Page 1 of 6 Life Cycle of Malaria Page 2 of 6 Malaria is an ancient disease transmitted by the Anopheles mosquito that predates recorded history. Historically it was common in the swampy areas around Rome, and was believed that the tainted air in those locations made people very sick, the disease was therefore named malaria for the Latin root words bad air. Malaria is caused by small parasitic protozoa of the genus Plasmodium which infects both humans and mosquitoes in a cyclical process. It is carried by only by female mosquitoes residing in tropical and subtropical areas and is injected into unsuspecting human hosts by the bite of an infected mosquito.
This particular Plasmodium is highly specific to infecting humans as we are the only vertebrates infected and the Anopheles mosquitoes are the vectors. (1).
This papers main focus shall be the process by which a malarial plasmodium colonizes and infects a human host, the methods the body employs to control the infection and the continuous life cycle completed between the two hosts. To understand any disease in humans one must first understand how it arrives into the body and what processes ensue. The following shall first describe the transition of the disease and then the colonization that takes place. During a blood meal on a human a female mosquito must inject her saliva containing an anticoagulant agent to ensure and even flow of blood into the mouth (1).
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The Malaria disease made its first appearance more than 4000 years ago. It used to be one of the diseases that people feared the most. About 655,000 people die from Malaria in 2010, about 200 people per day. In that year, 90% of the deaths occurred in the WHO region, Africa. Most of the Africans were women and children under the age of 5. (World Heath Organization, 2012) First of all, to know that ...
With the saliva comes malarial sporozoites which, within minutes of direct contact with the blood take an immediate route with the circulation of blood to the liver of the human (2).
Research has indicated that once the sporozoites arrive in the livers sinusoidal cavities they stop their movement by using two major surface proteins, the and the -related adhesive protein (3).
Research Page 3 of 6 conducted by Pradel et al. suggests that the sporozoites use these surface proteins to attach to in the sinusoidal extracellular matrix to slow their travel through the liver and then bind to and heparin sulfate on the Kupfer cells.
The Kupfer cells then become the doorways through which the sporozoite leaves the circulatory system and enters the underlying hepatocytes. Once the sporozoites invade the hepatocytes they are protected from the immune system by a (4) vacuole that does not co localize with the normal signals for acidifying organelles (2).
Because the body doesn’t recognize the vacuole as a threat at this point it remains safely with in the hepatic cell where it will stay for 9-16 days and differentiate into haploid cells called schizont which contain nearly 30, 000 compact cells called merozoites (1).
At the end of this period the mass production of merozoites within the schizont cause it to rupture, which releases the merozoites into the cytoplasm of the hepatic cell, killing it.
With the death of the hepatic cell thousands of merozoites spill into the blood stream, progressing the disease into what is known as liver stage malaria (4).
Once in the blood stream the merozoites immediately invade the closest erythrocytes. Once entering the cell they multiply rapidly through mitosis while feasting on hemoglobin. Each merozoite forms another schizont and after two days bursts open releasing 16-32 new merozoites which go on to colonize more red blood cells; this point is known as blood stage malaria.
Soon after, two out of every three red blood cells are colonized, producing fever and chills in the host (4).
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Once the erythrocyte is infected it becomes sticky and attaches to the walls of the blood vessels. If enough of Page 4 of 6 these cells build up in the same area blood vessels can become blocked and may rupture. If one ruptures in the brain (cerebral malaria) the damage caused to the surrounding tissue can be fatal due to localized ischemia. In addition, if left untreated the victim may suffer other severe complications including anemia, kidney failure and pulmonary edema (5, 6).
While it isn’t entirely understood how P.
manages to both invade the body and keep the immune system at bay, there has been research investigating this very mystery. A study conducted by Nobes et al. discovered that at the erythrocytic stage phagocytic Kupfer cells in the liver grow larger and begin to break down infected erythrocytes circulating though the sinusoidal cavities. While the exact trigger mechanism isn’t completely understood Nobes et al. hypothesized that the Kupfer cells are activated by particles, namely bits of exploded erythrocytes as well as actively infected erythrocytes. Once activated the Kupfer cells, also know as dendritic cells are supposed to be the leading crusader against the infection.
The typical response entails these cells transporting an antigen to the lymph nodes where they would activate T cells to enhance memory responses of other immune cells (7).
However the body is often not able to adequately respond to the mounting disease. Research involving circulating blood counts of dendritic cells has shown that those infected with malaria have severely diminished dendritic cells (8).
The protozoa impair the functions of these vital cells by interfering with their maturation and by stopping them from presenting antigens to naive T cells (5).
This is accomplished when the merozoites produce proteins that bind to the outside of the erythrocyte it is preying upon. These proteins attach to the Page 5 of 6 CD 36 proteins on the surface of dendritic cells ultimately inhibiting them from their immune function (5).
During this period of diminished immunity the plasmodium multiply exponentially infecting thousands of red blood cells until the host either dies or the malaria is eradicated with the aid of medications. So how is malaria a cyclical process as stated above if the host usually dies? How does the Plasmodium continue on if it the only transition of the disease it by mosquito and not through contact with other humans? The mosquito is the key, it can be infected when it takes blood from infected humans, thus continuing the cycle. This continuation is accomplished by the merozoites that invade the red blood cells. Not all of them differentiate into schizont’s.
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Rather, some develop into male and female gametocytes, thus entering the sexual stage of the parasite. When the mosquito takes a meal from an infected person the gametocytes are converted into male and female haploid gametes in the gut of the mosquito (6).
Once this metamorphosis occurs the male gamete fertilizes the female, resulting in a diploid zygote which then enters into mitosis and the ultimate formation of (6).
Ookinetes become flagellated and migrate to the edge of the pool of blood within the mosquito and cross the semi permeable peri trophic matrix containing the blood meal (6).
With the matrix behind them the settle in to a space between the gut wall and the basal lamina known as the cavity where they undergo another transformation to become oo cysts (6).
With in 10-24 days of feeding on an infected blood meal the oo cyst ruptures, releasing sporozoites which then advance to the front of the mosquito and Page 6 of 6 colonize the salivary glands (6).
Here they wait to be injected into another human host to begin the process of infection anew. Malaria is a complex disease with many steps in its life cycle. Once injected into a human the protozoa does its best to colonize, conquer and replicate for the next uptake by a mosquito to continue its process of infection. Through out time this parasite has evolved numerous ways to circumvent the bodies natural defenses against invaders and flourish.
While not all the methods employed by malaria to outwit the immune system are fully understood research is currently underway to discover this elusive information, with the hope that one day we may have a vaccine or a permanent cure. Reference 1. History of Plasmodium Parasites [monograph online] by Cann, Alan J PhD. University of Leicester department of Microbiology & Immunology; 1996 from: web accessed 2004 Mar 28. 2. Interactions between Malaria sporozoites and liver cells [monograph online] by Fr event, Ute NYU School of medicine 2002 retrieved from: web accessed 2004 Mar 28.
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3. Pradel, Gabriel, Garaphaty, Shiva ni, F revert, Ute. Proteoglycans mediate malaria sporozoite targeting to the liver, Molecular Biology 2002 45 (3) 637-651. 4. Silvia, Oliver et al.
Hepatocyte CD 81 is required for plasmodium and plasmodium sporozoite. Nature Medicine 2003; 9: (1) 93-96. 5. Heemels, Marie-Therese, A sticky situation with malaria. Nature Journal [serial online] 1999; 7 (1) Available: web Accessed 2004 Mar 28. 6.
Villa ” on, Jos’e M. Life Cycle of the Malaria Parasite [monograph online] Case Western Reserve University department of Microbiology from: web Nobes, Michael et al. Hepatic Kupfer cell function in rats with erythrocytic-stage malaria. Journal of gastroenterology & Hepatology 2002: 17 (5) 598-606. 8.
Urban, Britta et al. Peripheral blood dendritic cells in children with acute Plasmodium malaria. The American society of Hematology 2002: 98 (9) 2859-2861.
