The Mechanisms of Parasite Clearance after Antimalarial Treatment ofPlasmodium falciparumMalaria
Author(s) -
Kesinee Chotivanich,
Rachanee Udomsangpetch,
Arjen M. Dondorp,
Tyrone Williams,
Brian Angus,
J. A. Simpson,
S. Pukrittayakamee,
S. Looareesuwan,
Chris Newbold,
Nicholas J. White
Publication year - 2000
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/315718
Subject(s) - artesunate , malaria , quinine , plasmodium falciparum , artemisinin , parasite hosting , biology , red blood cell , immunology , clearance , hematocrit , parasitemia , pharmacology , virology , medicine , endocrinology , computer science , urology , world wide web
Studies were conducted to determine how malaria parasites are cleared from the blood after antimalarial treatment. Neither artesunate nor quinine decreased parasitized red cell deformability or increased antibody binding. In acute falciparum malaria, ring-infected erythrocyte surface antigen (RESA) was observed in erythrocytes without malaria parasites (RESA-red blood cell [RBC]), indicating prior parasitization. In uncomplicated malaria, RESA-RBC numbers increased significantly (P=.002) within 24 h of starting artesunate but rose much more slowly (7 days) after quinine treatment. In severe malaria, RESA-RBC increased significantly (P=. 001) within hours of starting artesunate but not with quinine treatment (P=.43). RESA-RBCs were not produced after drug treatment of malaria parasite cultures in vitro. Rapid malaria parasite clearance after treatment with artemisinin derivatives results mainly from the extraction of drug-affected parasites from host erythrocytes-presumably by the spleen. This explains why the fall in hematocrit after treatment of hyperparasitemia is often less than that predicted from loss of parasitized cells.
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