Reactive arthritis (ReA) is a systemic inflammatory disorder characterized by aseptic arthritis, which is triggered by an infection at a distant site, occurring in a genetically susceptible person. The term ReA has been used by some authors to refer to only genitourinary and gastrointestinal infections caused by specific agents, with the term postinfectious arthritis used for other aseptic forms of arthritis following an infection. Despite clinical differences and different treatments and mechanisms, most authors use the term ReA for both entities, however. Being considered as a member of spondyloarthritis group, it shares clinical, radiographic, and laboratory features with the other subgroups of the disease.
The mechanisms of ReA are under intensive research. Environmental and genetic factors are certainly involved. The human leukocyte antigen (HLA)-B27 has been described in 30–80% of patients with this condition. However, several bacteria have been described as causing ReA independently of the presence of HLA-B27, as well as viral, parasitic, and fungal infections. The exact role of HLA-B27 is still unclear.
There are no uniformly accepted diagnostic criteria for these conditions, and the diagnosis is essentially clinical. In this chapter several aspects of ReA and infection-associated arthritis, such as epidemiology, pathogenesis, clinical manifestations and treatment, will be discussed.