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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]
  • 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]
  • 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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Last updated: June 6, 2020