The mechanisms underlying ARDS are not entirely understood, but likely causes include endothelial dysfunction and altered capillary permeability because of parasitized erythrocyte adherence and sequestration and exaggerated host immune and inflammatory responses, particularly TNF-α, IL-1, IL-6, and IL-8.57, 58 However, ARDS can develop after apparently successful treatment and after the disappearance of parasites from the blood.11, 53 In these cases, ARDS may reflect persistence of inflammatory cytokines in the absence of any infected erythrocytes. This evidence concerns the gene IL6 and acute respiratory distress syndrome.