Acute onset of rash and oligoarthritis

The typical patient? A young, white man

Patients with RS are almost always Caucasian males in their early twenties and are typically HLA-B27 positive. Seronegativity for this HLA factor may portend a less severe version of the syndrome. Individuals infected with HIV show increased incidence of developing RS.³

A microbial antigen is likely responsible for the initial activation of RS. This is followed by an immune reaction involving the joints, skin, and eyes. This theory is supported by the absence of auto- antibodies, the frequent association with HLA-B27, and the fact that patients with advanced AIDS experience the same severity of RS symptoms, despite depressed CD4+ T cell function.¹

Bacteria trigger syndrome via 1 of 2 pathways

The bacteria that trigger RS typically enter the body through one of 2 pathways: the genitourinary tract or the gastrointestinal tract.

• The sexual transmission pathway involves infection with Chlamydia trachomatis or Ureaplasma urealyticum 1 to 4 weeks prior to development of urethritis and possibly conjunctivitis. The arthritic component follows later.
• The gastrointestinal pathway involves an enteric pathogen, such as Salmonella enteritidis, Yersinia enterocolitica, Campylobacter fetus, or Shigella flexneri that infects the host and follows the same time frame as noted earlier, though diarrhea rather than urethritis emerges as a chief complaint.⁴

Various forms of arthritis comprise the differential

A number of conditions must be ruled out before the RS diagnosis is considered definitive. The most likely imposters include:

• Gonococcal arthritis
• Rheumatoid arthritis
• Ankylosing spondylitis
• Psoriatic arthritis.

In addition, an attack of gouty arthritis, systemic lupus erythematosus, serum sickness, Behçet’s syndrome, rheumatic fever, Still’s disease, and HIV could also present in a similar fashion.

The lab work, detailed below, separates RS from the imposters.