Malaria is a vector-borne communicable humans and other animals’ disease that is caused by a protest microorganism of the Plasmodium genus. It starts with an infected female Anopheles mosquito bite that inserts the organism via saliva into the circulatory system. Once in the blood, the organism moves to the liver to grow up as well as reproduce. Characteristically, malaria symptoms include headache and fever, which in harsh instances can proceed to death or coma. Malaria is widespread in subtropical and tropical areas in a broad band all over the equator, including much of the Americas, Asia, and Sub-Saharan Africa (Cutler, Fung, Kremer, Singhal, & Vogl, 2007).
Malaria parasites are communicated to humans through an anopheline mosquitoes’ bite. Following injection, these parasites, which at this point are referred to as sporozoites, circulate for just a few minutes within the blood prior to getting into the liver cells of the host. In the liver, they divide fast for the following week, one parasite producing about 30000 daughter parasites, which are referred to as merozoites. Throughout this period of frantic division, the host stays totally well (Marsh, 2002).
Following about one week, the now dilated cells of the liver burst open, discharging the merozoites into the bloodstream, where they can merely endure if they quickly adhere to and get into the host’s red blood cells. The parasites are now protected, and they cannot be detected or attacked by the immune system of the host. Within the red blood cell, the parasite once more matures and divides, this time producing up to 32 daughter merozoites. After around two days, the red blood cell of the host bursts discharging merozoites into the blood to start the cycle again. This recurrent cycling of growth, discharge and reinvasion results in an exponential burst of parasites in the blood. The progeny from one parasite in the liver can result in the damage of all red blood cells of the host in 12 to 14 days (Marsh, 2002). This red blood cells’ damage causes anemia, which is among the typical problems contributed by Plasmodium falciparum malaria. While this progresses fast, the lack of ability to deliver enough oxygen to the fundamental organs of the body is enough to clarify many of the characteristics of disease and to result in the host’s death (Marsh, 2002).
Malaria is not only a disease usually related with poverty as a number of evidence advises that it also leads to poverty as well as a key obstruction to the development of economy (Worrall, Basu, & Hanson, 2005). Tropical areas are mostly affected even though the furthest extent of malaria extends to some temperate zones with severe seasonal modifications. This disease has been linked to key negative economic impacts on areas where it is spread widely. In the late 19th, as well as early 20th centuries, it was a key aspect in the sluggish development of the economy in the southern states of America (Humphreys, 2001).
A comparison of mean per capita gross domestic product in 1995, set for purchasing power’s parity, among nations with malaria and those without malaria produces fivefold dissimilarity. In nations where malaria is widespread, mean per capita gross domestic product has gone up with only 0.4% annually, compared to 2.4% annually in other nations (Sachs & Malaney, 2002).
Poverty can raise malaria risk, as those in poverty lack the financial capabilities to preclude or cure the disease. In its totality, the impact of malaria on the economy has been approximated to cost Africa $12 billion USD each year. The economic effect includes health care costs, working days wasted because of sickness, days wasted in education, reduced productivity because of brain destruction from cerebral malaria, and tourism and investment loss (Greenwood, Bojang, Whitty, & Targett, 2005). Malaria has a heavy load in a number of nations, where it might be accountable for 30–50% of admissions in hospital, up to 50% of visits by outpatients, and up to 40% of public health expenditure.
Cerebral malaria is among the leading neurological disabilities causes’ in African children (Idro, Marsh, John, & Newton, 2010). Studies that compare cognitive functions prior to and following treatment for harsh malarial sickness have demonstrated considerably afflicted school performance. These studies have, as well demonstrated cognitive capabilities even following healing (Fernando, Rodrigo, & Rajapakse, 2010). As a result, cerebral as well as severe malaria have important outcomes in socioeconomic outcomes that go beyond the instant consequences of the disease (Ricci, 2012).
Cutler, D., Fung, W., Kremer, M., Singhal, M., & Vogl, T. (2007, October). Mosquitoes: The Long-Term Effects of Malaria Eradication in India. Retrieved April 1, 2013, from http://www.nber.org/papers/w13539.pdf?new_window=1
Fernando, S., Rodrigo, C., & Rajapakse, S. (2010). The 'hidden' burden of malaria: Cognitive impairment following infection. Malaria Journal, 366.
Greenwood, B. M., Bojang, K., Whitty, C. J., & Targett, G. A. (2005). Malaria. Lancet, 365(9469), 1487–1498.
Humphreys, M. (2001). Malaria: Poverty, Race, and Public Health in the United States. Maryland: Johns Hopkins University Press.
Idro, R., Marsh, K., John, C. C., & Newton, C. R. (2010). Cerebral malaria: mechanisms of brain injury and strategies for improved neurocognitive outcome. Pediatric Research, 68(4), 267–274.
Marsh, K. (2002, October 1). Malaria and the human body, part 1: Danger cycle. Retrieved April 1, 2013, from http://malaria.wellcome.ac.uk/doc_WTD023879.html
Ricci, .. (2012). Social implications of malaria and their relationships with poverty. Mediterranean Journal of Hematology and Infectious Diseases, 4(1).
Sachs, J., & Malaney, P. (2002). The economic and social burden of malaria. Nature, 415(6872), 680–685.
Worrall, E., Basu, S., & Hanson, K. (2005). Is malaria a disease of poverty? A review of the literature. Tropical Health and Medicine, 10(10), 1047–1059.