All Chlamydiae share a common dimorphic life cycle, where the bacteria alternates between the infectious but non-dividing elementary body (EB) form, and the non-infectious but replicative reticulate body (RB) form. Following internalization of EBs through a poorly defined endocytic process, the bacteria reside in a membrane-bound vacuole termed the inclusion, where they convert into RBs and replication occurs over 24–72 hr. RBs eventually redifferentiate back to EBs in an asynchronous manner, and are then released to infect neighboring cells (Di Russo Case and Samuel, 2016; Hybiske, 2015; Ward, 1983). The encapsulating inclusion membrane provides the primary interface between the bacteria and the host cell’s cytoplasm and organelles. From the initial stages of invasion until eventual bacterial egress the chlamydial inclusion is extensively modified by insertion of numerous Type-III secreted bacterial effector proteins called inclusion membrane proteins or ‘Incs’. The Incs modulate host trafficking and signaling pathways to promote bacterial survival at different stages, including cell invasion, inclusion membrane remodeling, avoidance of the host cell innate immune defense system, nutrient acquisition and interactions with other host cell organelles (Elwell et al., 2016; Moore and Ouellette, 2014; Rockey et al., 2002).