The pathogen Listeria monocytogenes has an extraordinary intracellular life cycle, based on adaption to and exploitation of normal cellular mechanisms. Extracellular organisms induce their own phagocytosis, followed by destruction of the phagosomal membrane. Cytoplasmatic bacteria organize the intracellular protein actin into "comet tails", and thus gain motility. In contact with the plasma membrane, motile bacteria induce a pseudopodium, corresponding to an invagination of the plasma membrane of the neighbouring cell. Eventually, the pseudopodium is engulfed by the neighbouring cell, creating a double membrane vacuole. L. monocytogenes destroys the double membrane, and escapes into the cytoplasm. This article reviews the molecular biology of Listeria infection, and how research in this field has yielded increased insight into normal cellular processes. Finally, we propose that the neuroinvasive properties of L. monocytogenes is caused by actin-dependent transport within axons from the periphery to the central nervous system.