Plasmodium falciparum

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Classification

Higher order taxa

Kingdom: Protista Phylum: Apicomplexa Class: Aconoidasida Order: Haemosporida Family: Plasmadiidae

Species

Genus: Plasmodium Species: falciparum

Description and significance

Plasmodium falciparum lives in human red blood corpuscles. If one looks at a blood smear or blood film of a person infected with the malarial parasite, P. falciparum, they would probably see the immature trophozoites and gametophytes. The schizonts and the mature trophozoites are most likely not seen because they are imbedded in the tissues. The red blood cells that have been infected would be seen and they may contain more than one parasite. Faint comma-shaped red dots also appear on the surface of the erythrocytes and these are called the “Maurer’s dots”. They may cluster together in the form of a pear shape. After discovering the parasite, P. falciparum, researchers have attempted over the years to sequence its genome. The Malaria Genome Project was set up in the year 1995 to sequence its genome and in that same year its mitochondrion was sequenced. In 1996, the plastid (apicoplast) was sequenced. The genome of the nuclear chromosome 2 and chromosome 3 were sequenced in 1998 and 1999 respectively. And finally on October 3rd, 2002, the entire genome was sequenced. The Plasmodium falciparum genome is a difficult one to sequence because it is very complicated. Therefore, there were three institutions that divided the 14 chromosomes among themselves in the Malaria Genome Project. Stanford University sequenced chromosome 12, the Institute for Genomic Research and the Malaria Program of the Naval Medical Research Center worked on chromosomes 2, 10, 11 and 14 and the Sanger Centre sequenced chromosomes 1, 3-9, 13. The chromosome-by chromosome method was preferred instead of trying to sequence the entire genome by the shotgun method.

Genome structure

The Plasmodium falciparum genome is approximately 23 mega base pairs long. It consists of fourteen chromosomes with varying sizes from 0.643 to 3.29 mega base bairs long. The chromosomes are linear. The adenine to thymine composition is about 80.6% and about 90% in introns and intergenic areas. Fifty four percent of the genes contained introns and these genes were long about 2.3 kilo bases. In the genome, 5300 protein encoding genes were determined. That is about 1 gene for every 4338 base pairs. No transposable elements or retro-transposons were found. There were proteins on genes that were not recognized as well.

Cell structure and metabolism

When a human is bitten by an infected Anopheles mosquito, sporozoites are released in the human circulatory system. Soporzoites consist of an outer and a double inner membrane which lie on top of microtubules. They are approximately 10-15 micrometers long and contain three polar rings. After entering the circulatory system, the sporozoites travel to the liver where they replicate asexually producing merozoites. Merozoites then take over the erythocites and they develop into trophozoites (large rings). The trophozoites eat the host’s cytoplasm and break down hemoglobin to peptides. Exoerythrocytic schizonts are formed after numerous cycles of nuclear division of the trophozoites. The schizonts then undergo budding and merozoites are once again formed. The red blood cells rupture and the merozoites escape. They can now infect more red blood cells and when this happens, immature gametocytes may form instead of trophozoites. Another mosquito may feed on the infected individual and in turn accumulate these gametocytes in their bodies. A flagellated microgamete is formed after a male zygote undergoes fast nuclear division and this fuses with a female zygote. This fertilization produces an oocyte which resides in the gut wall of the mosquito. When this burst, sporozoites are released and they journey to the mosquito’s saliva. This mosquito then bites and infects another human and the cycle is repeated. In the erythrocytic stage of the life cycle, the hemoglobin in the host’s blood is used as food for Plasmodium falciparum. Hemoglobin is a protein and it is broken down into peptides. Hemazoin is the form in which the heme group is released and detoxified. In the same stage of the life cycle, the erythrocytic stage, Plasmodium falciparum makes it energy by the process of anaerobic glycolysis whereby the pyruvate molecule is converted to lactate. In P. falciparum, the main function of the Krebs cycle is to produce succinyl-CoA which is important in the catabolism of the heme group of hemoglobin. All the amino acids needed by the parasite are acquired from the host or from the metabolism of hemoglobin. The breakdown of lipids to fatty acids could probably be done by the apicoplast of P. falciparum. However, this is just hypothesized. It is yet to be determined. Purines are not metabolized by this parasite but it is obtained from the host. But, pyrimidines are metabolized from glutamine, bicarbonate and aspartate.

Ecology

Plasmodium falciparum is present throughout the world. It is most abundant in tropical/subtropical areas where it is warm and humid in order for the mosquitos vectors to replicate.

Pathology

How does this organism cause disease? Human, animal, plant hosts? Virulence factors, as well as patient symptoms.

Application to Biotechnology

Does this organism produce any useful compounds or enzymes? What are they and how are they used?

Current Research

Enter summaries of the most recent research here--at least three required

References

http://en.wikipedia.org/wiki/Plasmodium_falciparum http://www.tigr.org/tdb/edb2/pfa1/htmls/ http://microbewiki.kenyon.edu/index.php/Plasmodium http://www.ispub.com/ostia/index.php?xmlFilePath=journals/ijmb/vol1n2/plasmodium.xml http://en.wikipedia.org/wiki/Malaria http://justice.loyola.edu/~klc/BL472/Malaria/research.html http://en.wikipedia.org/wiki/Plasmodium_falciparum_biology http://www.dhpe.org/infect/malaria.html