Plasmodium falciparum
Aralık 08, 2018
Plasmodium falciparum
Plasmodium falciparum
• Multiple sporozoites can infect a single erythrocyte, and show multiple infections of cells with small ring forms.
• The trophozoite is often seen in the host cells at the very edge or periphery of cell membrane at accole position.
• Occasionally, reddish granules known as Maurer’s dots are observed
• Mature (large) trophozoite stages and schizonts are rarely seen in blood films, because their forms are sequestered in deep capillaries, liver and spleen.
• Peripheral blood smears characteristically contain only young ring forms and occasionally crescent shaped gametocytes.
Epidemiology
Clinical Features
Of all the four Plasmodia, P. falciparum has the shortest incubation period, which ranges from 7 to 10 days. After the early flu-like symptoms, P.falciparum rapidly produces daily (quotidian) chills and fever as well as severe nausea, vomiting and diarrhea. The periodicity of the attacks then becomes tertian (36 to 48 hours), and fulminating disease develops. Involvement of the brain (cerebral malaria) is most often seen in P.falciparum infection. Capillary plugging from an adhesion of infected red blood cells with each other and endothelial linings of capillaries causes hypoxic injury to the brain that can result in coma and death. Kidney damage is also associated with P.falciparum malaria, resulting in an illness called “black water” fever. Intravascular hemolysis with rapid destruction of red blood cells produces a marked hemoglobinuria and can result in acute renal failure, tubular necrosis, nephrotic syndrome, and death. Liver involvement is characterized byabdominal pain, vomiting of bile, hepatosplenomegally, severe diarrhea, and rapid dehydration.
P.falciparum occurs almost exclusively in tropical and subtropical regions. Weather (rainfall, temperature & humidity) is the most obvious cause of seasonality in malaria transmission. To date, abnormal weather conditions are also important causes of significant and widespread epidemics. Moreover, drug-resistant infection of P.falciparum is the commonest challenge in many parts of the world. In Ethiopia, even though all the four species of plasmodium infecting man have been recorded, P.falciparum is the one that most causes the epidemic disease and followed by vivax and malariae. P.ovale is rare. Infection rates in Ethiopia are 60%, 40%, 1%, and <1% for P. falciparum, P. vivax, P. malariae, and P. ovale, respectively.
Of all the four Plasmodia, P. falciparum has the shortest incubation period, which ranges from 7 to 10 days. After the early flu-like symptoms, P.falciparum rapidly produces daily (quotidian) chills and fever as well as severe nausea, vomiting and diarrhea. The periodicity of the attacks then becomes tertian (36 to 48 hours), and fulminating disease develops. Involvement of the brain (cerebral malaria) is most often seen in P.falciparum infection. Capillary plugging from an adhesion of infected red blood cells with each other and endothelial linings of capillaries causes hypoxic injury to the brain that can result in coma and death. Kidney damage is also associated with P.falciparum malaria, resulting in an illness called “black water” fever. Intravascular hemolysis with rapid destruction of red blood cells produces a marked hemoglobinuria and can result in acute renal failure, tubular necrosis, nephrotic syndrome, and death. Liver involvement is characterized byabdominal pain, vomiting of bile, hepatosplenomegally, severe diarrhea, and rapid dehydration.
Treatment
Because chloroquine – resistant stains of P.falciparum are present in many parts of the world, infection of P.falciparum may be treated with other agents including mefloquine, quinine, guanidine, pyrimethamine – sulfadoxine, and doxycycline. If the laboratory reports a mixed infection involving P.falciparum and P.vivax, the treatment must eradicate not only P.falciparum from the erythrocytes but also the liver stages of P.vivax to avoid relapses provided that the person no longer lives in a malaria endemic area.
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