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Reactive arthritis (ReA) is an autoimmune condition that develops in response to an infection in another part of the body. Coming into contact with bacteria and developing an infection can trigger reactive arthritis.[1] It has symptoms similar to various other conditions collectively known as “arthritis,” such as rheumatism. It is caused by another infection and is thus “reactive”, i.e., dependent on the other condition. The “trigger” infection has often been cured or is in remission in chronic cases, thus making determination of the initial cause difficult.
The symptoms of reactive arthritis very often include a combination of three seemingly unlinked symptoms—an inflammatory arthritis of large joints, inflammation of the eyes (conjunctivitis and uveitis), and urethritis. A useful mnemonic is “the patient can’t see, can’t pee and can’t bend the knee” or “the patient can’t see, can’t pee and can’t climb a tree”. Also known as Reiter’s syndrome, after German physician Hans Conrad Julius Reiter, it is also known as arthritis urethritica, venereal arthritis and polyarteritis enterica. It is a type of seronegative spondyloarthropathy.
Reactive arthritis is an RF-seronegative, HLA-B27-linked spondyloarthropathy[citation needed] (autoimmune damage to the cartilages of joints) often precipitated by genitourinary or gastrointestinal infections, some of which can be transmitted through sexual activities.
It most commonly strikes individuals aged 20-40, is more common in men than in women, and is more common in white men than in black men. This is owing to white individuals’ being more likely to have tissue type HLA-B27 than black individuals. People with HIV have an increased risk of developing reactive arthritis as well. Food poisoning is a common cause[citation needed].
Reactive arthritis was first described by Hans Conrad Julius Reiter, a German military physician, who in 1916 described the disease in a World War I soldier who had recovered from a bout of diarrhea, although the term has been found on Death Certificates dating back to 1877. (George Sherman, 4/10/1877, died of “Reiters Disease” at Randalls Island, NYC)[citation needed] . The term Reiter’s syndrome is being phased out, partly due to a move in the field of medicine to give descriptive names, rather than personal names, to conditions, and partly due to Dr. Reiter’s experiments in Nazi concentration camps. At least one reference[citation needed] states Reiter’s syndrome is to be used when areas other than joints are affected.
It is set off by a preceding infection, the most common of which would be a genital infection with Chlamydia trachomatis in the US. Other bacteria known to cause reactive arthritis which are more common worldwide are Neisseria gonorrhoeae, Ureaplasma urealyticum, Salmonella spp., Shigella spp., Yersinia spp., and Campylobacter spp.[2] A bout of food poisoning or a gastrointestinal infection may also precede the disease (those last four genera of bacteria mentioned are enteric bacteria). Reactive arthritis usually manifests about 1-3 weeks after a known infection. The mechanism of interaction between the infecting organism and the host is unknown. Synovial fluid cultures are negative, suggesting that ReA is caused either by an over-stimulated autoimmune response or by bacterial antigens which have somehow become deposited in the joints.
Symptoms generally appear within 1-3 weeks but can range from 4-35 days from the onset of the inciting episode of the disease.
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