SignificanceThe presence of more than two centrosomes is a hallmark of many types of cancer, including cervical and ovarian cancers of whichChlamydia trachomatis(C.t.) infection is a significant risk factor. Despite the importance of this problem, howC.t.orchestrates these drastic changes in the host cell remains poorly understood. Here, we describe howC.t.uses the effector protein CteG to drive centrosome amplification via manipulation of a key regulator of centriole duplication, centrin-2. This work begins to define howC.t.induces centrosome amplification to promote its replication while potentially contributing to devastating long-term negative consequences for normal host physiology. Furthermore, it may help elucidate why chlamydial infection leads to an increased cancer risk.