Chapter 20. Reactive Arthritis

John D. Carter

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Reactive Arthritis at a Glance

Reactive arthritis is one of the spondyloarthritides. It is an inflammatory syndrome that typically begins 1–4 weeks after certain genitourinary or gastrointestinal infections.
Most patients do not have the “classic triad” of symptoms (synovitis, urethritis, and conjunctivitis) and other organs are often involved (namely the skin).
Key clinical features are asymmetric arthritis of a few joints, most often large joints of the lower extremities, often accompanied by axial arthritis and enthesitis typically at the Achilles tendon or plantar fascia and sacroiliac joints.
Psoriasiform lesions on the soles—keratoderma blenorrhagicum—or penis—circinate balanitis—occur in one-third of patients and inflammatory eye disease is present in a similar proportion. Urethritis may occur with or without urogenital infection.
HLA-B27 appears to increase disease susceptibility and chronicity of reactive arthritis, but recent data suggest it might portend more fulminate symptoms thereby serving as a diagnostic bias.
Chlamydia, Salmonella, Campylobacter, Shigella, and Yersinia are definitive triggers of reactive arthritis, but other infections may also act as initiators.
Although reactive arthritis often is self-limited in weeks to months, as many as 30%–50% of patients will develop chronic disease that often waxes and wanes.

Reactive arthritis (ReA) is an inflammatory syndrome that results after certain genitourinary or gastrointestinal symptoms. The most common inciting infections include Chlamydia trachomatis, Salmonella, Shigella, Campylobacter, and Yersinia. The term reactive arthritis was introduced in 1973 to describe this type of arthritis that occurs after a triggering infection.1 There is considerable ambiguity in the literature in terms of the nomenclature of this condition for many terms and eponyms have been utilized. In 1942 two Harvard researchers, Bauer and Engelmann, recognized a case of ReA and upon their review of the literature they discovered that Hans Reiter had described this same syndrome in 1916.2 Reiter had described a German officer who developed the clinical triad of arthritis, nongonococcal urethritis, and conjunctivitis after an episode of acute dysentery. It was at that point that Bauer and Engelmann coined the term Reiter syndrome and this eponym was often used to describe the condition.

In recent years, the eponym Reiter syndrome became problematic for several reasons. First, most clinicians often demanded that a patient have the classic triad of symptoms involving the synovium, urethra, and conjunctiva before the diagnosis would be made. It is now known that most patients with ReA do not have the complete triad of symptoms.3 Further, many common features of ReA are not included in this “classic triad” including involvement of the skin and mucous membranes as well as other parts of the eye, namely the anterior uveal tract. More troubling is the acts of the man from which the eponym was coined. Although Hans Reiter was an erudite intellectual and a brilliant investigator who performed many useful studies early in his career including the discovery of the spirochete that causes leptospirosis and a nonpathogenic strain of Treponema, some of ...

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