Guinea. In spite of its admittedly poor transmission to chimpanzees given its discontigous spread, it is suspected that P. ovale is a zoonosis with an as yet unidentified host. If so, the host is likely to be a primate. The remaining species capable of infecting humans all have other primate hosts.

The only known host of P. falciparum and P. malariae is humans. P. vivax however can infect chimpanzees. Infection tends to be low grade but may be persistent and remain as source of parasites for humans for some time. P. vivax can also infect orangutans.[24]

Confusingly, P. tenue was proposed in the same year (1914) for a species found in birds. The human species is now considered probably a misdiagnosis, and the bird species is described on the P. tenue page.



The first four listed here are the most common species that infect humans. Nearly all human deaths from malaria are caused by the first species, P. falciparum, mainly in sub-Saharan Africa. With the use of the polymerase chain reaction additional species have been and are still being identified that infect humans.

The species of Plasmodium that infect humans include:

Trophozoites of the Plasmodium vivax parasite among human red blood cells

Species infecting humans

Unlike the mammalian and bird malarias those affecting reptiles have been more difficult to classify. In 1966 Garnham classified those with large schizonts as Sauramoeba, those with small schizonts as Carinamoeba and the single then known species infecting snakes (Plasmodium wenyoni) as Ophidiella.[20] He was aware of the arbitrariness of this system and that it might not prove to be biologically valid. Telford in 1988 used this scheme as the basis for the accepted (2007) system.[21]


The four subgenera Giovannolaia, Haemamoeba, Huffia and Novyella were created by Corradetti et al.[17] for the known avian malarial species. A fifth — Bennettinia — was created in 1997 by Valkiunas.[18] The relationships between the subgenera are a matter of current investigation. Martinsen et al. 's recent (2006) paper outlines what was known at the time.[19]

Parasites infecting other mammals including lower primates (lemurs and others) are classified in the subgenus Vinckeia. The distinction between P. falciparum and P. reichenowi and the other species infecting higher primates was based on morphological findings but have since been confirmed by DNA analysis. Vinckeia, while previously considered to be something of a taxonomic 'rag bag', has been recently shown to form a coherent grouping. The remaining groupings here are based on the morphology of the parasites. Revisions to this system are likely as more species are subject to DNA analysis.





The genera Plasmodium, Fallisia and Saurocytozoon all cause malaria in lizards. All are carried by Diptera (true two-winged flies). Pigment is absent in the Garnia. Non pigmented gametocytes are typically the only forms found in Saurocytozoon: pigmented forms may be found in the leukocytes occasionally. Fallisia produce non pigmented asexual and gametocyte forms in leukocytes and thrombocytes.

Plasmodium belongs to the family Plasmodiidae (Levine, 1988), order Haemosporidia and phylum Apicomplexa. There are 450 recognised species in this order. Many species of this order are undergoing reexamination of their taxonomy with DNA analysis. It seems likely that many of these species will be reassigned after these studies have been completed.[15][16]

