The statement that arthritides developing after a distant infection are called reactive or post-infectious is contrary to the proposal that they also should be called ReA. However, several other arthritides fulfil the original definition, which has led to the suggestion that ReA can be divided into a B27-associated and non- associated form. The disease was classified as a subgroup within the family of spondyloarthritis, also termed reactive spondyloarthritis. After discovery of the association between HLA-B27 and ReA, the term “HLA-B27 associated reactive arthritides” became common, preferentially following infections with Enterobacteria and Chlamydia. The term ReA was introduced by Ahvonen and colleagues to describe acute arthritis triggered by an extra-articular bacterial infection, often in the gastrointestinal or urogenital tract, and in which the causative organism cannot be cultured from synovial specimens. This group consists of inflammatory arthritis triggered by microbes, where neither the organism nor its product or specific antigen is established in the joint. This group includes reactive arthritis (ReA), with the infection originating in the urogenital or gastrointestinal system causing inflammatory joint disease however, the microbes are usually not detected in the joint. This group comprises post-infectious arthritis with bacterial antigens being detected in the joint. This group includes septic or infectious arthritis with the causative organism identified in joints secondary to an infection elsewhere in the body. The World Health Organization, in association with the Arthritis and Rheumatism Research Council, classified the relationship between joints and infection into the following four groups : The association between microbes and joints has attracted medical interest for decades and more, and that association remains a complex issue. Inclusion of these newly identified etiologic agents must necessitate increased research into the pathogenic mechanisms variously involved, which will engender important insights for treatment and management of ReA. Diagnostic procedures cannot be restricted to the well-known HLA-B27-associated group of ReA, but must also cover the large number of rare forms of arthritis following infections and vaccinations, as well as those elicited by the newly identified members of the ReA group summarized herein.

In view of the increasingly large spectrum of causative agents, diagnostic consideration for the disease must include the entire panel of post-infectious arthritides termed ReA. The most prominent new infectious agents implicated as causative in ReA are Staphylococcus lugdunensis, placenta- and umbilical cord–derived Wharton’s jelly, Rothia mucilaginosa, and most importantly the SARS-CoV-2 virus. Recent reports of ReA cover several rare causative microorganism such as Neisseria meningitides, Clostridium difficile, Escherichia coli, Hafnia alvei, Blastocytosis, Giardia lamblia, Cryptosporidium, Cyclospora cayetanensis, Entamoeba histolytica/dispar, Strongyloides stercoralis, β-haemolytic Streptococci, Mycobacterium tuberculosis, Mycoplasma pneumoniae, Mycobacterium bovis bacillus Calmette-Guerin, and Rickettsia rickettsii. Additional information is included on microbial products detected in the joint, as well as on the positivity of HLA-B27. Further, we include reports that present at least a hint of effective antimicrobial therapy for ReA as documented in case reports or in double-blind controlled studies. The discussion is set within the context of changing disease terminology, definition, and classification over time. We discuss the entire spectrum of microbial agents known to be the main causative agents of ReA, those reported to be rare infective agents, and those reported to be new candidates causing the disease. This article presents a comprehensive narrative review of reactive arthritis (ReA) with focus on articles published between 20.

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