The culminating step of the intraerythrocytic development of Plasmodium 
falciparum, the causative agent of malaria, is the spectacular release of 
multiple invasive merozoites on rupture of the infected erythrocyte membrane. 
This work reports for the first time that the whole process, taking place in 
time scales as short as 400 milliseconds, is the result of an elastic 
instability of the infected erythrocyte membrane. Using high-speed differential 
interference contrast (DIC) video microscopy and epifluorescence, we demonstrate 
that the release occurs in 3 main steps after osmotic swelling of the infected 
erythrocyte: a pore opens in ~ 100 milliseconds, ejecting 1-2 merozoites, an 
outward curling of the erythrocyte membrane is then observed, ending with a fast 
eversion of the infected erythrocyte membrane, pushing the parasites forward. It 
is noteworthy that this last step shows slight differences when infected 
erythrocytes are adhering. We rationalize our observations by considering that 
during the parasite development, the infected erythrocyte membrane acquires a 
spontaneous curvature and we present a subsequent model describing the dynamics 
of the curling rim. Our results show that sequential erythrocyte membrane 
curling and eversion is necessary for the parasite efficient angular dispersion 
and might be biologically essential for fast and numerous invasions of new 
erythrocytes.