Reactive arthritis

Causes and mechanism of development (pathogenesis)

Reactive arthritis is triggered by a combination of an infectious agent and genetic predisposition. A key risk factor is being a carrier of the gene encoding the HLA-B27 antigen. Microbes can persist the longest specifically in cells carrying this antigen.

"Arthritogenic" strains penetrate through mucous membranes, evade destruction, and multiply inside phagocytes (macrophages, leukocytes). Then, phagocytes transport the pathogen and its antigens to target organs—the joints.

Using chlamydial arthritis as an example, the immune response develops in stages:

• First, macrophages and cellular immunity are activated.
• Secretory immunoglobulin A (IgA) is produced at the site of infection.
• Early class M antibodies (IgM) are synthesized within the first two days.
• Later, a switch to the production of class G antibodies (IgG) occurs.

Clinical presentation

The classic manifestation of the pathology is Reiter's syndrome (urethro-oculo-synovial syndrome). It develops after a urogenital or intestinal infection and includes the triad: urethritis, conjunctivitis, and arthritis.

In children, especially against the background of chlamydia, the syndrome debuts sequentially. First, the urogenital tract is affected, often with mild and subtle symptoms. Then, catarrhal conjunctivitis occurs, and the joints are involved last. Joint syndrome manifests as asymmetric mono-, oligo-, or polyarthritis.

Features of joint syndrome:

• The knee and ankle joints are predominantly affected.
• The inflammation is acute, with pronounced effusion (exudation) and elevated temperature (sometimes up to febrile levels).
• A specific sign is dactylitis ("sausage-like" digit deformity), with the first toe frequently affected.
• Tenosynovitis and bursitis frequently occur (e.g., Achilles bursitis).
• Joint destruction is absent for a long time, despite relapses.

The severity of the course depends on the trigger. Post-enterocolitic reactive arthritis is significantly more aggressive than urogenital arthritis, accompanied by severe intoxication, fever, and high inflammatory markers.

Diagnostics

To establish a diagnosis, the Berlin diagnostic criteria (1996) are used. They include the assessment of peripheral arthritis (asymmetric, typically affecting 1–4 lower extremity joints) and a link to a preceding infection (an episode of diarrhea or urethritis within 4 weeks prior to arthritis).

If the clinical signs of the infection are overt, laboratory confirmation is desirable but not mandatory. In cases of occult infection, verification of the pathogen becomes mandatory. It is important to exclude septic and microcrystalline arthritides, other spondyloarthropathies, Lyme disease, and streptococcal arthritis.

Laboratory identification:

• Antigen detection: identifying antigens in the epithelium or synovial fluid using direct immunofluorescence assay (DFA).
• Antibody detection: determining Ig against chlamydia (CFT, immunofluorescence) or intestinal bacteria (PHA, CFT) in the blood.
• Morphology and culture: visualization of structures or culture inoculation.
• PCR: detection of pathogen DNA.

Class and exam questions

What else to study on this topic

• Detailed analysis of the Berlin diagnostic criteria
• Differential diagnosis with septic and streptococcal arthritis
• Features of the immune response (IgM to IgG switch)
• The role of HLA-B27 in the pathogenesis of spondyloarthrites
• Laboratory diagnostic methods (DFA, CFT, PHA)

Other topics of «Chapter 9. Rheumatic Diseases»

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.