Plasmodium is a genus of parasitic protists. Infection by these organisms is known as malaria. The genus Plasmodium was created in 1885 by Marchiafava and Celli. Currently over 200 species of this genus are recognized and new species continue to be described. 
Of the over 200 known species of Plasmodium, at least 10 species infect humans. Other species infect animals, including monkeys, rodents, birds, and reptiles. The parasite always has two hosts in its life cycle: a mosquito vector and a vertebrate host.
The organism itself was first seen by Laveran on November 6, 1880 at a military hospital in Constantine, Algeria, when he discovered a microgametocyte exflagellating. In 1885, similar organisms were discovered within the blood of birds in Russia. There was brief speculation that birds might be involved in the transmission of malaria; in 1894 Patrick Manson proposed the existence of an exoerythrocytic stage in the life cycle: this was later confirmed by Short, Garnham, Covell and Shute (in 1948) who found Plasmodium vivax in the human liver.
All the Plasmodium species causing malaria in humans are transmitted by mosquito species of the genus Anopheles. Species of the mosquito genera Aedes, Culex, Culiseta, Mansonia and Theobaldia can also transmit malaria but not to humans.
Both sexes of mosquitos live on nectar. Because nectar's protein content alone is insufficient for oogenesis (egg production) one or more blood meals is needed by the female. Only female mosquitoes bite.
The life cycle of Plasmodium is complex. Sporozoites from the saliva of a biting female mosquito are transmitted to either the blood or the lymphatic system of the recipient. The sporozoites then migrate to the liver and invade hepatocytes. The parasite matures in the hepatocyte to a schizont containing many merozoites in it. In some Plasmodium species, such as Plasmodium vivax and Plasmodium ovale, the parasite in the hepatocyte would not achieve maturation to a schizont but remain as a latent or dormant form and called a hypnozoite. Although Plasmodium falciparum is not considered to have a hypnozoite form.  this may not be entirely correct (vide infra).
The development from the hepatic stages to the erythrocytic stages has, until very recently, been obscure. In 2006 it was shown that the parasite buds off the hepatocytes in merosomes containing hundreds or thousands of merozoites. These merosomes lodge in the pulmonary capillaries and slowly disintegrate there 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.
Within the erythrocytes the merozoite grow first to a ring-shaped form and then to a larger trophozoite form. In the schizont stage, the parasite divides several times to produce new merozoites, which leave the red blood cells and travel within the bloodstream to invade new red blood cells. The parasite feeds by ingesting haemoglobin and other materials from red blood cells and serum. The feeding process damages the erythrocytes. Details of this process have not been studied in species other than Plasmodium falciparum so generalizations may be premature at this time.
Invasion of erythrocyte precursors has only recently been studied. The earliest stage susceptible to infection were the orthoblasts - the stage immediately preceding the reticulocyte stage which in turn is the immediate precursor to the mature erythrocyte.
At the molecular level a set of enzymes known as plasmepsins which are aspartic acid proteases are used to degrade hemoglobin. The parasite digests 70-80% of the erythrocyte's haemoglobin The reason proposed for this apparently excessive digestion of haemoglobin is the colloid-osmotic hypothesis which suggests that the digestion of haemoglobin increases the osmotic pressure within the infected erythrocyte leading to its premature rupture and subsequent death of the parasite. To avoid this fate much of the haemoglobin is digested and exported from the erythrocyte. This hypothesis has been experimentally confirmed.
Most merozoites continue this replicative cycle but some merozoites differentiate into male or female sexual forms (gametocytes) (also in the blood), which are taken up by the female mosquito.
In the mosquito's midgut, the gametocytes develop into gametes and fertilize each other, forming motile zygotes called ookinetes. The ookinetes penetrate and escape the midgut, then embed themselves onto the exterior of the gut membrane. Here they 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 and subcutaneous tissue of the next host the mosquito bites. The majority appear to be injected into the subcutaneous tissue from which they migrate into the capillaries. A proportion are ingested by macrophages and still others are taken up by the lymphatic system where they are presumably destroyed. The sporozoites which successfully enter the blood stream move to the liver where they begin the cycle again.
Reactivation of the hypnozoites has been reported for up to 30 years after the initial infection in humans. The factors precipating this reactivation are not known. In the species Plasmodium malariae, Plasmodium ovale and Plasmodium vivax hypnozoites have been shown to occur. It is not yet known if hypnozoite reactivaction occurs with any of the remaining species that infect humans but this is presumed to be the case.
The pattern of alternation of sexual and asexual reproduction which may seem confusing at first is a very common pattern in parasitic species. The evolutionary advantages of this type of life cycle were recognised by Gregor Mendel.
Under favourable conditions asexual reproduction is superior to sexual as the parent is well adapted to its environment and its descendents share these genes. Transferring to a new host or in times of stress, sexual reproduction is generally superior as this produces a shuffling of genes which on average at a population level will produce individuals better adapted to the new environment.
A report of P. falciparum malaria in a patient with sickle cell anemia four years after exposure to the parasite has been published. A second report that P. falciparum malaria had become symptomatic eight years after leaving an endemic area has also been published.
A third case of an apparent recurrence nine years after leaving an endemic area of P. falciparum malaria has now been reported . A fourth case of recurrence in a patient with lung cancer has been reported. Two cases in pregnant women both from Africa but who had not lived there for over a year have been reported.
It seems that at least occasionally P. falciparum has a dormant stage. If this is in fact the case, eradication or control of this organism may be more difficult than previously believed.
A small number of potentially dormant forms of Plasmodium parasites both in vitro and in vivo have been observed.
The schizont stage-infected erythrocyte in an experimental culture of P. falciparum, F32 was suppressed to a low level with the use of atovaquone. The parasites resumed growth several days after the drug was removed from the culture.
More than a hundred late-stage trophozoites or early schizont infected erythrocytes of P. falciparum in a case of placental malaria of a Tanzanian woman were found to form a nidus in an intervillous space of placenta. While such a concentration of parasites in placental malaria is rare, placental malaria cannot give rise to persistent infection as pregnancy in humans normally lasts only 9 months.
Macrophages containing merozoites dispersed in their cytoplasm, called 'merophores', were observed in P. vinckei petteri - an organism that causes murine malaria. Similar merophores were found in the polymorph leukocytes and macrophages of other murine malaria parasite, P. yoelii nigeriensis and P. chabaudi chabaudi. All these species unlike P. falciparum are known to produce hyponozoites that may cause a relapse. The finding of Landau et al. on the presence of malaria parasites inside lymphatics suggest a mechanism for the recrudescence and chronicity of malaria infection.
As of 2007 DNA sequences are available from fewer than sixty species of Plasmodium and most of these are from species infecting either rodent or primate hosts. The evolutionary outline given here should be regarded as speculative and subject to revision as data becomes available.
The Apicomplexa — the phylum to which Plasmodium belongs - are thought to have originated within the Dinoflagellates — a large group of photosynthetic protists. It is thought that the ancestors of the Apicomplexa were originally prey organisms that evolved the ability to invade the intestinal cells and subsequently lost their photosynthetic ability. Many of the species within the Apicomplexia still possess a plastid (the organelle in which photosynthesis occurs in photosynthetic eukaryotes), and some that do not have evidence of plastid genes within their genomes. These plastids are not capable of photosynthesis. Their function is not known, but there is suggestive evidence that they may be involved in reproduction.
Some extant dinoflagelates, however, can invade the bodies of jellyfish and continue to photosynthesize, which is possible because jellyfish bodies are almost transparent. In other organisms with opaque bodies this ability would most likely rapidly be lost. The recent (2008) description of a photosynthetic protist related to the Apicomplexia with a functional plastid supports this hypothesis.
Current (2007) theory suggests that the genera Plasmodium, Hepatocystis and Haemoproteus evolved from one or more Leukocytozoon species. Parasites of the genus Leukocytozoan infect white blood cells (leukocytes), liver and spleen cells and are transmitted by 'black flies' (Simulium species) — a large genus of flies related to the mosquitoes.
It is thought that Leukocytozoon evolved from a parasite that spread by the orofaecal route and 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. Once vector transmission was firmly established, the previous orofecal route of transmission was lost.
Molecular evidence suggests that a reptile - specifically a squamate - was the first vertebrate host of Plasmodium. Birds were the second vertebrate hosts with mammals being the most recent group of vertebrates infected..
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.
The genus Plasmodium evolved (presumably from its Leukocytozoon ancestor) about 130 million years ago, a period that is coincidental 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.
Mosquitoes evolved in what is now South America about 230 million years ago. There are over 3500 species recognized, but to date their evolution has not been well worked out, so a number of gaps in our knowledge of the evolution of Plasmodium remain. There is evidence of a recent expansion of Anopheles gambiae and Anopheles arabiensis populations in the late Pleistocene in Nigeria.
The reason why a relatively limited number of mosquitoes should be such a sucessful vectors of multiple diseases is not yet known. It has been shown that among the most common disease spreding mosquitoes the symbiont bacterium Wolbachia are not normally present. It has been shown that infection with Wolbachia can reduce the ability of some viruses and Plasmodium to infect the mosquito and that this effect is Wolbachia strain specific.
All Plasmodium species examined to date have 14 chromosomes, with one mitochondrion and one plastid genome. The chromosomes which have been sequenced vary in length from 500 kilobases to 3.5 megabases. It is presumed that this is the pattern throughout the genus. The typical chormosome number of Leukcytozoon has not yet been established.
The genome of four Plasmodium species have been sequenced. These species are Plasmodium falciparum, Plasmodium knowlesi, Plasmodium vivax and Plasmodium yoelli. All these species have 14 chromosomes and genomes of about 25 megabases, results consistent with earlier estimates.
The biology of these organisms is more fully described on the Plasmodium falciparum biology page.
Plasmodium belongs to the family Plasmodiidae (Levine, 1988), order Haemosporidia and phylum Apicomplexa. There are currently 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 re-assigned after these studies have been completed. For this reason the entire order is outlined here.
While this tree contains a considerable number of species, DNA sequences from many species in this genus have not been included - probably because they are not available yet. Because of this problem, this tree and any conclusions that can be drawn from it should be regarded as provisional.
Three additional trees are available from the American Museum of Natural History.
These trees agree with the Tree of Life. Because of their greater number of species in these trees, some additional inferences can be made:
It is also known that the species infecting humans do not form a single clade. In contrast, the species infecting Old World monkeys seem to form a clade. Plasmodium vivax may have originated in Asia and the related species Plasmodium simium appears to be derived through a transfer from the human P. vivax to New World monkey species in South America.
Another tree concetrating on the species infecting the primates is available here: PLOS site
This tree shows that the 'African' (P. malaria and P. ovale) and 'Asian' (P.cynomogli, P. gonderi, P. semiovale and P. simium) species tend to cluster together into separate clades. P. vivax clusters with the 'Asian' species. The rodent species (P. bergei, P. chabaudi and P. yoelli) form a separate clade. As usual P. falciparum does not cluster with any other species. The bird species (P. juxtanucleare, P. gallinaceum and P. relictum) form a clade that is related to the included Leukocytozoan and Haemoproteus species.
An analysis of ten 'Asian' species (P. coatneyi, P. cynomolgi, P. fieldi, P. fragile, P. gonderi, P. hylobati, P. inui, P. knowlesi, P. simiovale and P. vivax) suggests that P. coatneyi and P. knowlesi are closely related and that P. fragile is the species most closely related to these two. P. vivax and P. cynomolgi appear to be related.
Unlike other eukaryotes studied to date Plasmodium species have two or three distinct SSU rRNA (18S rRNA) molecules encoded within the genome. These have been divided into types A, S and O. Type A is expressed in the asexual stages; type S in the sexual and type O only in the oocyte. Type O is only known to occur in Plasmodium vivax at present. The reason for this gene duplication is not known but presumably reflects an adaption to the different environments the parasite lives within.
The Asian simian Plasmodium species - Plasmodium coatneyi, Plasmodium cynomolgi, Plasmodium fragile, Plasmodium inui, Plasmodium fieldi, Plasmodium hylobati and Plasmodium simiovale - have a single single S-type-like gene and several A-type-like genes. It seems likely that these species form a clade within the subgenus Plasmodium.
P. vivax appears to have evolved between 45,000 and 82,000 years ago from a species that infects south east Asian macques. This is consistent with the other evidence of a south eastern origin of this species.
It has been reported that the C terminal domain of the RNA polymerase 2 in the primate infecting species (other than P. falciparum and probably P. reichenowei) appears to be unusual suggesting that the classification of species into the subgenus Plasmodium may have an evolutionary and biological basis.
A report of a new species that clusters with P. falciparum and P. reichenowi in chimpanzees has been published, although to date the species has been identified only from the sequence of its mitochondrion. Further work will be needed to describe this new species, however, it appears to have diverged from the P. falciparum- P. reichenowi clade about 21 million years ago.
It has been shown that P. falciparum forms a clade with the species P reichenowi. This clade may have originated between 3 million and 10000 years ago. It is proposed that the origin of P. falciparum may have occurred when its precursors developed the ability to bind to sialic acid Neu5Ac possibly via erythrocyte binding protein 175. Humans lost the ability to make the sialic acid Neu5Gc from its precursor Neu5Ac several million years ago and this may have protected them against infection with P. reichenowi.
A recently (2009) described species (Plasmodium hydrochaeri) that infects capybaras (Hydrochaeris hydrochaeris) may complicate the phylogentics of this genus. This species appears to be most similar to Plasmodium mexicanum a lizard parasite. Further work in this area seems indicated.
The full taxonomic name of a species includes the subgenus but this is often omitted. The full name indicates some features of the morphology and type of host species. Sixteen subgenera are currently recognised.
The only two species in the subgenus Laverania are P. falciparum and P. reichenowi. A third species - Plasmodium gaboni - may also exist but a full description of this species has not yet been published. The presence of elongated gametocytes in several of the avian subgenera and in Laverania in addition to a number of clinical features suggested that these might be closely related. This is no longer thought to be the case.
The type species is Plasmodium falciparum.
Species infecting monkeys and apes (the higher primates) with the exceptions of P. falciparum and P. reichenowi are classified in the subgenus Plasmodium. The distinction between P. falciparum and P. reichenowi and the other species infecting higher primates was based on the morphological findings but have since been confirmed by DNA analysis.
The type species is Plasmodium malariae.
Parasites infecting other mammals including lower primates (lemurs and others) are classified in the subgenus Vinckeia. Vinckeia while previously considered to be something of a taxonomic 'rag bag' has been recently shown - perhaps rather surprisingly - to form a coherent grouping.
The type species is Plasmodium bubalis.
This is known as Malaria
The remaining groupings are based on the morphology of the parasites. Revisions to this system are likely to occur in the future as more species are subject to analysis of their DNA.
The four subgenera Giovannolaia, Haemamoeba, Huffia and Novyella were created by Corradetti et al. for the known avian malarial species. A fifth—Bennettinia—was created in 1997 by Valkiunas. The relationships between the subgenera are the matter of current investigation. Martinsen et al. 's recent (2006) paper outlines what is currently (2007) known. The subgenera Haemamoeba, Huffia, and Bennettinia appear to be monphylitic. Novyella appears to be well defined with occasional exceptions. The subgenus Giovannolaia needs revision.
P. juxtanucleare is currently (2007) the only known member of the subgenus Bennettinia.
Nyssorhynchus is an extinct subgenus of Plasmodium. It has one known member - Plasmodium dominicum
Unlike the mammalian and bird malarias those species (>90 known) that infect 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. 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 currently accepted (2007) system.
These species have since been divided in to 8 genera - Asiamoeba, Carinamoeba, Fallisia, Garnia, Lacertamoeba, Ophidiella, Paraplasmodium and Sauramoeba. Three of these genera (Asiamoeba, Lacertamoeba and Paraplasmodium) were created by Telford in 1988. Another species (Billbraya australis) described in 1990 by Paperna and Landau and is the only known species in this genus. This species may turn out to be another subgenus of lizard infecting Plasmodium.
There are ~40 recognised bird species. Although over 50 species have been described, several have been rejected as being invalid.
With the exception of P. elongatum the exoerythrocytic stages occur in the endothelial cells and those of the macrophage-lymphoid system. The exoerythrocytic stages of P. elongatum parasitise the blood forming cells.
The various subgenera are first distinguished on the basis of the morphology of the mature gametocytes. Those of subgenus Haemamoeba are round or oval while those of the subgenera Giovannolaia, Huffia and Novyella are elongated. These latter genera are distinguished on the basis of the size of the schizonts: Giovannolaia and Huffia have large schizonts while those of Novyella are small.
Species in the subgenus Bennettinia have the following characteristics:
The type species is Plasmodium juxtanucleare.
Species in the subgenus Giovannolaia have the following characteristics:
The type species is Plasmodium circumflexum.
Species in the subgenus Haemamoeba have the following characteristics:
The type species is Plasmodium relictum.
Species in the subgenus Huffia have the following characteristics:
The type species is Plasmodium elongatum.
Species in the subgenus Novyella have the following characteristics:
The type species is Plasmodium vaughani.
All species in these subgenera infect lizards.
Species in the subgenus Asiamoeba have the following characteristics:
Species in the subgenus Carinamoeba have the following characteristics:
The type species is Plasmodium minasense.
Species in the subgenus Fallisia have the following characteristics:
Species in the subgenus Garnia have the following characteristics:
Species in the subgenus Lacertaemoba have the following characteristics:
Species in the subgenus Paraplasmodium have the following characteristics:
Species in the subgenus Sauramoeba have the following characteristics:
The type species is Plasmodium agamae.
All species in Ophidiella infect snakes
The type species is Plasmodium weyoni.
Plasmodium (Asiamoeba) clelandi
Plasmodium (Asiamoeba) draconis
Plasmodium (Asiamoeba) lionatum
Plasmodium (Asiamoeba) saurocordatum
Plasmodium (Asiamoeba) vastator
Plasmodium (Bennettinia) juxtanucleare
Plasmodium (Carinamoeba) basilisci
Plasmodium (Carinamoeba) clelandi
Plasmodium (Carinamoeba) lygosomae
Plasmodium (Carinamoeba) mabuiae
Plasmodium (Carinamoeba) minasense
Plasmodium (Carinamoeba) rhadinurum
Plasmodium (Carinamoeba) volans
Plasmodium (Fallisia) siamense
Plasmodium (Giovannolaia) anasum
Plasmodium (Giovannolaia) circumflexum
Plasmodium (Giovannolaia) dissanaikei
Plasmodium (Giovannolaia) durae
Plasmodium (Giovannolaia) fallax
Plasmodium (Giovannolaia) formosanum
Plasmodium (Giovannolaia) gabaldoni
Plasmodium (Giovannolaia) garnhami
Plasmodium (Giovannolaia) gundersi
Plasmodium (Giovannolaia) hegneri
Plasmodium (Giovannolaia) lophurae
Plasmodium (Giovannolaia) pedioecetii
Plasmodium (Giovannolaia) pinnotti
Plasmodium (Giovannolaia) polare
Plasmodium (Haemamoeba) cathemerium
Plasmodium (Haemamoeba) coggeshalli
Plasmodium (Haemamoeba) coturnixi
Plasmodium (Haemamoeba) elongatum
Plasmodium (Haemamoeba) gallinaceum
Plasmodium (Haemamoeba) giovannolai
Plasmodium (Haemamoeba) lutzi
Plasmodium (Haemamoeba) matutinum
Plasmodium (Haemamoeba) paddae
Plasmodium (Haemamoeba) parvulum
Plasmodium (Haemamoeba) relictum
Plasmodium (Haemamoeba) tejera
Plasmodium (Huffia) elongatum
Plasmodium (Huffia) hermani
Plasmodium (Lacertaemoba) floridense
Plasmodium (Lacertaemoba) tropiduri
Plasmodium (Laverania) falciparum
Plasmodium (Laverania) reichenowi
Plasmodium (Ophidiella) pessoai
Plasmodium (Ophidiella) tomodoni
Plasmodium (Ophidiella) wenyoni
Plasmodium (Novyella) ashfordi
Plasmodium (Novyella) bertii
Plasmodium (Novyella) bambusicolai
Plasmodium (Novyella) columbae
Plasmodium (Novyella) corradettii
Plasmodium (Novyella) dissanaikei
Plasmodium (Novyella) globularis
Plasmodium (Novyella) hexamerium
Plasmodium (Novyella) jiangi
Plasmodium (Novyella) kempi
Plasmodium (Novyella) lucens
Plasmodium (Novyella) megaglobularis
Plasmodium (Novyella) multivacuolaris
Plasmodium (Novyella) nucleophilum
Plasmodium (Novyella) papernai
Plasmodium (Novyella) parahexamerium
Plasmodium (Novyella) paranucleophilum
Plasmodium (Novyella) rouxi
Plasmodium (Novyella) vaughani
Plasmodium (Nyssorhynchus) dominicum
Plasmodium (Paraplasmodium) chiricahuae
Plasmodium (Paraplasmodium) mexicanum
Plasmodium (Paraplasmodium) pifanoi
Plasmodium (Plasmodium) bouillize
Plasmodium (Plasmodium) brasilianum
Plasmodium (Plasmodium) cercopitheci
Plasmodium (Plasmodium) coatneyi
Plasmodium (Plasmodium) cynomolgi
Plasmodium (Plasmodium) eylesi
Plasmodium (Plasmodium) fieldi
Plasmodium (Plasmodium) fragile
Plasmodium (Plasmodium) georgesi
Plasmodium (Plasmodium) girardi
Plasmodium (Plasmodium) gonderi
Plasmodium (Plasmodium) inui
Plasmodium (Plasmodium) jefferyi
Plasmodium (Plasmodium) joyeuxi
Plasmodium (Plasmodium) knowlei
Plasmodium (Plasmodium) hyobati
Plasmodium (Plasmodium) malariae
Plasmodium (Plasmodium) ovale
Plasmodium (Plasmodium) petersi
Plasmodium (Plasmodium) pitheci
Plasmodium (Plasmodium) rhodiani
Plasmodium (Plasmodium) schweitzi
Plasmodium (Plasmodium) semiovale
Plasmodium (Plasmodium) semnopitheci
Plasmodium (Plasmodium) silvaticum
Plasmodium (Plasmodium) simium
Plasmodium (Plasmodium) vivax
Plasmodium (Plasmodium) youngi
Plasmodium (Sauramoeba) achiotense
Plasmodium (Sauramoeba) adunyinkai
Plasmodium (Sauramoeba) aeuminatum
Plasmodium (Sauramoeba) agamae
Plasmodium (Sauramoeba) balli
Plasmodium (Sauramoeba) beltrani
Plasmodium (Sauramoeba) brumpti
Plasmodium (Sauramoeba) cnemidophori
Plasmodium (Sauramoeba) diploglossi
Plasmodium (Sauramoeba) giganteum
Plasmodium (Sauramoeba) heischi
Plasmodium (Sauramoeba) josephinae
Plasmodium (Sauramoeba) pelaezi
Plasmodium (Sauramoeba) zonuriae
Plasmodium (Vinckeia) achromaticum
Plasmodium (Vinckeia) aegyptensis
Plasmodium (Vinckeia) anomaluri
Plasmodium (Vinckeia) atheruri
Plasmodium (Vinckeia) berghei
Plasmodium (Vinckeia) booliati
Plasmodium (Vinckeia) brodeni
Plasmodium (Vinckeia) bubalis
Plasmodium (Vinckeia) bucki
Plasmodium (Vinckeia) caprae
Plasmodium (Vinckeia) cephalophi
Plasmodium (Vinckeia) chabaudi
Plasmodium (Vinckeia) coulangesi
Plasmodium (Vinckeia) cyclopsi
Plasmodium (Vinckeia) foleyi
Plasmodium (Vinckeia) girardi
Plasmodium (Vinckeia) incertae
Plasmodium (Vinckeia) inopinatum
Plasmodium (Vinckeia) landauae
Plasmodium (Vinckeia) lemuris
Plasmodium (Vinckeia) melanipherum
Plasmodium (Vinckeia) narayani
Plasmodium (Vinckeia) odocoilei
Plasmodium (Vinckeia) percygarnhami
Plasmodium (Vinckeia) pulmophilium
Plasmodium (Vinckeia) sandoshami
Plasmodium (Vinckeia) traguli
Plasmodium (Vinckeia) tyrio
Plasmodium (Vinckeia) uilenbergi
Plasmodium (Vinckeia) vinckei
Plasmodium (Vinckeia) watteni
Plasmodium (Vinckeia) yoelli
Host range among the mammalian orders is non uniform. At least 29 species infect non human primates; rodents outside the tropical parts of Africa are rarely affected; a few species are known to infect bats, porcupines and squirrels; carnivores, insectivores and marsupials are not known to act as hosts.
The listing of host species among the reptiles has rarely been attempted. Ayala in 1978 listed 156 published accounts on 54 valid species and subspecies between 1909 and 1975. The regional breakdown was Africa: 30 reports on 9 species; Australia, Asia & Oceania: 12 reports on 6 species and 2 subspecies; Americas: 116 reports on 37 species.
Because of the number of species parasited by Plasmodium further discussion has been broken down into following pages:
The literature is replete with species initially classified as Plasmodium that have been subsequently reclassified. With DNA taxonomy some of these may be once again be classified as Plasmodium. Some of these species are listed here for completeness.
The following species are currently (2007) regarded as belonging to the genus Hepatocystis rather than Plasmodium:
The following species are now considered to belong to the genus Haemoemba rather than to Plasmodium:
The following species been reclassified as a species of Garnia:
Host note: Hepatocystis epomophori infects the bat (Hypsignathus monstruosus)
The following species are currently regarded as questionable validity (nomen dubium). While most of these 'species' have been reported in the literature it has in general been difficult to independently confirm their existence. Some of these may be reclassified into different taxa while others seem likely to be declared to be non species i.e. that a mistake was made by the authors. Until a ruling on these species has been made their status is likely to remain unclear.
Some history of malaria - http://muse.jhu.edu/journals/bulletin_of_the_history_of_medicine/v079/79.2slater.html
Subgenera: P. (Asiamoeba) - P. (Bennettinia) - P. (Carinamoeba) - P. (Giovannolaia) - P. (Haemamoeba) - P. (Huffia) - P. (Lacertaemoba) - P. (Laverania) - P. (Novyella) - P. (Plasmodium) - P. (Paraplasmodium) - P. (Sauramoeba) - P. (Vinckeia)
Species overview: P. accipiteris - P. achiotense - P. achromaticum - P. acuminatum - P. adunyinkai - P. aegyptensis - P. aeuminatum - P. agamae - P. alloelongatum - P. anasum - P. anomaluri - P. arachniformis - P. ashfordi - P. atheruri - P. audaciosum - P. aurulentum - P. australis - P. attenuatum - P. azurophilum - P. balli - P. bambusicolai - P. basilisci - P. beebei - P. beltrani - P. berghei - P. bertii - P. bigueti - P. bitis - P. biziurae - P. booliati - P. bouillize - P. bowiei - P. brodeni - P. brasilianum - P. brasiliense - P. brumpti - P. brucei - P. brygooi - P. bubalis - P. bucki - P. bufoni - P. buteonis - P. capistrani - P. carinii - P. cathemerium - P. causi - P. cephalophi - P. cercopitheci - P. chabaudi - P. chalcidi - P. chiricahuae - P. circularis - P. circumflexum - P. clelandi - P. cordyli - P. cnemaspi - P. cnemidophori - P. coatneyi - P. coggeshalli - P. colombiense - P. columbae - P. corradettii - P. coturnixi - P. coulangesi - P. cuculus - P. cyclopsi - P. cynomolgi - P. diminutivum - P. diploglossi - P. dissanaikei - P. divergens - P. dominicana - P. draconis - P. durae - P. effusum - P. egerniae - P. elongatum - P. eylesi - P. fabesia - P. fairchildi - P. falciparum - P. falconi - P. fallax - P. fieldi - P. fischeri - P. foleyi - P. formosanum - P. forresteri - P. floridense - P. fragile - P. galbadoni - P. garnhami - P. gallinaceum - P. gemini - P. georgesi - P. giganteum - P. giganteumaustralis - P. giovannolai - P. girardi - P. gonderi - P. globularis - P. gologoense - P. gonatodi - P. gracilis - P. griffithsi - P. guangdong - P. gundersi - P. guyannense - P. heischi - P. hegneri - P. hermani - P. herodiadis - P. heteronucleare - P. hexamerium - P. holaspi - P. holti - P. huffi - P. hylobati - P. incertae - P. icipeensis - P. iguanae - P. inconstans - P. inopinatum - P. inui - P. japonicum - P. jefferi - P. jiangi - P. josephinae - P. joyeuxi - P. juxtanucleare - P. kempi - P. kentropyxi - P. knowlesi - P. koreafense - P. lacertiliae - P. lagopi - P. lainsoni - P. landauae - P. leanucteus - P. lemuris - P. lepidoptiformis - P. limnotragi - P. lionatum - P. lophurae - P. loveridgei - P. lutzi - P. lygosomae - P. mabuiae - P. mackerrasae - P. mackiei - P. maculilabre - P. maior - P. majus - P. malariae - P. marginatum - P. matutinum - P. megaglobularis - P. megalotrypa - P. melanoleuca - P. melanipherum - P. mexicanum - P. michikoa - P. minasense - P. minuoviride - P. modestum - P. morulum - P. multiformis - P. murinus - P. narayani - P. necatrix - P. neotropicalis - P. neusticuri - P. nucleophilium - P. octamerium - P. odocoilei - P. osmaniae - P. ovale - P. paddae - P. papernai - P. paranucleophilum - P. parvulum - P. pedioecetii - P. pelaezi - P. percygarnhami - P. pessoai - P. petersi - P. pifanoi - P. pinotti - P. pinorrii - P. pitheci - P. pitmani - P. polare - P. pulmophilum - P. pythonias - P. quelea - P. reichenowi - P. relictum - P. rhadinurum - P. rhodaini - P. robinsoni - P. rousetti - P. rousseloti - P. rouxi - P. sandoshami - P. sasai - P. saurocaudatum - P. schweitzi - P. scelopori - P. scorzai - P. semiovale - P. semnopitheci - P. shortii - P. siamense - P. silvaticum - P. simium - P. simplex - P. smirnovi - P. stuthionis - P. tanzaniae - P. tenue - P. tejerai - P. telfordi - P. tomodoni - P. torrealbai - P. toucani - P. traguli - P. tribolonoti - P. tropiduri - P. tumbayaensis - P. tyrio - P. uilenbergi - P. uluguruense - P. uncinatum - P. uranoscodoni - P. utingensis - P. uzungwiense - P. watteni - P. wenyoni - P. vacuolatum - P. vastator - P. vaughani - P. vautieri - P. venkataramiahii - P. vinckei - P. vivax - P. volans - P. voltaicum - P. wenyoni - P. yoelii - P. youngi - P. zonuriae
Plasmodium Marchiafava & Celli, 1885