a, Salmonella. Intracellular Salmonella reside and replicate within a vacuole known as the SCV (Salmonella-containing vacuole). Maintenance of this vacuole as a permissive environment for the bacteria involves altering normal vacuolar transport pathways. SifA is involved in the formation of tubular extensions to the SCV (Sifs) which, are involved in maintaining vacuolar integrity. Sifs form along microtubules and it is likely that Salmonella uses microtubules and their associated motor proteins to deliver membrane vesicles destined for fusion to the SCV, or to send out membranous SCV tentacles that fuse with vesicular compartments. An unknown SPI-2 effector mediates recruitment of actin to the SCV and is also involved in maintaining vacuolar integrity. This may involve recruitment and fusion of actin-containing or actin-propelled vesicles to the SCV. An actin coat may also protect the SCV from fusion with unfavourable compartments. SpvB modifies actin by ADP-ribosylation, and may be involved in a subsequent disassembly of actin at the SCV and other cellular sites, such as stress fibres. SseJ may be involved in membrane removal from the SCV, through budding or scission. b, Mycobacteria. Coronin is recruited to mycobacterial vacuoles during their formation. Retention of coronin on the vacuolar membrane may serve to protect the mycobacterial vacuole from undergoing unfavourable fusion events. Mycobacteria also disrupt the actin cytoskeleton, through an unknown mechanism. This disruption causes the vacuole to arrest during phagosomal maturation at a stage where it can fuse with early endosomes but not lysosomes. The mechanisms involved in this maturation arrest have not been described, but may involve downregulation of actin-mediated vesicle rocketing.