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| Malaria |
There are two stages of development of malaria, namely the exoerthrocitic stage and the erythrocitic stage. The exoeryhrocitic stage is the stage where infection occurs in the human liver system caused by the plasmodium parasite, while the erythrocitic stage is the stage of infection in red blood cells (erythrocytes).
After entering through the blood and reaching the human liver system, this parasite will multiply rapidly which then exits and infects red blood cells, which is the process that causes fever in malaria sufferers. Furthermore, the plasmodium parasite will continue to multiply in red blood cells which then come out to infect other red blood cells that are still healthy, this is what causes symptoms of fever or fluctuating fever in malaria sufferers.
Although the human spleen system can actually destroy red blood cells infected by parasites, the Plasmodium falciparum parasite can make red blood cells stick to small blood vessels by releasing adhesive proteins, so that infected red blood cells cannot enter the spleen system to be destroyed. With this ability, Plasmodium falciparum often becomes an acute malaria disease, due to the ability to attach infected red blood cells to the walls of small blood vessels simultaneously so that it can block blood circulation to the brain which often results in a coma in malaria sufferers.
In contrast, some plasmodium vivax or ovale parasites do not have a lethal tendency like Plasmdium falciparum, but have the ability to produce hypnosoites that remain active for months or even years. So that people with malaria caused by Plasmodium often experience new malaria relapses and relapses for several months or even years after being infected for the first time and is very difficult to eradicate completely from the infected human body.
The pathophysiology of malaria is not known with certainty. The pathophysiology of malaria is multifactorial and may be related to the following:
1. Erythrocyte destruction.
The destruction of erythrocytes is not only by rupture of erythrocytes containing parasites, but also by phagocytosis of erythrocytes containing parasites and those that do not contain parasites, causing anemia and tissue anoxia. With severe intravascular hemolysis, hemoglobinuria (blackwater fever) may occur and may result in renal failure.
2. Endotoxin-macrophage mediators.
During schizogony, erythrocytes containing parasites trigger endotoxin-sensitive macrophages to release various mediators that play a role in changes in the pathophysiology of malaria. Endotoxin is not present in the malaria parasite, probably from the gastrointestinal tract. The malaria parasite itself can release tumor necrosis factor (TNF). TNF is a monokine, found in the blood of animals and humans infected with the malaria parasite. TNF and other related cytokines cause fever, hypoglycemia and adult respiratory distress syndrome (ARDS) with sequestration of neutrophil cells in the pulmonary vasculature. TNF can also destroy Plasmodium falciparum in vitro and can increase the attachment of parasitized erythrocytes to the capillary endothelium. Serum TNF concentrations in children with acute falciparum malaria are directly related to mortality, hypoglycemia, hyperparasitemia and disease severity.
3. Sequestration of infected erythrocytes.
Erythrocytes infected with Plasmodium falciparum at an advanced stage can form knobs on their surface. These protrusions contain malaria antigens and react with malaria antibodies and are related to the affinity of erythrocytes containing Plasmodium falciparum to the endothelium of blood capillaries in the internal organs, so that schizogony takes place in the internal circulation, not in the peripheral circulation. Infected erythrocytes adhere to the endothelium of the blood capillaries and form a clot (sludge) that blocks the capillaries in the internal organs.
Proteins and fluids seep through the leaky capillary membrane (become permeable) and cause tissue anoxia and edema. Sufficiently widespread tissue anoxia can cause death. Histidine-rich protein P. falciparum was found in the protrusions, there were at least four kinds of protein for the cytoplasm of erythrocytes infected with Plasmodium P. falciparum.
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