Plasmodium
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MICROBIOLOGY
- Malaria is caused by intraerythrocytic Plasmodium protozoa belonging to the Apicomplexa group, transmitted by night-time or pre-dawn biting female Anopheles sp. mosquitoes.
- CDC confirmed 2,078 U.S. cases in 2016, a 36% increase compared to 2105 (N=1,524), and the highest number of cases since 1972.[2] No case in 2016 was acquired by mosquito-borne transmission in the US.
- P. falciparum (77% of U.S. cases)
- Invades RBCs of all stages
- Causes the most severe and lethal illness
- Endothelial cytoadherence causes mature-staged infected RBCs to sequester in the microvasculature and damage the heart, brain, kidney, lung, placenta.[15]
- P. vivax
- The most common type outside of sub-Saharan Africa survives at lower temperatures and higher elevations.
- Preferentially invades reticulocytes via Duffy binding proteins and reticulocyte binding proteins.
- Less prevalent in sub-Saharan Africa due to the Duffy blood group antigen-negative populations.
- Cases diagnosed in Duffy-negative populations attributed to improved detection versus recent adaptation.[17]
- Persists in hepatocytes as hypnozoites for months to years
- Eradication requires treatment of both liver (hypnozoite) and blood (schizont) stages.
- P. ovale
- Can persist in hepatocytes as hypnozoites for months to years
- Eradication requires treatment of both liver and blood stages.
- P. malariae
- Infects older RBCs and causes low-level parasitemia and chronic, low-grade infection
- P. knowlesi: a monkey malaria parasite, causes human malaria in Southeast Asia, morphologically resembles P. malariae
- Both uncomplicated and severe diseases occur at low parasitemia. IV artesunate recommended for parasitemia > 15,000/μL.[16]
- P. falciparum (77% of U.S. cases)
- Life cycle: female anopheline mosquito bites a human host and injects sporozoites, which invade hepatocytes and mature into schizonts (exo-erythrocytic schizogony), which rupture and release merozoites that invade RBCs. In RBCs, ring stage trophozoites mature into schizonts (erythrocytic schizogony), followed by rupture of RBCs and a new cycle of RBC invasion.
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MICROBIOLOGY
- Malaria is caused by intraerythrocytic Plasmodium protozoa belonging to the Apicomplexa group, transmitted by night-time or pre-dawn biting female Anopheles sp. mosquitoes.
- CDC confirmed 2,078 U.S. cases in 2016, a 36% increase compared to 2105 (N=1,524), and the highest number of cases since 1972.[2] No case in 2016 was acquired by mosquito-borne transmission in the US.
- P. falciparum (77% of U.S. cases)
- Invades RBCs of all stages
- Causes the most severe and lethal illness
- Endothelial cytoadherence causes mature-staged infected RBCs to sequester in the microvasculature and damage the heart, brain, kidney, lung, placenta.[15]
- P. vivax
- The most common type outside of sub-Saharan Africa survives at lower temperatures and higher elevations.
- Preferentially invades reticulocytes via Duffy binding proteins and reticulocyte binding proteins.
- Less prevalent in sub-Saharan Africa due to the Duffy blood group antigen-negative populations.
- Cases diagnosed in Duffy-negative populations attributed to improved detection versus recent adaptation.[17]
- Persists in hepatocytes as hypnozoites for months to years
- Eradication requires treatment of both liver (hypnozoite) and blood (schizont) stages.
- P. ovale
- Can persist in hepatocytes as hypnozoites for months to years
- Eradication requires treatment of both liver and blood stages.
- P. malariae
- Infects older RBCs and causes low-level parasitemia and chronic, low-grade infection
- P. knowlesi: a monkey malaria parasite, causes human malaria in Southeast Asia, morphologically resembles P. malariae
- Both uncomplicated and severe diseases occur at low parasitemia. IV artesunate recommended for parasitemia > 15,000/μL.[16]
- P. falciparum (77% of U.S. cases)
- Life cycle: female anopheline mosquito bites a human host and injects sporozoites, which invade hepatocytes and mature into schizonts (exo-erythrocytic schizogony), which rupture and release merozoites that invade RBCs. In RBCs, ring stage trophozoites mature into schizonts (erythrocytic schizogony), followed by rupture of RBCs and a new cycle of RBC invasion.
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