Inflammatory joint disease can develop following an extra-articular infection. The term reactive arthritis was coined in order to differentiate this arthritis, which is often characterized by lack of culturable organisms in the joint, from septic arthritides. Bacteria known to trigger reactive arthritis include Campylobacter, Chlamydia, Salmonella, Shigella and Yersinia. Demonstration of bacteria or bacterial macromolecules in the joint has elicited the idea that reactive arthritis is a sterile process induced and maintained by antigenic material in the synovium. Continued synthesis of antigens to maintain synovial inflammation probably requires establishment of persistent bacterial infection in the joint, or at the primary site of infection. In the case of Chlamydia trachomatis, viable, metabolically-active organisms have been demonstrated to exist for extended periods in the joints of patients with reactive arthritis. In this chapter, we review the aetiological agents, and their molecular biology and phagocyte-host interactions, that are involved in reactive arthritis and spondylarthropathy.