Pathophysiology and Epidemiology of Malaria - Essay Example

Pathophysiology and Epidemiology of malaria Introduction Malaria, a mosquito-borne, protozoal illness, recognized as a parasite disease with the mosquito as the vector in early 19th century. In spite of concentrated efforts by government and NGOs, malaria is the most fatal parasitic disease today. Malaria infections manifest in humans results from infection with Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale or Plasmodium malariae with Plasmodium falciparum accountable for the mass of the clinical cases and mortalities. The female anopheles mosquito is the one that transmits the plasmodium parasite. The mosquito leaves the parasite in the human blood while feeding it’s a blood meal. Anopheles gambiae, Anopheles arabiensis and Anopheles funestus are first and foremost the main parasites responsible for transmitting the majority of human being malaria (Gutierrez 2000). Pathogenesis of Malaria All types of malaria manifest through common symptoms like fever, though some patients progress to severe malaria often caused by the P. falciparum species. It takes 24-72 hours after infection for the infecting parasites to schizogonise, depending on species. Newly developed merozoites are released through the lysis of infected erythrocytes together with other waste substances like, red cell membrane products, hemozoin pigment and glycosylphosphatidylinositol (GPI) (Gutierrez 2000). These toxins released into the blood, lymphotoxin, as well as superoxide and nitric oxide (NO). The end part of GPI has been implicated as a key parasite toxin by several experts. The various cytokines released in response to malaria parasites and red cell membrane products released after lysis are largely responsible for the systemic form of malaria such as head pain, fever , unsettled stomach and vomiting, diarrhea, weariness, painful joints and muscles, thrombocytopenia, immunosuppressant,.(Palmer and Reeder 2001). The plasmodial DNA is also highly proinflammatory and can induce cytokinemia and fever. Plasmodial DNA presented by hemozoin, produced during schizogony, interacts intracellularly with the Toll-like receptor-9, which leads to the discharge of proinflammatory cytokines that bring on COX-2-upregulating prostaglandins leading to the initiation of other uncomfortable body feeling like fever (Palmer and Reeder 2001). Pathogenesis of Severe Malaria The infectivity of red cells by malaria parasites, P. falciparum, brings about progressive together with mechanical alteration of the red cells that can deteriorate over time into life-threatening complications of malaria (Choffnes and Relman). While P. falciparum has been overwhelmingly castigated as the main cause of severe malaria, other species can be equally culpable (Root and Waldvogel). For example, cases of severe infection and even death have been reported following infections of P. vivax and P. knowlesi. More than a few pathophysiological features such as the sponge biomass, reset and confiscation alter formability and restraint of parasitized erythrocytes. Endothelial activation, dysfunction, injury and altered thrombostasis have been found to be involved in the acquisition of severe malaria. This is most profound in cases of P. falciparum infection (Root and Waldvogel). Role of Cytokines in Severe Malaria On detecting infection by malaria parasites, proinflammation cytokines go into overdrive cascading like tumor necrosis factor, while interleukins, interferon-γ, and nitric oxide responds to the invasion and cause damage to the human body. But, cytokines failure to down regulate inflammatory response results in immune pathology causing complication. Excessive production of cytokines can lead to reduced mitochondrial oxygen use and enhance lactate production (Merson 2005). Increased cytoadherence causes micro vascular obstruction and more hypoxia. Disturbed auto-regulation of local blood flow leads to deprived movement and further tissue hypoxia, dyserythropoiesis, deprived red cell deformability, and anemia, abridged gluconeogenesis and hypoglycemia and cardiac insufficiency, discriminating regulation of vascular and intercellular adhesion molecules predominantly in the mind and placenta, leading to cerebral malaria and placental dysfunction (Merson 2005). Activation of leukocytes and platelets promotes procoagulant activity. Thus it cannot be over and done with that the outcome of malaria illness is determined by the equilibrium in the middle of the pro- and anti-inflammatory cytokines (Merson 2005). Cytoadherence, Sequestration, and Rosetting Structural changes in the infected red cells increase in their rigidity and adhesiveness make P. falciparum particularly virulent. Due to the increased tackiness, the red cells contaminated with late stages of P. falciparum adhere to the capillary and post capillary venular endothelium in the deep microvasculature. (Coleman and Tsongalis). It is the sequestration of the maturing P. falciparum parasites in the deeper tissues that present them the microaerophilic venous environment. (Coleman and Tsongalis). Some of The previously discussed factors help out the falciparum vermin to take on uninhibited multiplication, thereby increasing the parasite load profusely. (Gutierrez 2000). Red cell membrane rigidity and deformability The conventional method of diagnosis for malaria is the microscopic examination of Giemsa-stained blood smears. This method has been criticized as time wasting, misleading in identifying Plasmodium species especially in cases with low level of parasitemia, a mixed parasite infection, or when modified by anti-malarial drug treatment. Molecular methods of testing most notably, the polymerase chain reaction (PCR) have been employed in recent years for routine diagnosis to provide information about drug resistance and genetic diversity of the parasites (Moxham and Souhami). Epidemiology Epidemiological analysis is critical to any malaria control programs. However, this method requires knowledge and expertise in planning, management and evaluation of malaria control programs. The epidemiological approach utilizes scientific tools to describe and measure the distribution of the disease, explain the distribution by its determinant factors, and predict the expected changes in the distribution through human intervention. The chain of infection has six links; a pathogen or causative (infectious) agent, a reservoir, a porch of way out from the pool, a mode of transmission, a doorway of entrance into the host and a susceptible host(Moxham and Souhami). Illustrative figure; Infectious agent, reservoir, portal of exit, mode of transmission, portal of entry and susceptible host (Insert rectangular diagrams) An infection can be prevented by breaking any link in the chain of infection. The causative organism in this case is the P. falciparum protozoa, which are spread by the arthropod vector, anopheles mosquito. The intervention can take forms of, Sterilizing surgical instruments and anything that comes into contact with sterile spaces of the body and treating the infected. Vector control involves decreasing malaria morbidity and mortality by lowering levels of transmission, for example, an individual can reduce contact with the vectors by using insect repellants (Moxham and Souhami). Use of insecticide treated mosquito nets and indoor residual spraying (IRS) have been effective in mosquito endemic areas. IRS seeks to destroy mosquitoes that rlax on the walls after taking a blood meal therefore, preventing further transmission; however, mosquito can develop IRS resistance through evolution. To control breeding of mosquitoes people are advised by epidemiologists to cover stagnant water. Intermittent preventive therapy is used to prevent infection of children and pregnant women. Scientists have also contemplated introducing transgenic mosquitoes that cannot carry the parasites therefore decimating its prevalence by denying it access and sustenance by a vector (Gutierrez 2000). Conclusion Early diagnosis and treatment prevents the parasite load in the community from accumulating. Presumptive treatment with chloroquine should be done for all cases of fever and second line antimalarials administered in case of resistance and radical treatment using primaquine should be administered for confirmed cases of malaria fever. Complete treatment should be adhered to control the spread of parasites. Individuals and communities should be educated on malaria prevention and treatment and health institutions should adopt the best equipment and practices in treating malaria. Bibliography: Choffnes, E. R. and Relman, D. A., 2011. The causes and impacts of neglected tropical and zoonotic diseases: opportunities for integrated intervention strategies: workshop summary. Washington, D.C.: National Academies Press Coleman, W. B. and Tsongalis G.J., 2009. Molecular pathology: the molecular basis of human disease. Burlington, Mass.: Academic Press. Gutierrez, Y. 2000. Diagnostic pathology of parasitic infections with clinical correlations. New York [u.a.]: Oxford University Press. Merson, H. M., 2005. International public health: diseases, programs, systems, and policies. Sudbury, Mass. [u.a.]: Jones and Bartlett Publ. Moxham, J. and Souhami, R., L. 2002. Textbook of medicine. Edinburgh [u.a.]: Churchill Livingstone. Palmer, E. S. and Reeder, M., 2001. Imaging of tropical diseases: with epidemiological, pathological, and clinical correlation. Heidelberg, Germany; New York: Springer- Verlag. Root, R. K. and Waldvogel, F. 1999. Clinical infectious diseases: a practical approach, New York, NY [u.a.]: Oxford Univ. Press. Read More