The paper "Life Cycle of Plasmodium Falciparum" is a great example of medical research. The life cycle of Plasmodium Falciparum comprises two separate hosts, female anopheles mosquito and human beings. Female anopheles mosquito ingests gametocytes by feeding on an infected human host, which fertilizes, forming a zygote, and matures into sporozoites. These sporozoites reside in the salivary glands of female anopheles and are transmitted to humans during a mosquito bite. In humans, the cycle consists of two separate phases; exoerythrocytic and erythrocytic phases. (Jones 2009, p. 2) Sporozoites enter the human bloodstream and migrate to the liver to begin the exoerythrocytic phase that lasts for about 2 weeks.
After invading the parenchymal cells of the liver, these sporozoites reproduce asexually to form tens of thousands of merozoites which again enter the bloodstream by membrane blebbing. Merozoites invade red blood cells to mark the beginning of the erythrocytic phase. In this phase, these merozoites again replicate asexually and further increase in number eventually bursting the red blood cell and invading a new erythrocyte upon release. Some merozoites divide sexually within the red blood cells to produce the gamete forms that are transferred back to the anopheles mosquito thus completing the cycle.
(Jones 2009, p. 2) Stages of the erythrocytic phase are important for the pathogenesis of Plasmodium falciparum. This is because the invasion of these red blood cells not only causes replication of the parasites but it also leads to other fatal complications. (Jones 2009, p. 4). RBC lysis results in periodic fever and chills and a decrease in hemoglobin concentration leading to anemia. Furthermore, the invasion of RBCs by these parasites results in some modification of surface proteins, making them susceptible to aggregation.
Occlusion of important blood vessels by infected cells results in cerebral edema, multi-organ dysfunction, and other fatal complications characteristic of plasmodium falciparum infection. 2. The cuticle is the outer surface layer of nematodes and is a critical structure for their protection. This layer acts as a hydroskeleton for the maintenance of body shape and allows mobility at the same time. Important properties of cuticle such as toughness and flexibility make it a perfect barrier to the environment and also allow movement of opposed muscles within the tubular infrastructure.
Moreover, in the parasitic species of nematodes, the cuticle is the surface that comes in contact with the host’ s immune cells and provides protection against them. The outer surface of the cuticle is covered with a surface coat that can be shed off when immune killer cells come in contact with it. Therefore, the cuticle provides a perfect evasion mechanism that is crucial for the survival and protection of nematodes. (Perry 2011, p. 29) Just like cuticles in nematodes, the tegument in Platyhelminthes is a host-parasite interface.
It is the outermost covering of the helminth that comes in direct contact with the host immune cells. But unlike cuticle, tegument consists of a syncytium that bears various structures such as microvilli and microtreches. An important layer of tegument known as membranocalyx plays a vital role in providing defense against the host immune system. This membrane can also be shed as an evasion mechanism. Moreover, the glycocalyx is also responsible for the neutralization of various host enzymes aiding in the survival of helminths and providing them protection from an external hostile environment.
JONES, M. L. (2009). Erythrocyte invasion by Plasmodium falciparum. Birmingham, Ala, University of Alabama at Birmingham. https://www.mhsl.uab.edu/dt/2009r/jonesm.pdf.
PERRY, R. N., & WHARTON, D. A. (2011). Molecular and physiological basis of nematode survival. Wallingford, Oxfordshire, CABI.