Orientia tsutsugamushi (Ot) is a mite-borne, obligate intracellular bacterium and a causative agent of the human disease scrub typhus. Ot targets a wide range of tissues, leading to CNS complications, multi-organ failure and mortality in severe cases. Previous investigation has focused on the initial stages of the Ot lifecycle, including entry into cells, intracellular motility and bacterial replication in the cytosol. However, it is not known how the bacterium exits host cells, nor how this process is induced. To address this, I have developed a microscopy-based assay to quantify bacterial maturation and egress. It is not known whether bacterial exit is purely time-dependent, or whether bacterial copy number impacts maturation, implying that bacteria may sense each other or conditions in the host cell. Using this assay, I show that initial bacterial number impacts maturation, with high MOI infections reaching a maturation state earlier. To address the question of whether bacteria need to be metabolically active to mature, I combine this assay with antibiotic treatments. I show that Ot require active bacterial protein synthesis to move to the cell periphery, but not to egress. It is unclear whether Ot maturation is triggered by intracellular conditions or by a maturation process intrinsic to bacteria. To untangle this complexity, I use a panel of chemical inhibitors to disrupt specific host and bacterial pathways. Preliminary results suggest that maturation may be triggered early by changes in nutrient availability or actin polymerisation; further work will focus on understanding how these changes induce Ot maturation.