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 U.S.
  
  • 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.