Whereas bacterial pathogens take over the control of their host cell actin cytoskeleton by delivering an array of protein effectors through specialized secretion systems, promastigotes of the protozoan parasite Leishmania donovani rely entirely upon a cell surface glycolipid to achieve this feat. Here, we review recent evidence that L. donovani promastigotes subvert host macrophage actin dynamics during the establishment of infection and we discuss the potential mechanisms involved.