**15. Evolution**

As of 2007, DNA sequences are available from less 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 more data becomes available.[31,32,]

The 'Apicomplexa (the phylum to which *Plasmodium* belong) are thought to have originated within the Dinofagellates -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 Apicomplexa still possess plastids (the organelle in which photosynthesis occur in photosynthetic eukaryotes), and some that lack plastids nonetheless have evidence of plastid genes within their genomes. In the majority of such species, the plastids are not capable of photosynthesis. Their function is not known, but there is suggestive evidence that they may be involved in reproduction.[33]

Some extant dinoflagellates, however, can invade the bodies of jellyfish and continue to photosynthesise, which is possible because jellyfish bodies are almost transparent. In host organisms with opaque bodies, such an ability would most likely rapidly be lost. The 2008 description of a photosynthetic protist related to the Apicomplexa with a functional plastid supports this hypothesis.[32]

Current (2007) theory suggests that the genera *Plasmodium Hepatocystis* and *Haemoprotus* evolved from one or more *Leucoytozoon* species. Parasites of the genus *Leucocytozoon* infect white blood cells (Leukocytes) and liver and spleen cells, and are transmitted by 'black flies' (*Simulium* species) ----- a large genus related to the mosquitoes.

Biology of Malaria Parasites 19

• Subgenus *Haemoproteus*

• Genus *Fallisia* Lainson, Landau & Shaw 1974

• Subgenus *Asiamoeba* Telford 1988 • Subgenus *Bennettinia* Valkiunas 1997 • Subgenus *Carinamoeba* Garnham 1996

• Subgenus *Ophidiella* Garnham 1966

• Genus *Polychromophilus*

• Genus *Ravella* • Genus *Saurcytozoon*

*vivax* than *P. malaria.*

• Subgenus *paraplasmodium* Telford 1988 • Subgenus *Sauramoeba* Garnham 1966 • Subgenus *Vinekeia* Garnham 1964

• Subgenus *Haemamoebe* Grassi & Feletti 1890 • Subgenus *Huffia* Garnham & Laird 1963 • Subgenus *Lucertaemoba* Telford 1988 • Subgenus *Laverania* Bray 1963

• Subgenus *Giovannolaia* Corradetti, Garnham & Laird 1963

• Subgenus *Novyella* Corradtti, Garnham & Laird 1963

*P. coatneyi* and *P. inui* appear to be closely related to *P. vivax.[38]* 

• Subgenus *Plasmodium* Bray 1963 emend, Garnham 1964

The eleven 'Asian' species included here form a clade with *P.* vivax being clearly closely related as are *P. knowsell* and *P. coatneyi;* similarly *P. brazilium* and *P. malaria* are related. *P. hylobati* and *P. inui* are closely related. *P. gonderi* appear to be more closely related to *P.* 

Family Garniidae

• Genus *Garnia* • Genus *Progarnia*

• Subgenus *Fallisia* • Subgenus *Plasmodioides*

Family Leucocytozoidae • Genus *Leucocytozoon* • Subgenus *Leucocytozoon*

• Subgenus *Akiba* Family Plasmodiidae • Genus *Bioccala* • Genus *Billbraya* • Genus *Dionisiu* • Genus *Hepatocystis* • Genus *Mesnilium* • Genus *Nycteria* • Genus *Plasmodium*

It is thought that *Leucocytozoon* evolved from a parasite that spread through the orofaecal route and which infected intestinal wall. At some point parasites 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 cell 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 squamte – 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 phagocytes particulate matter, which makes the parasite's entry into the cell easier. The mechanism of entry of *Plasmodium* species into erythrocytes is still very unclear, as it takes place in less than 30 seconds. It is not yet known if this mechanism evolved before mosquitoes became the main vectors for transmission of *Plasmodium*.[35]

The genus *Plasmodium* evolved (presumably from its *Leucocytozoon* 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 gene 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.[36]

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.[37]

The reason why a relatively limited number of mosquitoes should be such successful vectors of multiple diseases is not yet known. It has been shown that, among the most common disease – spreading 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.
