Plasmodium malaria life cycle

Over 100 Plasmodium species contribute to the spread of malaria, but only four of these (P. falciparum, P. vivax, P. ovale, and P. malariae) account for human infection, the deadliest being P. falciparum. The malaria life cycle exists first in a mosquito, and then it passes to a human host. An infected female Anopholes mosquito is the host of the parasite s sporogonic hfe cycle. Mature P. falciparum sporozoites reach the salivary glands of the mosquito, and the parasite is transmitted to a human host when the mosquito feeds. During this blood meal, sporozoites are released into the bloodstream where they penetrate hepatic cells and mature into schizonts. The liver cells rupture after approximately two weeks, discharging merozoites into the bloodstream whereupon they infect red blood cells (RBCs). Every 48 to 78 hours, mature merozoites rupture from... 

Detection by LDMS and structural elucidation of other secondary metabolite products, generated in the host during the onset of the parasite disease, is discussed. These molecules may serve as additional biomarkers for rapid malaria diagnosis by LDMS. For instance, choline phosphate (CP) is identified as the source of several low-mass ions observed in parasite-infected blood samples in addition to heme biomarker ions. The CP levels track the sample parasitemia levels. This biomarker can provide additional specificity and sensitivity when compared to malaria detection based on heme ion signals alone. Furthermore the observed elevated CP levels are discussed in the context of Plasmodium metabolism during its intra-erythrocytic life cycle. These data can... 

To date, no effective vaccine has been developed for many parasites, notably the malaria-causing parasitic protozoa Plasmodium. One of the major difficulties in such instances is that parasites go through a complex life cycle, often spanning at least two different hosts. 

The malaria parasite Plasmodium has a complex life cycle with several forms and spends much of its life hiding within red blood cells.1 It may also suppress the immune system. The unicellular sporozoites, which are injected into the bloodstream by mosquitos, are protected by an external coat protein that is unusual in containing many short repeated sequences. For example, that of P. falciparum, which causes the most deadly form of malaria, contains the sequence Asn-Ala-Asn-Pro repeated 37 times.q These coat proteins undergo unusually rapid evolution, which makes the preparation of vaccines difficult.1... 

The life cycle of Plasmodium requires two vectors for completion. The definitive hosts are female mosquitoes from the genus Anopheles. Anophelesgambiae and Anopheles funestus are two such definitive hosts in the African Region, while Anopheles darlingi transmits malaria in South and Central America (6-8). The second host is a vertebrate that may be a bird, reptile, or small mammal. The malaria species listed above are all able to utilize humans as a vertebrate host. 

Alphonse Laveran, a French Army physician working in North Africa in the 1880s, was the first to observe malarial parasites in human blood. Their mode of transmission was not understood, however, until Ronald Ross, a British medical officer in India, found the organisms within the bodies of Anopheles mosquitoes. Malaria is caused by four species of parasitic protozoa Plasmodium vivax, P. ovale, P. malariae, satid P. falciparum. These organisms have complex life cycles involving several different developmental stages in both human and mos-... 

Protozoal infections. Malaria is the major transmissible parasitic disease in the world. The life cycle of the plasmodium that is relevant to prophylaxis and therapy is described. Drug resistance is an increasing problem and differs with geographical location, and species of plasmodium. 

Since then, her focus has been on the cell biology of malaria in the mammalian liver. Her interests include sporozoite targeting to the liver, molecular communication between sporozoites and Kupffer cells, EE development in hepatocytes, mode of release and fate in the body of hepatic merozoites, and the comparative biology of the exo-erythrocytic phase of mammalian and avian malaria infections. Establishment of the methodology to observe fluorescent parasites in various organs of live animals has provided a window into the complex life cycle of Plasmodium in the mammalian host. 

Malaria is a devastating human disease that causes more than 850 000 deaths each year. The disease is caused by a protozoan parasite of the genus Plasmodium, which is obligate intracellular protozoan parasites of humans and animals, and the symptoms of the disease are largely a consequence of the asexual multiplication of these parasites within erythrocytes in the host. The Human disease is caused by the Plasmodium species P. falciparum, P. vivax, P. ovale and P. malariae. The life cycle of the Malaria parasite is extremely complex involving distinct cellular morphologies for infection of the host organism (human or other animal) and the infectious vector, the mosquito... 

The symptoms of malaria are entirely due to the proliferation of Plasmodium parasites within the erythrocytes of infected individuals. The treatment of this is currently accomplished through the use of drugs such as Chloroquine. Whilst the erythrocytic phase of the life cycle is an obvious opportunity, a... 

At present, there are two streams of drug discovery activity that could lead to the successful development of a kinase inhibitor as a drug for Plasmodium Malaria, namely in vitro screening activities around validated kinase targets and deconvolution of key targets revealed from the screening of various Malaria Boxes on various stages of the life cycle of the parasite. 

In any case, it is clear that artemisininoids act by an alkylant mechanism and that this mechanism differs from that shown by other alkylant STLs as discussed above. It is highly noteworthy that selective toxicity occurs towards various states in the life-cycle of Plasmodium since heme-associated toxification by the described mechanism should occur also in uninfected cells. This selectivity is likely to be -at least in part- due to selective sequestration in infected erythrocytes as mentioned above. Evidence has been presented that -apart from targeting malaria-specific proteins- processes consuming metabolic energy, i.e. active transport, is involved in this selective uptake [92] but the transport mechanism is not known in detail. 

Malaria parasites have a complex life cycle that permits drug action at several points. Plasmodium species that infect humans P falciparum, P malariae, P ovale, P vivax) tire spread by the female Anopheles mosquito and, after inoculation into the human host, undergo a primary developmental stage in the liver (primary tissue phase). They then enter the blood and parasitize erythrocytes (erythrocytic phase). P falciparum and P malariae have only one cycle of liver cell invasion thereafter, multiplication is confined to erythrocytes. The other species have a dormant hepatic stage (in which they become bypnozoites) that is responsible for recurrent infections and relapses after apparent recovery of the host from the initial infection. 

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