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Malaria - Research Paper Example

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Malaria [Insert Name] [Course and Unit] [Professor] [Institution] [Date] Malaria Introduction One moment a person is fine, the next they complain of fatigue, paint in the joints, lethargy, and a slight headache. In a few hours time, they have fever approaching 39 degrees Celsius, have headache, joints are weak, hot flashes and may be accompanied by vomiting and loss of appetite…
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Download file to see previous pages This article will discuss malaria as a human disease, its epidemiology, and mode of transfer, its current prevalence, and mitigating measures and make a conclusion Literature review Cause of malaria Malaria is caused by eukaryotic protists belonging to the genus Plasmodium, phylum Amicomplexa that is transmitted by the female anopheles mosquito, which are its vectors, when they bite human beings. Once bitten, the parasites multiply within the body specifically in the red blood cells and liver and gestate for two weeks. Five types of Plasmodium cause malaria: Plasmodium vivax, Plasmodium falciparum, Plasmodium ovale, Plasmodium knowlesli and Plasmodium malariae . P. vivax is the most common type while P. falciparum is the most virulent and accounts for 90 percent of malaria deaths. Within the malaria causing parasites are found organelles called apicoplasts that are important for the parasites’ metabolism through production of various proteins. The parasites have a life cycle that starts upon entry into the secondary host; humans from the primary host; the female anopheles mosquito, which also are the parasites vectors (Sherman, 1998). Younger mosquitoes suck the blood of an infected human and ingest the parasites, whose gametes differentiate to form an okinete that further produces a cyst. The cyst with time will rapture to produce spores that migrate to the mosquitoes’ salivary glands where they infect a new person when the mosquito bites (Sherman, 1998). Pathogenesis of malaria There are two malaria development phases, the first phase being liver infection (exoerythrocytic phase) where they infect hepatocytes within the liver and multiply asexually, without showing symptoms for between 8 to 30 days (Sherman, 1998). In the liver, they stay dormant for some time, differentiating into numerous merozoites that move into the blood stream when their host cells erupt. The red blood cells (erythrocytes) are infected by merozoites starting the second phase of infection (Sherman, 1998). They further multiply within the erythrocytes where they infect other red blood cells while multiplying and produce periodic bursts that usually coincide with periods of high fever in the infected person. The fever is caused by the body’s reaction to the copious numbers of cell debris coming from the ruptured erythrocytes. The bursting of erythrocytes destroys them, this causes the feeling of tiredness and malaise as red blood cells that carry oxygen to muscles are destroyed (Marsh, 2002). When red blood cells burst, the parasite releases damaged host cell debris into the bloodstream together with its toxins. At this point the parasites are visible to the human immune system that respond by producing cytokines that can destroy the parasites but can equally destroy the hosts’ cells. Too much production of cytokines can kill the host while too little production will allow the parasites to kill the host. By living and reproducing within liver and red blood cells, the immune cells do not detect them, allowing their multiplication but the spleen destroys those parasites found in the circulatory system. As an adaptation, the parasites then adhere to the walls of blood capillaries and can cause total blockage in crucial areas like the blood brain barrier causing coma (cerebral malaria). The parasites adhere to blood vessels using PFEMP1 (“Plasmodium falciparum erythrocyte membrane protein 1” ...Download file to see next pagesRead More
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