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Essays > Malaria (October 19, 1999 by Pat Heyman)
"It canna be malaria. Something else."
"The island’s accursed."
"Now you’re talking like a woman, Culum."
"The fever wasn’t here before the coolies. Get rid of the coolies and you’ll be rid of the plague. They’re carrying it with them. They’re doing it."
"How do we know that? I’ll admit it started in the coolie lines. And I’ll agree they live in the low-lying parts. And I’ll agree that as far as we know you can only get malaria by breathing the poisoned night air. But why is there only fever in the valley? Is it only Happy Valley that’s got bad air? Air’s air, for the love of Christ, and there’s a fine breeze blowing there most of the day and night. It does na make sense."
"It makes very good sense. It’s the will of God."
"A pox on that for an answer."
"I’ll thank you not to blaspheme."
"And I’ll thank you to remember that not so many years ago men were burned at the stake just for saying the earth went round the sun! It’s na the will of God!" –Tai-Pan, James Clavell (1966)
- Anemia and reticulocytosis:
- The primary cause for morphological changes in malaria is the destruction of erythrocytes. Their destruction causes a hemolytic anemia as well as anemia of chronic disease. The body responds by accelerating erythrocyte production and patients with malaria may exhibit chronic reticulocytosis. Individuals with hemoglobinopathies—particularly Sickle Cell Anemia and beta-thalassemia—have fewer symptoms and morphological changes at every level. This is probably due to a difficulty in digesting hemoglobin.
- Splenic enlargement:
- The first organ to show morphological changes is the spleen. Changes in the spleen can be seen as early as two weeks after infection, but the size of the spleen is not a good indicator of infection time. The spleen actively participates in the destruction of red blood cells and hematopoiesis; malaria also results in the hyperplasia of splenic lymphocytes and macrophages. So with stimulation of both splenic activities, splenomegaly is common. Individuals with malaria are at risk for splenic rupture with very small amounts of trauma. (Aikawa, 1980).
- Liver enlargement:
- Hepatomegaly in malaria seems to be associated with the level of nutrition, but can occur in well-nourished individuals. Kupfer cells are hypertrophied and contain parasite infested erythrocytes. Liver changes are not associated with the sporozoite infection (besides the initial destruction of a few parenchymal cells) (Russell**). Endothelial cells in the sinusoids transform into Kupfer cells and rapidly divide to increase the number macrophages (Aikawa, 1980). Parasitized red blood cells adhere to the sinusoid endothelium, causing slowed blood flow through the liver, resulting in portal hypertension, ischemia, and eventually focal necrosis. Fatty infiltration can be found throughout the liver, especially around the centrilobular vein. As the disease goes on, phagocytes become rounded instead of elongated and can be found floating free in the sinusoid. The liver eventually turns black from the deposition of malaria pigment (hemozosin).
- Capillary Occlusion and Cerebral Malaria:
- Cerebral malaria is the most dangerous form of malaria, and most U.S. deaths from malaria in World War II resulted from this complication. Cerebral malaria is an indirect complication arising from capillary occlusion. Agglutinated parasitized erythrocytes mass together forming a plug. All malarias cause some occlusion of capillaries, but only P. falciparum malaria causes the erythrocyte mass and its cause is not understood. The occlusions can occur in any system, but brain occlusions are the most dangerous (Russell, 1963).
- Renal Pathology:
- Renal changes vary with the species of Plasmodium, but generally speaking, malaria can cause nephrotic syndrome and glomerulonephritis. Both are associated with changes in the basement membrane, which begins to thicken and become less elastic (Aikawa, 1980).
- Pulmonary changes:
- The most important pulmonary change is sudden, massive pulmonary edema, most likely caused by increased hydrostatic pressure as blood flow through the lungs decrease (Dunn and Palmer, 1998).
Etiology
Pathogenesis
Morphology
Clinical Manifestations