Reactive arthritis and post-infectious inflammatory syndromes: SAQ

This child has the textbook presentation of the classic reactive arthritis, and the task is to outline the diagnosis and the differential, then to discuss the stepwise management with the sepsis exclusion as the first priority. ^[4][9]

Question 1 (10 marks)

Outline the diagnosis of the reactive arthritis, the mechanism, and the differential from the septic arthritis, the post-streptococcal reactive arthritis and the acute rheumatic fever. ^[4]

A full-mark answer covers the definition with the latency, the trigger organisms, the HLA-B27 association, the mechanism of the molecular mimicry, and the four-way differential with the discriminating features. ^[4][5]

The definition and the latency (2 marks). Reactive arthritis is the sterile inflammatory arthritis that erupts one to four weeks after a distant gastrointestinal or genitourinary infection, in a joint that contains no cultivable organism. The latency is the single most discriminating feature, and the one-to-four-week window separates it from the septic arthritis, which has no latency, and from the post-streptococcal reactive arthritis, which has the latency under ten days. This child has the three-week latency after the diarrhoea, which anchors the diagnosis. ^[4]

The trigger organisms and the HLA-B27 (2 marks). The classic triggers are the enteric bacteria Salmonella, Shigella, Campylobacter and Yersinia, and the genitourinary Chlamydia trachomatis. The HLA-B27 allele is present in roughly half to three-quarters of the patients, and it is a susceptibility marker that modifies the severity and the risk of the chronicity, the sacroiliitis and the uveitis, but it is not diagnostic on its own because it is present in a substantial fraction of the healthy population. This child has the positive HLA-B27 and the enthesitis at the Achilles tendon, which are the spondyloarthritis hallmarks. ^[5][4]

The mechanism (2 marks). The central mechanism is the molecular mimicry. The HLA-B27 molecule on the antigen-presenting cell picks up the bacterial peptide, and it presents it to the CD8-positive T cell. The activated T cell cross-reacts with the self-antigens in the synovium because the bacterial peptide and the self-peptide share a similar shape, and the interleukin-23 and interleukin-17 axis sustains the sterile synovitis. The joint remains sterile because the live organisms do not seed it, though the bacterial antigens persist in the synovial macrophages. ^[5]

The differential from the septic arthritis (1 mark). The febrile, unwell child with a single hot joint and a refusal to bear weight is the septic arthritis, which is excluded by the Kocher criteria, the blood cultures and the joint aspirate. This child is afebrile and well, and the aspirate is sterile, which excludes the septic arthritis. ^[9]

The differential from the post-streptococcal reactive arthritis and the acute rheumatic fever (3 marks). The post-streptococcal reactive arthritis follows the group A streptococcal pharyngitis with the latency under ten days, the additive and persistent pattern, the prominent enthesitis and the absent carditis, and it is distinguished from this child by the streptococcal trigger and the shorter latency. The acute rheumatic fever follows the streptococcal pharyngitis with the latency of two to three weeks, the migratory polyarthritis, the dramatic response to the non-steroidal anti-inflammatory drugs, and the carditis as the hallmark, and the 2015 revised Jones criteria require the two major or the one major and two minor criteria with the evidence of the preceding streptococcal infection. This child has the enteric trigger and the enthesitis, and the streptococcal serology is normal, which excludes both the streptococcal syndromes. ^[3][1]