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Chapter 15 : Malaria

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Malaria, Page 1 of 2

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Abstract:

Malaria is classically known as a disease of fever, anemia, and splenomegaly, with clinical descriptions dating back 6,000 years. The parasites are entirely confined to the bloodstream, bone marrow, and spleen. The genome of the most lethal human species, , along with that of murine malaria , was completed initially. Chronic parasitemia causes chronic sequelae or permanently selects for genetic disorders which protect from severe malaria disease but cause other human disease, such as sickle cell anemia. , in addition to the classic triad of fever, anemia, and spenomegaly, can cause reversible dysfunction of almost any organ, unless malaria progresses to death. The human parasites increase destruction and decrease production of erythrocytes. The pathogenesis of cerebral malaria is multi-factorial and begins with sequestration of parasitized erythrocytes to brain endothelial cells in postcapillary venules. Chronic malaria antigen stimulation of the immune system by persistent parasitemia has been associated with oncogenic translocation by Epstein-Barr virus (EBV) to produce Burkitt’s lymphoma. The quinolines target hemozoin formation in the lipid environment of the acidic digestive vacuole and therefore are stage specific to the erythrocyte stages rather than to the gametocyte or liver stages. Acute malaria is entirely preventable and can be completely curable in settings with rapid accurate diagnosis and effective chemotherapy.

Citation: Sullivan, Jr. D, Gandhi N. 2009. Malaria, p 259-274. In Fratamico P, Smith J, Brogden K (ed), Sequelae and Long-Term Consequences of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555815486.ch15

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Figures

Image of Figure 1.
Figure 1.

Surface changes of infected trophozoite-stage erythrocyte. The normal erythrocyte (left) has a smooth surface and minimizes its volume with the biconcave disc. In contrast, the infected trophozoite-stage erythrocyte has been transformed to contain knobs which act as ligands to host receptors on endothelial cells or leukocytes.

Citation: Sullivan, Jr. D, Gandhi N. 2009. Malaria, p 259-274. In Fratamico P, Smith J, Brogden K (ed), Sequelae and Long-Term Consequences of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555815486.ch15
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Image of Figure 2.
Figure 2.

Malaria fever curves. Typical fever curves from patients with or tertian malaria (A), or quotidian malaria (B), and quartan malaria (C), with temperatures every 48, 24 and 72 h.

Citation: Sullivan, Jr. D, Gandhi N. 2009. Malaria, p 259-274. In Fratamico P, Smith J, Brogden K (ed), Sequelae and Long-Term Consequences of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555815486.ch15
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Image of Figure 3.
Figure 3.

Imported malaria cases in the United States and the United Kingdom from 1966 to 2005. Total number of malaria cases from the United Kingdom (filled triangles) and the United States (filled squares) and total deaths in the United Kingdom (empty triangles) and the United States (empty squares). In the United States, total civilian cases (filled circles) outnumber military cases (empty circles) almost 10-fold.

Citation: Sullivan, Jr. D, Gandhi N. 2009. Malaria, p 259-274. In Fratamico P, Smith J, Brogden K (ed), Sequelae and Long-Term Consequences of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555815486.ch15
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Image of Figure 4.
Figure 4.

Onset of malaria case presentation, 1992 to 2005. The time to clinical presentation in months after travel by species, with (solid bar), (hatched bar), (stippled bar), and (vertical bar). Values are averages of 12 years with standard deviations of the means.

Citation: Sullivan, Jr. D, Gandhi N. 2009. Malaria, p 259-274. In Fratamico P, Smith J, Brogden K (ed), Sequelae and Long-Term Consequences of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555815486.ch15
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Image of Figure 5.
Figure 5.

Age-dependent prevalence of severe malaria and deaths. (A) Increasing how often the mosquitoes deliver an infectious bite or the entomologic inoculation rate determines an age-dependent pattern for severe disease, anemia, cerebral malaria, or renal disease, varying from holoendemic (parasite prevalence greater than 60 to 70%), hyperendemic (parasite prevalence between 50 to 70%), mesoendemic (parasite prevalence between 20 and 50%), and hypoendemic (parasite prevalence less than 10%) forms of malaria. The entomologic inoculation rate can vary from 1 to over 1,000 each year. (B) Peak prevalence in a region where malaria is holoendemic follows by a few years the peak risk period for deaths, which is under age 5.

Citation: Sullivan, Jr. D, Gandhi N. 2009. Malaria, p 259-274. In Fratamico P, Smith J, Brogden K (ed), Sequelae and Long-Term Consequences of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555815486.ch15
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