Check to include Clear and return to Menu Close Closed captions. Press the spacebar to toggle captions on and off. Continue Continue Exit Filter FINISH finish Definition definition Glossary Terms Menu Please rotate your device NEXT next Notes Notes Bio More info Captions pause play Send an email PREV previous Question List replay Resources resources Restart Search... search Search in: Search Results Skip Navigation. Hit enter to return to the slide. Slide Text SUBMIT ALL submit all SUBMIT submit volume A combination of artemisinin or one of its derivatives with an antimalarial drug or antimalarial drugs of a different class. The life cycle of the malaria parasite in a host from merozoite invasion of red blood cells to schizont rupture (merozoite → ring stage → trophozoite → schizont → merozoites). Duration is approximately 48 hours in Plasmodium falciparum, P. ovale, and P. vivax and 72 hours in P. malariae. The presence in host red blood cells of asexual parasites. The level of asexual parasitemia can be expressed in several different ways: the percentage of infected red blood cells, the number of infected cells per unit volume of blood, the number of parasites seen in one microscopic field in a high-power examination of a thick blood film, or the number of parasites seen per 200 to 1000 white blood cells in a high-power examination of a thick blood film. Severe P. falciparum malaria with cerebral manifestations, usually including coma (Glasgow Coma Scale <11, Blantyre Coma Scale <3). Malaria with coma persisting for >30 minutes after a seizure is considered to be cerebral malaria. A combination of two or more different classes of antimalarial medicines with unrelated mechanisms of action. Elimination of the symptoms and asexual blood stages of the malaria parasite that caused the patient or caregiver to seek treatment. Resistance to antimalarial drugs is the ability of a parasite strain to survive and/or to multiply despite the administration and absorption of a medicine given in doses equal to or higher than those usually recommended but within the tolerance of the subject, provided drug exposure at the site of action is adequate. Resistance to antimalarial drugs arises because of the selection of parasites with genetic mutations or gene amplifications that confer reduced susceptibility. Sexual stages of malaria parasites present in the host red blood cells. Persistent liver stages of P. vivax and P. ovale malaria that remain dormant in host hepatocytes for an interval (most often 3 to 45 weeks) before maturing to hepatic schizonts. These schizonts then burst and release merozoites, which infect red blood cells. Hypnozoites are the source of relapses. A dark brown granular pigment formed by malaria parasites as a byproduct of hemoglobin catabolism. The pigment is evident in mature trophozoites and schizonts. They also may be present in white blood cells (peripheral monocytes and polymorphonuclear neutrophils) and in the placenta. Parasites released into the host bloodstream when a hepatic or erythrocytic schizont bursts. These parasites then invade the red blood cells. Antimalarial treatment with a single medicine (either a single active compound or a synergistic combination of two compounds with related mechanism of action). A genus of protozoan vertebrate blood parasites that includes the causal agents of malaria. Plasmodium falciparum, P. malariae, P. ovale, and P. vivax cause malaria in humans. Human infections with the monkey malaria parasite P. knowlesi also have been reported from forested regions of Southeast Asia. The life cycle of the malaria parasite when it first enters the host. Following inoculation into a human by the female anopheline mosquito, sporozoites invade parenchyma cells in the host liver and multiply within the hepatocytes (liver cells) for 5 to 12 days, forming hepatic schizonts. These schizonts then burst, liberating merozoites into the bloodstream, which subsequently invade red blood cells. In P. vivax and P. ovale infections only, a radical cure is a cure as previously defined plus prevention of relapses by killing hypnozoites. An antigen-based stick, cassette, or card test for malaria in which a colored line indicates that plasmodial antigens have been detected. The recurrence of asexual parasitemia after treatment of the infection with the same infection that caused the original illness. This recurrence results from incomplete clearance of parasitemia because of inadequate or ineffective treatment. It therefore is different from a relapse in P. vivax and P. ovale infections and differs from a new infection or re-infection (as identified by molecular genotyping in endemic areas). The recurrence of asexual parasitemia following treatment that can be caused by a recrudescence, a relapse (in P. vivax and P. ovale infections only), or a new infection. The recurrence of asexual parasitemia in P. vivax and P. ovale malaria deriving from persisting liver stages. Relapse occurs when the blood stage infection has been eliminated but hypnozoites persist in the liver and mature to form hepatic schizonts. After variable intervals of weeks to months, the hepatic schizonts burst and liberate merozoites into the bloodstream. Young, usually ring-shaped intra-erythrocytic malaria parasites, before malaria pigment is evident under microscopy. Mature malaria parasites in host liver cells (hepatic schizonts) or red blood cells (erythrocytic schizonts) that are undergoing nuclear division. This process is called schizogony. Resistance to antimalarial drugs emerges and spreads because of the selective survival advantage that resistant parasites have in the presence of antimalarial drugs to which they are resistant. Selection pressure describes the intensity and magnitude of the selection process; the greater the proportion of parasites in a given parasite population exposed to concentrations of an antimalarial that allows proliferation of resistant, but not sensitive, parasites, the greater the selection pressure. Hemoglobin concentration of <5 g/100 mL (hematocrit <15%). Acute falciparum malaria with signs of severity and/or evidence of vital organ dysfunction. Motile malaria parasites that are infective to humans, inoculated by a feeding female anopheline mosquito. The sporozoites invade hepatocytes. The intensity of malaria transmission measured by the frequency with which people living in an area are bitten by anopheline mosquitoes carrying sporozoites. This often is expressed as the annual entomological inoculation rate (EIR), which is the number of inoculations of malaria parasites received by one person in one year. Stage of development of the malaria parasites within host red blood cells from the ring stage and before nuclear division. Mature trophozoites contain visible malaria pigment. Symptomatic infection with malaria parasitemia without signs of severity and/or evidence of vital organ dysfunction. Number of new infections the population of a given vector would distribute per case per day at a given place and time, assuming conditions of non immunity.