Legionella species are environmental bacteria and accidental human pathogens that can cause severe pneumonia termed Legionnaires’ disease. These bacteria utilise a Type IVB Dot/Icm secretion system to translocate effectors into the host cell. These effectors manipulate host cell trafficking pathways which enables the establishment of a replicative vacuole, the Legionella-containing vacuole (LCV). Our understanding of the development and dynamics of this vacuole is based on extensive analysis of Legionella pneumophila. However, little is known about the LCV of non-pneumophila species of Legionella. We have characterised the Legionella longbeachae replicative vacuole and demonstrated that, despite important genomic differences, during early infection the host Rab GTPase, Rab1, and the v-SNARE Sec22b are recruited to the longbeachae-LCV with similar dynamics to the recruitment of these host proteins to the pneumophila-LCV. We constructed a Dot/Icm deficient L. longbeachae strain by deleting dotB and demonstrated that this mutant was attenuated for intracellular growth in THP-1 macrophages. Using this mutant and a TEM-1 ß-lactamase reporter assay, we demonstrated the Dot/Icm-dependent translocation of a novel family of proteins, the Rab-like effectors (Rle). Immunofluorescent analysis confirmed that these proteins enter the host cell during infection, with RleA and RleC present on the longbeachae-LCV. Future work will explore the mechanism through which L. longbeachae recruits Rab1 and Sec22b to the LCV, and the roles of the Rles during infection.