Life Cycle And Factors Influencing The Plasmodium Infection

The Life Cycle of Plasmodium

Question:

Discus About The Community Expansion Gene Geography Sickle?

Plasmodium is a genus that belongs to unicellular parasites that have been identified responsible for the incidence of malaria among host organisms. This unicellular parasite has a life cycle that occurs inside the body of two hosts, namely, a vertebrate and a dipteran insect host (Ariey et al., 2014). These species are found to contain several features that resemble other eukaryotes. The genome is present in the nucleus. It doubles the genome in the insect host’s midgut for a brief time (Bushell et al., 2017). The essay will discuss its life cycle and the various host factors that influence its infection.

The Plasmodium life cycle involves several changes inside the insect and vertebrate hosts. The parasites present in the salivary glands of infected mosquitoes, are called sporozoites that are injected in the bosy of the host, along with the saliva when a mosquito bites the vertebrate. They enter the bloodstream and are transported to the liver, following which they undergo invasion and replication in the hepatocytes (Delves et al., 2012). Merozoites emerge from the infected hepatocytes and form a ring-shaped structure that enlarges to form a trophozoite. These are then found to mature to form schizonts that multiply and produce new merozoites. This is followed by bursting of the infectred RBCs, thereby allowing the merozoites to travel and infect new cells (Ke et al., 2015). Upon infection, sime merozoites are found to differentiate into male and female gametocytes that are taken up by a mosquito, when it feeds on the vertebrate host. They move to the vector’s midgut and develop into male and female gametes, followed by fertilization and subsequent zygote formation. An ookinete is gradually formed from the zygote that penetrates the midgut wall and develops an oocyst, which in turn forms elongated sporozoites (Theisen et al., 2014).

Several differences exist in the physiology of the human host that directly influences the pattern of transmission of the Plasmodium infection. These factors also affect the severity of the disease. Due to the fact that the stages of the lifecycle are quite complex, human beings are either immune or non-immune to malaria, the disease caused by Plasmodium. Innate or natural immunity to malaria is regarded as the host’s inherent refractoriness that prevents infection establishment or inhibitory response against parasite introduction (Boyle et al., 2015). This immunity is naturally present in human body and independent of previous infections. Alterations in hemoglobin structure or certain enzymes confer protection against severe manifestation of the infection. People living in areas of high malaria prevalence commonly exhibit these traits. Duffy glycoprotein is a receptor for chemicals, secreted during inflammation of blood cells. Presence of Duffy negativity in RBCs also protects against Plasmodium infection (Wright & Rayner, 2014). Acute infection is also found to induce non-specific, immediate immune response that limits progression of the infection. This is primarily mediated by extrathymic, primordial T cells, and autoantibody producing-B1 cells. Several genetic conditions, such as, thalassemia, inherited hemoglobin disorders and Glucose-6-phosphate dehydrogenase (G6PD) polymorphism plays an essential role in protecting against this infection (S Balgir, 2012). Children and women with weak immunity are more susceptible to malaria infection in endemic areas. Poor socio-economic factors and lack of adequate prevention literacy also influence transmission (Cdc.gov, 2018).

Host Factors Influencing Plasmodium Infection

Plasmodium infection is generally caused due to several parasite factors. The female Anopheles mosquito picks up the parasite from bloodstream of infected people while biting them and obtains that blood to nurture their eggs. Inside the mosquito host body, the parasites are found to develop and reproduce. Upon biting a person for another time, these parasites present in the salivary glands of the mosquitoes get injected inside the host and are passed into the blood of the host. Therefore, salivary glands invasion is one of the major events that result in vector-borne disease transmission. Microvasculature obstruction and parasite biomass have been strongly correlated with the severity of Plasmodium infection, which often results in death. The parasites do not have any specific predilection for the stages of circulating RBCs and are found to invade them all, regardless of the stage. This contributes to high rates of parasitemias (Barber et al., 2015). Parasite biomass of Plasmodium is found to increase on failure to initiate appropriate treatment strategies, or due to the presence of weak immune system in the host. This eventually makes the infection more severe and results in death of the person (Bernabeu et al., 2016). Thus, elevated parasite biomass is regarded as a major independent risk factor that contributes to Plasmodium associated mortality. An increase in parasite biomass leads to erythrocyte loss and subsequent sequestration of the infected RBCs in microvascular beds, commonly referred to as cerebral malaria (Cunnington, Riley & Walther, 2013). This sequestration is another major parasite factor that influences the severity of Plasmodium infection. It refers to adherence of infected erythrocytes that contain the parasite’s late developmental stages such as, the trophozoites and schizonts, to the endothelium of the venules and the capillaries. This sequestration results in malfunctioning of various organs, thereby resulting in coma or brain death (Milner Jr et al., 2015).

Climatic factors, such as, temperature, rainfall, and relative humidity are directly responsible for the infection transmission. A decrease in temperature results in an increase in the number of days required by Plasmodium to complete its life cycle. Maximum temperature needed for its development is 40°C. The life cycle gets limited at temperatures lower than 18°C (Cottrell et al., 2012). On the other hand, higher temperatures increase number of blood meals and eggs laid by the mosquitoes. An increase in altitude also decreases temperature, thereby affecting transmission (Mordecai et al., 2013). Appropriate amount of water is needed for breeding of the mosquitoes. Stagnant water collection supports vector breeding and increases infection rates. In addition, mosquitoes have been found to survive better under high humidity (Bomblies, 2012). Non-climatic factors that influence transmission rates include urbanization, migration, and population movement. Incidence of the infection rates are lower in urban areas due to lack of empty spaces that act as breeding grounds and improved access to healthcare and prevention strategies (Qi et al., 2012). Furthermore, drug resistance to the parasite also prevents its transmission.

Prevention strategies include determining the risk or likelihood of getting affected, staying in well-screened areas, using mosquito repellents, protective clothing and bed netting (Cullen & Arguin, 2014). Prophylactic use of antimalarial drugs, such as, chloroquine while travelling in endemic areas also helps in preventing infection transmission (Ouédraogo et al., 2014).

Parasite Factors Influencing Plasmodium Infection

To conclude, it can be stated that the protozoan parasite, Plasmodium is responsible for causing a deadly, yet curable disease among vertebrates. This parasite is transmitted by the bite of mosquitoes, and creates life-threatening conditions that can cause significant morbidity, if not treated. People living in warmer regions are at an increased likelihood of suffering from this infection. Although, there are two hosts needed for completion of the parasite’s life cycle, the insect acts as the definitive host because it acts as the feasible location where sexual reproduction of the parasite always occurs. Thus, it can be concluded that a range of host and parasite factors are responsible for transmission of the disease.

References

Ariey, F., Witkowski, B., Amaratunga, C., Beghain, J., Langlois, A. C., Khim, N., ... & Lim, P. (2014). A molecular marker of artemisinin-resistant Plasmodium falciparum malaria. Nature, 505(7481), 50.

Barber, B. E., William, T., Grigg, M. J., Parameswaran, U., Piera, K. A., Price, R. N., ... & Anstey, N. M. (2015). Parasite biomass-related inflammation, endothelial activation, microvascular dysfunction and disease severity in vivax malaria. PLoS pathogens, 11(1), e1004558.

Bernabeu, M., Danziger, S. A., Avril, M., Vaz, M., Babar, P. H., Brazier, A. J., ... & Gomes, E. (2016). Severe adult malaria is associated with specific PfEMP1 adhesion types and high parasite biomass. Proceedings of the National Academy of Sciences, 113(23), E3270-E3279.

Bomblies, A. (2012). Modeling the role of rainfall patterns in seasonal malaria transmission. Climatic change, 112(3-4), 673-685.

Boyle, M. J., Reiling, L., Feng, G., Langer, C., Osier, F. H., Aspeling-Jones, H., ... & McCarthy, J. S. (2015). Human antibodies fix complement to inhibit Plasmodium falciparum invasion of erythrocytes and are associated with protection against malaria. Immunity, 42(3), 580-590.

Bushell, E., Gomes, A. R., Sanderson, T., Anar, B., Girling, G., Herd, C., ... & Mather, M. W. (2017). Functional profiling of a Plasmodium genome reveals an abundance of essential genes. Cell, 170(2), 260-272.

Cdc.gov. (2018). CDC - Malaria - About Malaria - Biology - Human Factors and Malaria.  Retrieved 3 March 2018, from https://www.cdc.gov/malaria/about/biology/human_factors.html

Cottrell, G., Kouwaye, B., Pierrat, C., Le Port, A., Bouraïma, A., Fonton, N., ... & Garcia, A. (2012). Modeling the influence of local environmental factors on malaria transmission in Benin and its implications for cohort study. PLoS One, 7(1), e28812.

Cullen, K. A., & Arguin, P. M. (2014). Malaria surveillance—United States, 2012. Morbidity and Mortality Weekly Report: Surveillance Summaries, 63(12), 1-22.

Cunnington, A. J., Riley, E. M., & Walther, M. (2013). Stuck in a rut? Reconsidering the role of parasite sequestration in severe malaria syndromes. Trends in parasitology, 29(12), 585-592.

Delves, M., Plouffe, D., Scheurer, C., Meister, S., Wittlin, S., Winzeler, E. A., ... & Leroy, D. (2012). The activities of current antimalarial drugs on the life cycle stages of Plasmodium: a comparative study with human and rodent parasites. PLoS medicine, 9(2), e1001169.

Ke, H., Lewis, I. A., Morrisey, J. M., McLean, K. J., Ganesan, S. M., Painter, H. J., ... & Vaidya, A. B. (2015). Genetic investigation of tricarboxylic acid metabolism during the Plasmodium falciparum life cycle. Cell reports, 11(1), 164-174.

Milner Jr, D. A., Lee, J. J., Frantzreb, C., Whitten, R. O., Kamiza, S., Carr, R. A., ... & Dzamalala, C. (2015). Quantitative assessment of multiorgan sequestration of parasites in fatal pediatric cerebral malaria. The Journal of infectious diseases, 212(8), 1317-1321.

Mordecai, E. A., Paaijmans, K. P., Johnson, L. R., Balzer, C., Ben?Horin, T., Moor, E., ... & Lafferty, K. D. (2013). Optimal temperature for malaria transmission is dramatically lower than previously predicted. Ecology letters, 16(1), 22-30.

Ouédraogo, A. L., Bastiaens, G. J., Tiono, A. B., Guelbéogo, W. M., Kobylinski, K. C., Ouédraogo, A., ... & Lanke, K. H. (2014). Efficacy and safety of the mosquitocidal drug ivermectin to prevent malaria transmission after treatment: a double-blind, randomized, clinical trial. Clinical infectious diseases, 60(3), 357-365.

Qi, Q., Guerra, C. A., Moyes, C. L., Elyazar, I. A. F., Gething, P. W., Hay, S. I., & Tatem, A. J. (2012). The effects of urbanization on global Plasmodium vivax malaria transmission. Malaria journal, 11(1), 403.

S Balgir, R. (2012). Community expansion and gene geography of sickle cell trait and G6PD deficiency, and natural selection against malaria: experience from tribal land of India. Cardiovascular & Hematological Agents in Medicinal Chemistry (Formerly Current Medicinal Chemistry-Cardiovascular & Hematological Agents), 10(1), 3-13.

Theisen, M., Roeffen, W., Singh, S. K., Andersen, G., Amoah, L., van de Vegte-Bolmer, M., ... & Adu, B. (2014). A multi-stage malaria vaccine candidate targeting both transmission and asexual parasite life-cycle stages. Vaccine, 32(22), 2623-2630.

Wright, G. J., & Rayner, J. C. (2014). Plasmodium falciparum erythrocyte invasion: combining function with immune evasion. PLoS pathogens, 10(3), e1003943.