Enteroinvasive pathogens, such as Shigella and Salmonella, induce their uptake into non-phagocytic epithelial cells through the injection of effectors by the type-3-secretion system. The bacteria are ingested in tight bacterial-containing vacuoles (BCVs) that are surrounded by in situ formed infection-associated macropinosomes (IAMs). In contrast to previous reports, we have recently shown via novel 3D imaging techniques that macropinocytosis is not required for the entry of these bacterial pathogens, however the IAMs regulate their subsequent intracellular trafficking. In the case of Shigella, IAMs do not fuse with the BCV, and contact between these two compartments results in the destabilization of the BCV and membrane rupture. In the case of Salmonella two scenarios occur; IAMs either fuse with the BCV, which results in the generation of the Salmonella containing vacuole surrounded by Salmonella induced filaments (Sifs). Simple contact between IAMs and the BCV also promote vacuolar rupture in the case of Salmonella leading to cytoplasmic hyper-replication. Interestingly, BCV contacts with the surrounding compartments also dictates intravuolar bacterial growth or dormancy. We have performed ultra-structural studies, combined with dynamic imaging and proteomics of the involved compartments to identify the molecules that drive these complex interactions. This has shown a regulatoy network of Rab GTPases, the Exocyst complex, and SNAREs that is hijacked by injected bacterial effectors. I will describe how these factors determine the intracellular niche formation for both, Shigella and Salmonella.