About Reactive Arthritis

From the nation’s leading law firm representing victims of campylobacter and other foodborne illness outbreaks.

Chapter 1

What is Reactive Arthritis?

Formerly known as Reiter syndrome, reactive arthritis (ReA) is joint inflammation that occurs after a bacterial infection originating outside the joints (i.e., “extra-articular”). These infections are either gastrointestinal (e.g., Salmonella, Campylobacter, Yersinia, Shigella, and sometimes E. coli) or urogenital (most commonly Chlamydia trachomatis, but also Neisseria gonorrhea and Mycoplasma). Acute ReA occurs several days or weeks after the antecedent infection. It is typically monoarticular (involving one joint) or oligoarticular (involving just a few joints, usually less than six). The lower extremities are most commonly involved, but it can also involve the arms and spine. Other names for ReA are post-infectious arthritis, post-dysenteric arthritis, and seronegative arthritis. When it lasts more than six months, it is called chronic reactive arthritis.

A small subset of patients with ReA may have two additional symptoms: conjunctivitis (redness and eye pain) and urethritis (burning and pain with urination).


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Source: HealthSoul

Epidemiology

ReA is relatively uncommon and can affect both men and women. While it can occur at any age, it is more common in younger adults. Overall rates of ReA are 0-15% after a gastrointestinal (GI) infection. The most common GI infections associated with ReA are Campylobacter, Salmonella, Shigella, and Yersinia. A systematic review of relevant literature found the incidence after specific intestinal pathogens to be 9 per 1,000 persons for Campylobacter and 12 per 1,000 persons for Salmonella and Shigella.

The incidence of ReA after urogenital infections is 2-4% and is more common in men than women. Chlamydia infection is the most common cause of this sexually-acquired reactive arthritis.

Reactive arthritis is uncommon in children, especially in those under nine years of age.

Pathophysiology

ReA is an immune-mediated syndrome that is triggered by a recent bacterial infection. The theory is that the invasive bacteria (or their fragments) in the blood stream induce T-lymphocytes (a type of white blood cell), which then attack the soft tissue lining the joint, called the synovium. While the synovial cavity does not normally contain bacteria, it is possible for microbes to enter either directly during recurrent episodes of bacteremia or by transport within lymphoid cells or monocytes, other types of white blood cells.


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Source: https://cmr.asm.org/content/17...

Some people may have a genetic predisposition for ReA. Thirty to fifty percent of individuals with ReA have a genotype called Human Leukocyte Antigen-B27 (or HLA-B27). The HLA system is the major histocompatibility complex in humans, an important part of the immune system. It is comprised of glycoproteins on the surface of all nucleated body cells and found in high concentrations in white blood cells. There are multiple theoretical reasons why HLA-B27 might increase the likelihood of acquiring ReA. For example, HLA-B27 appears to enhance the invasion of Salmonella into intestinal epithelial cells.


Next Chapter

What are the Symptoms of Reactive Arthritis?

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