**11. Infection of mosquito**

In the mosquito's midgut, the gametocytes develop into gametes and fertilize each other, forming motile zygotes called ookinetes. It has been shown that up to 50% of the ookinetes may undergo apoptosis within the mighut. The reason for this behavior is unknown. While in the mosquito gut the parasites form thin cytoplasmic extensions to communicate with each other. These structures persist from the time of gametocyte activation until the zygote transforms into an ookinete. The function of these tubular structures remains to be discovered.[20]

The ookinetes penetrate and escape the midgut, then embed themselves onto the exterior of the gut membrane. As in the liver the parasite tends to invade a number of cells before choosing one to reside in. the reason for the behavior is not known. Here they divide many times to produce large number 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.

Biology of Malaria Parasites 17

Developmental arrest was induced by *in vitro* culture of *P. falciparum* in the presence of sub lethal concentration of artemisinin. The drug induced a subpopulation of ring stage into developmental arrest. At the molecular level this is associated with over- expression of heat shock and erythrocyte binding surface protein with the reduced expression of a cell-cycle

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 parasite resumed growth several

Macrophages containing merozoites dispersed on their cytoplasm. Called 'merophores', were observed in *P. vinkei 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. chabudi chaaudi.* 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

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

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

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

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'

**13. Drug induced** 

**14. Biological refuges** 

**15. Evolution** 

becomes available.[31,32,]

they may be involved in reproduction.[33]

supports this hypothesis.[32]

regular and a DNA biosynthesis protein.

days after the drug was removed from the culture.[28]

for the recrudescence and chronicity of malaria infections.[29,30,]

(*Simulium* species) ----- a large genus related to the mosquitoes.

The escape of the gametocytes from the erythrocytes has been until recently obscure. The parasitophorous vacuole membrane ruptures at multiple sites within less than a minute following ingestion. This process may be inhibited by cysteine protease inhibitors. After this rupture of the vacuole the subpellicular membrane begins to disintegrate. This process also can be inhibited by aspartic and the cysteine/ serine protease inhibitors. Approximately 15 minutes post-activation. The erythrocytes membrane rupture at a single breaking point a third process that can be interrupted by protease inhibitors.

Infection of the mosquito has noticeable effects on the host. The presence of the parasite induces apoptosis of the egg follicles.
