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Plasmodium falciparum:

The Causative Agent of Malaria

by Micah Benson


The protozoan Plasmodium falciparum is responsible for causing 500 million cases of malaria per year as well as 100-200 million deaths per year worldwide (Kuby, p438). The majority of these deaths occur in sub-Saharan Africa, especially among malnourished children. Malaria is endemic in 92 countries, where 40% of the world’s population is at risk of the disease (WHO). Documentation of malaria occurs as far back as 4000BC, with mentions of the disease on clay tablets. The name of the disease originates from the late 1800’s and is derived from ‘mal aria,’ meaning bad air. There are four members of Plasmodium that cause malaria along with P. falciparum, with P. vivax, P. ovale, P. malariae (Schaechter, p450). P. falciparum is considered the most important as it is by far the most deadly species. The primary vector of P. falciparum is the female anopheline mosquito, which uses humans as a host for blood meals. The male anopheline feeds only on plant juices, and is not a competent vector for the disease. Humans compromise the only suitable reservoir in the enzootic cycle of the protozoa (Schaechter, p450). Both the P. falciparum and Anopheles gambiae genomic sequences have been recently published (Gardner et al. Holt et al. 2002), thus giving rise to invaluable tools in the development of new and much needed anti-malarial drugs and vaccines, as well as new targets in mosquito control.


Encounter and Entry

The female Anopheles interacts with the human host by piercing the host’s epithelium and releasing Plasmodium falciparum from its salivary glands into the human bloodstream while obtaining a blood meal. The form of P. falciparum injected into the human host is the sporozoite stage in the pathogen's life cycle (Kuby, Schaechter). As humans compromise the only competent reservoir for P. falciparum, the female Anopheles must have acquired the protozoan via blood meal from another infected human 9 to 17 days prior to being able to infect a new human host.

Spread and Multiplication

The sporozoites enter the human host and then travel via the bloodstream to the liver, where they enter liver cells and mature into schizonts after a period of 8-14 days. Sporozoites are covered with a 45-kDa protein called circumsporozoite which mediates adhesion to hepatocytes (Kuby, p439). Schizonts are released into the bloodstream as merozoites after a week, and are capable of entering and lysing erythrocytes and thus causing disease. The erythrocyte-attacking merozoites multiply asexually, and further mature into the ring-shaped trophozoites within the bloodstream (Schaechter, p451). Some protozoa remain dormant in the liver cells as hypnozoites, which cause relapsing malaria. Within the erythrocytes, some P. falciparum differentiate into gametocytes, which multiply sexually, and which can be ingested by female Anopheles mosquitoes through a blood meal of the infected human reservoir. Within the mosquito, the male and female gametocytes produce zygotes, which develop into oocytes within the mosquitoes’ gut, and the oocytes produce sporozoites that migrate to the Anopheles salivary gland, thus completing the P. falciparum life cycle (Schaechter, p451).

Response to Host Defenses

In young children where malaria is endemic, notably sub-Saharan Africa, the host response to P. falciparum is poor (Roll Back Malaria). This inadequate immune response among children yields almost 1 million deaths a year in children alone, with a mortality rate of 50% (Kuby, p439). Among adults in endemic regions, 84% have detectable antibodies to P. falciparum, and many have chronic P. falciparum infection. The ability of P. falciparum to evade the human’s immune system is due to it having multiple morphologies within its life cycle while present within the human body, allowing it to constantly change surface antigens, and is also due to the protozoan living a portion of its life intracellularly within liver and red blood cells (Kuby, p439).


The symptoms of malaria typically reside on a 48 hour cycle in which the most vicious of the symptoms occur with the lysis of erythrocytes and the subsequent release of merozoites. Symptoms include fever, chills, anemia, and severe flu-like symptoms (Schaechter, p451). The human host may even contribute to the pathology of the parasite through the excessive release of tumor necrosis factor (TNF) and interleukin-1 (IL-1), leading to sickness (Kuby, p439).


Common anti-malarial drugs include chloroquine, doxycycline, mefloquine, malarone, and hydroxychloroquine sulfate. Travelers are often advised to take these prescription drugs all though their trip into endemic areas. Other preventative measures include wearing DEET, an insect repellant that repels mosquitoes. Measures taken to avoid contact with mosquitoes also lower the chances of infection (CDC).


There are many problems caused by P. falciparum that need to be resolved. Drug resistance to choloroquine, formerly the most ubiquitous and useful anti-malarial drug, is bestowed upon P. falciparum by a pfcrt mutation in the greater parts of Africa (Sidhue et at, 2002), and resistance to other drugs is increasing. Vaccines have generally proven ineffective or unreasonable, due to the ability of P. falciparum to ‘hide’ its surface antigens. Recently, 90% of patients immunized with irradiated sporozoites were protected against infection for ten months, however, protection was not conferred beyond that, and the great difficulty in culturing sporozoites makes this an unreasonable vaccine (Kuby, p440). The disease has been described as dealing out "the greatest harm to the greatest number (Schaechter, p449)," and its impact on the world has yet to be repelled by modern medicine. New drugs, and effective vaccines must be created, as well as new means of mosquito control.




CDC website:

Garner et al. 2002. Genome sequence of the human malaria parasite Plasmodium falciparum. Nature 419:498-512

Holt, Robert et al. 2002. The Genome Sequence of the Malaria Mosquito Anopheles gambiae. Science, 298: 129-149

Kuby. 2000, 4th ed. Immunology. W. H. Freeman and Co, NY, New York

Roll Back Malaria:

Schaechter, Moselio. Engleberg, N Cary. Eisenstein, Barry. Medoff, Gerald. 1999, 3rd ed. Mechanisms of Microbial Disease. Lippincott Williams and Wilkins, NY, New York.

Sidhu, Amar Bir Singh. Verdier-Pinard, Dominik. Fidock, David. 2002. Chloroquine Resistance in Plasmodium falciparum Malaria Parasites Conferred by pfcrt Mutations. Science 298:210-213

World Health Organization. World malaria situation in 1994. Wkly Epidemiol Rec 1997;72:269-76


Related Links of Interest

Center for Disease Control:

A malaria database for the serious scientist:

World Health Organization:



© 2010, J.Graf. Site made by Micah Benson, for comments please contact