MICROBIOLOGY

Malaria is caused by intraerythrocytic Plasmodium protozoa belonging to the Apicomplexa group and is transmitted by night-time or pre-dawn-biting female Anopheles sp. mosquitoes.

• In 2018, the CDC confirmed 1,823 cases of malaria in the U.S. Most cases originated in Africa (85%); of those cases, 70% were imported from West Africa.[15]
• Since June of 2023, 9 malaria cases were locally acquired by mosquito-borne transmission in the U.S.: 1 of P. falciparum in Maryland, 7 of P. vivax in Florida, and 1 of P. vivax in Texas.[8]
  
  • P. falciparum causes 70% of cases in the U.S.
    • P. falciparum invades red blood cells (RBCs) of all life stages and causes the most severe and lethal disease.
    • Endothelial cytoadherence causes infected RBCs to sequester in the microvasculature and damage the heart, brain, kidney, lung, and placenta.[19]
  • P. vivax causes 10% of cases in the U.S.
    • P. vivax is the most common type of Plasmodium spp. diagnosed outside sub-Saharan Africa and survives at lower temperatures and higher elevations.
    • It preferentially invades reticulocytes via Duffy binding proteins and reticulocyte binding proteins.[22]
    • Due to its persistence in hepatocytes for months to years as hypnozoites, eradicating P. vivax requires treatment to eliminate both stages: liver stage (hypnozoite) and blood stage (schizont).
  • P. ovale causes 5% of cases in the U.S.
    • Due to hepatocyte persistence for months to years, eradicating P. ovale requires liver and blood stages treatment.
  • P. malariae causes 3% of cases in the U.S.
    • This species infects older RBCs and causes low-level parasitemia and chronic, low-grade infection.
  • P. knowlesi is a monkey malaria parasite that causes human malaria in Southeast Asia and morphologically resembles P. malariae.
    • Both uncomplicated and severe diseases occur at low parasitemia. IV artesunate is recommended to treat parasitemia > 15,000/μL.[21]
• Life cycle: Female anopheline mosquito bites a human host and injects sporozoites, which invade hepatocytes and mature into schizonts (exo-erythrocytic schizogony). Schizonts rupture and release merozoites that invade RBCs. In RBCs, ring-stage trophozoites mature into blood schizonts (erythrocytic schizogony), followed by rupture of RBCs and a new cycle of RBC invasion.