Chapter 151 Reactive and Postinfectious Arthritis
The role of infectious agents in the pathophysiology of arthritis is a topic of intense study. In addition to causing arthritis by means of direct infection (i.e., septic arthritis; Chapter 677), infection can lead to the generation and deposition of immune complexes as well as antibody or T cell–mediated cross-reactivity with self. Evidence continues to grow that microorganisms also play a role in the development of classic autoimmune diseases, such as systemic lupus erythematosus and juvenile idiopathic arthritis. Reactive and postinfectious arthritis are defined as joint inflammation due to a sterile inflammatory reaction following a recent infection. For historical reasons, we use reactive arthritis to refer to arthritis that occurs following enteropathic or urogenital infections and postinfectious arthritis to describe arthritis that occurs after infectious illnesses not classically considered in the reactive arthritis group, such as infection with group A streptococcus or viruses. In some cases, nonviable components of the initiating organism have been demonstrated in affected joints, and the presence of viable, yet nonculturable, bacteria within the joint remains an area of investigation.
The course of reactive arthritis is variable and may remit or progress to a chronic spondyloarthritis including ankylosing spondylitis (Chapter 150). In postinfectious arthritis, the pain or joint swelling is usually transient, lasting less than 6 wk, and does not share the typical spondyloarthritis pattern. The distinction between postinfectious arthritis and reactive arthritis is not always clear, either clinically or in terms of pathophysiology.
Pathogenesis
Reactive arthritis typically follows enteric infection with Salmonella, Shigella, Yersinia enterocolitica, Campylobacter jejuni, Cryptosporidium parvum, or Giardia intestinalis, or genitourinary tract infection with Chlamydia trachomatis or Ureaplasma. Though similar in some respects to reactive arthritis, acute rheumatic fever caused by group A streptococcus (Chapter 176.1), arthritis associated with infective endocarditis (Chapter 431), and the tenosynovitis associated with Neisseria gonorrhoeae are considered later.
Clinical Manifestations and Differential Diagnosis
Symptoms of reactive arthritis present approximately 2-4 wk following infection. The classic triad of arthritis, urethritis, and conjunctivitis (formerly referred to as Reiter syndrome) is relatively uncommon in children. The arthritis is typically oligoarticular, with a lower extremity predilection. Dactylitis may occur, and enthesitis (Fig. 151-1) is common (Chapter 150). Cutaneous manifestations can occur and may include circinate balanitis, ulcerative vulvitis, oral lesions, and keratoderma blennorrhagica, which is similar in appearance to pustular psoriasis (Fig. 151-2). Systemic symptoms may include fever, malaise, and fatigue. Early in the disease course, markers of inflammation—erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and platelets—may be markedly elevated.
Figure 151-1 Enthesitis—swelling of the posterior aspect of the left heel and lateral aspect of the ankle.
(Courtesy of Nora Singer, Case Western Reserve University and Rainbow Babies’ Hospital.)
Figure 151-2 Keratoderma blennorrhagica.
(Courtesy of Dr. M.F. Rein and The Centers for Disease Control and Prevention Public Health Image Library, 1976. Image #6950.)
Familiarity with other causes of postinfectious arthritis is vital when a diagnosis of reactive arthritis is being considered. Numerous viruses are associated with postinfectious arthritis (Table 151-1
