Determining The Serum Protein Levels And CIC Level

Determining The Serum Protein Levels And CIC Level In Cerebral Malaria Patients Essay Assignment Paper

Determining The Serum Protein Levels And CIC Level In Cerebral Malaria Patients Essay

Malaria is a febrile illness characterized by fever and related symptoms (WHO, 1990). It is a disease caused by a blood borne protozoan parasite which is an intracellular parasite belonging to the class Sporozoa and of the genus Plasmodium and it is transmitted through the bite of an infected female anopheles mosquito (CDC, 2002). There are four different parasites of this genus which may give rise to malaria in man. Malaria is probably one of the oldest diseases known to mankind that has profound impact on our history. History of malaria and its terrible effects is as ancient as the history of civilization, therefore history of mankind itself (Ray et al., 1992). This ancient disease is still the scourge of the tropic and subtropics Africa, the Middle East, Asia and China and Central and South America are all endemic zones with tens of Ilion cases annually (Lucas, 1992). Determining The Serum Protein Levels And CIC Level In Cerebral Malaria Patients Essay

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Plasmodium falciparum is one of the genus and cause the most ere and virulent form of the disease and the only one to cause acute ality. In this study Plasmodium falciparum will be on focus since it is most prevalent in Nigeria. This genus of malaria spend a part of their cycle in the red cell of the host where the erythrocyticschizogony. They develop into merozoites and undergo a cycle producing schizonts. Each cycle terminates when the red cell rupture releasing merozoites into the circulation to infect new red cells eliciting an immune response. Malaria infection leads to the formation of circulating immune complexes (Mibeiet al., 2005). The importance of circulating immune complexes (CIC) and their relationship to various diseases has been the subject of investigation for number of years. Formation of immune complexes is a protective, on-going and usually benign process of a normally functioning immune system. However, in some individual CIC are deposited in the walls of blood vessels, especially in the glomerular capillaries where they cause tissue damage. The biospecific binding between sites of the antibody and the determinant group of the antigen result in the formation of antigen-antibody complex (AgAb) known as immune complexes (McDougal and McDuffie, 1985). Since malaria has been known to cause mortality this study is aimed at assessing the magnitude of circulating immune Complexes and some biochemical parameters which include serum total rein, albumin and globulin. Determining The Serum Protein Levels And CIC Level In Cerebral Malaria Patients Essay

Malaria is an important neglected disease and one of the most important global health problems, potentially affecting more than one third of the world’s population. Cerebral malaria (CM) is a deadly complication of Plasmodium falciparum infection, associated with a 10–14% mortality rate and approximately 1–2 million annual deaths among young children predominantly in sub-Saharan Africa and Southeast Asia, yet its pathogenesis remains incompletely understood. In Ghana, malaria has a wide spectrum of presentations: from asymptomatic carriers to mild malaria to multifactorial severe disease, including CM and severe malarial anemia (SMA) [1–5].

CM, a clinically complex syndrome of coma and potentially reversible encephalopathy, is associated with increased levels of proinflammatory cytokines like tumor necrosis factor (TNF)-α, interferon (IFN)-γ and lymphotoxin [6, 7], and increasingly recognized long-term sequelae in survivors [7–15]. Although the physiopathology of CM has been extensively investigated, the exact cellular and molecular basis of the neuropathology is still unclear. Recent studies have shown that mechanical blockage caused by sequestration of parasitized red blood cells (pRBCs), leukocytes and platelets [3, 4, 8–12], secretion of cytokines and chemokines [2, 6, 7, 13], angiogenic failure [14, 15], immune status and the genetic background of the host, and parasite factors [7, 16] are involved in the pathogenesis of CM. However, it is generally accepted that two major factors are involved: (i) metabolic insufficiencies due to the sequestration of pRBCs, leukocytes and platelets within brain vessels via upregulated adhesion molecules [3, 4, 8–12], and (ii) immunological reactions with the local involvement of T cells and monocytes activated by Plasmodium antigens [7, 11]. These two major mechanisms appear to act together under the control of cytokines [7], and chemokines [2] to exacerbate CM. Determining The Serum Protein Levels And CIC Level In Cerebral Malaria Patients Essay

Postmortem data in humans and murine models of CM show that neuronal damage in brain tissue occurs in CM, although the parasites remain confined to the intravascular space (with no contact with neurons). This strongly suggests that the blood-brain barrier (BBB) is perturbed, and thus the BBB represents a key interface between the intraerythrocytic stages of the parasite and the human host. The functional and morphological evidence supports mild-to-moderate impairment of the BBB, but whether this is sufficient to cause neurological complications such as CM is inconclusive [16, 17]. Mechanical blockage could occur from the ability of pRBC’s to adhere to unparasitized erythrocytes and endothelial cells, and sequester in the deep cerebral microvasculature [3, 4, 8–12]. Parasite sequestration alone, however, cannot account for fatal CM pathogenesis as there is evidence that survivors of CM have the same degree of sequestration during comas as those succumbing to disease. It is evident that host immune factors play an important role in the pathogenesis of CM. [8, 16]. Although parasite sequestration during severe malaria is central to pathogenesis of severe malaria, the role of cytokines, chemokines, apoptotic, and angiogenic factors in exacerbating disease severity remains unclear.