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Reactive Arthritis

🎧 Reactive Arthritis — deep-dive podcast

📋 Key Information Summary

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  • Definition: Reactive arthritis (ReA) is a sterile, inflammatory arthritis occurring 1–4 weeks after a genitourinary or gastrointestinal infection, typically involving the lower limbs asymmetrically.
  • Classic triad (Reiter syndrome): Arthritis + urethritis/cervicitis + conjunctivitis — though the full triad is present in only ~30% of cases.
  • Key triggers: Chlamydia trachomatis (urogenital) and enteric pathogens — Salmonella, Yersinia, Campylobacter, Shigella.
  • HLA-B27: Present in 60–80% of patients; associated with more severe disease, sacroiliitis, and chronicity.
  • Diagnosis: Clinical — no single confirmatory test. Arthritis with characteristic timing following a documented infection; exclude septic arthritis and crystal arthropathy.
  • Extra-articular features: Anterior uveitis (15–25%), circinate balanitis, keratoderma blennorrhagicum, enthesitis, dactylitis.
  • First-line treatment: NSAIDs (naproxen 500 mg BD or indomethacin 25–50 mg TDS); use lowest effective dose for shortest duration.
  • Intra-articular corticosteroids for persistent mono- or oligoarthritis; systemic corticosteroids reserved for refractory cases.
  • DMARDs: Sulfasalazine 500 mg BD up to 1 g BD (PBS Authority Required) for chronic/remitting disease ≥6 weeks; methotrexate if sulfasalazine fails.
  • Antibiotics: NOT recommended for established arthritis (no benefit in RCTs); however, treat any active concurrent Chlamydia infection with doxycycline 100 mg BD × 7 days.
  • Prognosis: ~60–75% achieve complete remission within 6–12 months; ~15–20% develop chronic disease; HLA-B27-positive patients have higher relapse risk.
  • ATSI considerations: Higher rates of enteric infections in remote communities; increased Chlamydia prevalence; barriers to rheumatology access.
  • Referral: Ophthalmology urgently if uveitis suspected (red eye + pain + photophobia); rheumatology if arthritis persists >6 weeks or DMARD therapy considered.
🎬 Reactive Arthritis — clinical explainer

Introduction & Australian Epidemiology

Reactive arthritis (ReA) is a form of spondyloarthropathy characterised by sterile inflammation of the joints and entheses following a remote infection, typically of the genitourinary or gastrointestinal tract. The term "reactive" was introduced by Ahvonen et al. in 1969 to describe arthritis developing after Yersinia infection, and has largely replaced the older eponym "Reiter syndrome," which is now considered eponymously inappropriate given Hans Reiter's association with Nazi-era human experimentation.

In Australia, ReA is estimated to account for approximately 3–5% of new presentations to rheumatology clinics. The urogenital form predominates in sexually active adults aged 20–40 years, while the post-enteric form affects all age groups and is often linked to foodborne outbreaks. The Australian Institute of Health and Welfare (AIHW) data indicate that spondyloarthropathy collectively affects approximately 0.3–0.5% of the Australian population, with ReA representing a significant proportion of new-onset inflammatory arthritis referrals.

Post-Chlamydia ReA is likely underdiagnosed because many genitourinary infections are asymptomatic. Enteric-triggered ReA may present in clusters following documented outbreaks of Salmonella or Campylobacter, which are notifiable conditions under Australian state and territory public health legislation. The incidence is higher in Aboriginal and Torres Strait Islander communities due to greater exposure to enteric pathogens and higher rates of sexually transmitted infections (STIs).

Reactive Arthritis clinical infographic — pathophysiology, clinical clues, diagnosis, imaging, and management
Tap or click image to enlarge — Reactive Arthritis: pathophysiology, clinical clues, diagnosis, imaging, and management.
Reactive Arthritis infographic, full size

Postinfectious Arthritis

Reactive arthritis is the prototypical postinfectious arthritis — an inflammatory joint disease triggered by a distant infection but with no viable organisms recovered from synovial fluid or tissue. The mechanism involves molecular mimicry, whereby microbial antigens (particularly peptides from Chlamydia or enteric bacteria) share structural homology with self-antigens in the joint, leading to a cross-reactive immune response.

Pathogenic Mechanisms

  • Molecular mimicry: Bacterial heat-shock proteins (GroEL/Hsp60) and outer-membrane proteins resemble human joint antigens, driving CD4+ and CD8+ T-cell responses within the synovium.
  • Bacterial persistence: Particularly with Chlamydia trachomatis, there is evidence of aberrant, persistent forms (reticulate bodies) within the synovium that may drive ongoing inflammation without replicating.
  • Innate immune activation: Toll-like receptor (TLR) stimulation by bacterial lipopolysaccharide (LPS) and peptidoglycan fragments activates macrophages and neutrophils in the synovial membrane.
  • Genetic susceptibility: HLA-B27 presents microbial peptides aberrantly, promoting cytotoxic T-cell responses; the MHC class I allele also alters intracellular bacterial handling (HLA-B27 misfolding hypothesis).

Temporal Relationship

Arthritis typically develops 1–4 weeks after the inciting infection, though intervals of up to 6 weeks have been described. The index infection may be clinically apparent (diarrhoea, urethritis) or entirely subclinical — particularly relevant for Chlamydia, where up to 70–80% of urogenital infections in women and 50% in men are asymptomatic.

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Diagnostic pitfall: Because the triggering infection may be asymptomatic or resolved by presentation, clinicians must actively seek a history of recent urethritis, diarrhoeal illness, sexual contacts, or travel. Routine STI screening (including nucleic acid amplification testing for Chlamydia and Gonorrhoea) should be offered to all patients presenting with undifferentiated inflammatory arthritis.

Distinguishing Postinfectious Arthritis from Septic Arthritis

Feature Reactive Arthritis Septic Arthritis
Synovial fluid culture Sterile Positive (usually S. aureus)
WBC count 10,000–50,000/µL Usually >50,000/µL
Pattern Asymmetric, oligoarticular, lower limb Usually monoarticular
Systemic toxicity Mild–moderate Fever, rigors, sepsis
Extra-articular features Uveitis, skin, enthesitis Absent
Antibiotic response No benefit for arthritis Essential treatment

Chlamydia-Associated Triggers

Chlamydia trachomatis (serovars D–K) is the most common trigger for urogenital reactive arthritis in Australia and globally. The estimated incidence of ReA following urogenital Chlamydia infection is 1–4%, though this may be an underestimate given asymptomatic carriage.

Key Features of Chlamydia-Triggered ReA

  • More common in males (M:F ratio approximately 5:1 for urogenital form).
  • HLA-B27 present in 60–80% of affected individuals.
  • Conjunctivitis and anterior uveitis are more common with Chlamydia-triggered ReA than enteric forms.
  • Circinate balanitis (painless shallow ulcers on the glans penis) occurs in ~20–40% of male patients.
  • Asymptomatic Chlamydia persistence is the putative mechanism — aberrant reticulate bodies within the synovium drive chronic inflammation.

Diagnosis of Chlamydia Trigger

  • Nucleic acid amplification test (NAAT): First-line investigation — urine or urogenital swab for C. trachomatis DNA. Available through all Australian pathology providers; MBS-rebated.
  • Serology: Anti-Chlamydia IgG/IgA may indicate past infection but is not specific for the reactive arthritis trigger and has limited diagnostic utility.
  • Synovial fluid/tissue PCR: Research setting; not routinely available in Australia. May demonstrate Chlamydia DNA in synovial tissue even when urogenital NAAT is negative.
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Australian practice point: All sexually active patients presenting with undifferentiated inflammatory arthritis should be offered Chlamydia and Neisseria gonorrhoeae NAAT, regardless of symptomatic urethritis. Testing is available at sexual health clinics, GP surgeries, and community health services, including bulk-billed options.

Enteric Triggers

Post-dysenteric reactive arthritis follows gastrointestinal infection with Salmonella (non-typhoidal), Shigella, Yersinia, or Campylobacter species. These organisms are notifiable under Australian state and territory public health legislation, and outbreaks are monitored by OzFoodNet and state health departments.

Organism ReA Incidence Post-Infection HLA-B27 Prevalence Australian Context
Salmonella spp. 6–15% 60–70% Common cause; linked to poultry and egg outbreaks. Notifiable nationally.
Campylobacter spp. 1–5% ~50% Most common bacterial enteric pathogen in Australia; linked to undercooked poultry.
Shigella spp. 7–15% 70–80% Endemic in some Aboriginal communities; MSM transmission increasing.
Yersinia spp. 10–25% 60–75% Less common in Australia; associated with pork and dairy products.

Clinical Features of Enteric-Reactive Arthritis

  • Onset 1–4 weeks after the diarrhoeal illness (which may be mild or self-limiting).
  • Asymmetric oligoarthritis predominantly affecting the knees, ankles, and metatarsophalangeal joints.
  • Lower frequency of urethritis and circinate balanitis compared with Chlamydia-triggered ReA.
  • HLA-B27-positive patients more likely to develop sacroiliitis and chronic disease.
  • Enteric-triggered ReA tends to have a more self-limiting course than urogenital-triggered ReA.

Investigation of Enteric Trigger

  • Stool culture and multiplex PCR (GI pathogen panel) — available at all major Australian pathology providers (MBS-rebated).
  • Serology for Yersinia (anti-Yop antibodies) — limited availability; request through reference laboratories.
  • Blood cultures if febrile or systemically unwell (to exclude concurrent bacteraemia).

Extra-Articular Features

Reactive arthritis is a systemic inflammatory condition with multiple potential extra-articular manifestations. Recognition of these features is essential for diagnosis and comprehensive management.

Mucocutaneous Manifestations

  • Circinate balanitis: Painless shallow erosions on the glans penis or urethral meatus; present in 20–40% of male patients. Does not require specific treatment beyond topical emollients.
  • Keratoderma blennorrhagicum: Hyperkeratotic, psoriasiform lesions on the soles, palms, and around nails. Resembles pustular psoriasis. Topical corticosteroids or vitamin D analogues (calcipotriol) may be used.
  • Oral ulcers: Painless shallow erosions on the palate, tongue, or buccal mucosa; usually transient.
  • Nail changes: Onycholysis, subungual hyperkeratosis — indistinguishable from psoriatic nail disease.

Ocular Manifestations

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Urgent ophthalmology referral: Anterior uveitis (iritis) occurs in 15–25% of ReA patients and may be the presenting feature. Symptoms include unilateral red eye, pain, photophobia, and blurred vision. Untreated anterior uveitis may lead to posterior synechiae, secondary glaucoma, and visual loss. Same-day ophthalmology assessment should be arranged through the emergency department or urgent referral clinics.
  • Conjunctivitis: Bilateral, mild, self-limiting; part of the classic triad but may be missed.
  • Anterior uveitis: Typically unilateral; may be recurrent. HLA-B27-positive patients have higher recurrence rates.
  • Episcleritis: Less common; presents with sectoral injection and mild discomfort.

Urethritis

  • Sterile urethral discharge, dysuria, or increased urinary frequency.
  • May be triggered by or coexist with active Chlamydia trachomatis infection — always perform NAAT.
  • Cervicitis in female patients may be asymptomatic.

Enthesitis & Dactylitis

  • Enthesitis: Inflammation at tendinous insertions — Achilles tendon insertion (most common), plantar fascia, patellar tendon, tibial tuberosity. Present in 40–70% of cases.
  • Dactylitis: "Sausage digits" — diffuse swelling of an entire digit due to flexor tenosynovitis and joint inflammation. A hallmark of spondyloarthropathy.

Constitutional Symptoms

  • Fatigue, malaise, low-grade fever, and weight loss may occur, particularly in the acute phase.
  • Psoriasiform skin lesions, onychodystrophy, and conjunctivitis can mimic psoriatic arthritis — differentiation requires careful history regarding the preceding infection.

HLA-B27 Association

Human leucocyte antigen B27 (HLA-B27) is a major histocompatibility complex (MHC) class I molecule present in 6–8% of the general Australian population but in 60–80% of patients with reactive arthritis. Its presence is a major determinant of disease susceptibility, severity, and chronicity.

Role of HLA-B27 in Reactive Arthritis

  • Increased susceptibility: HLA-B27-positive individuals are 10–50× more likely to develop ReA following a triggering infection.
  • Sacroiliitis and axial disease: HLA-B27 is strongly associated with sacroiliac joint involvement and progression to ankylosing spondylitis-like phenotype.
  • Chronicity: Patients who are HLA-B27-positive have higher rates of persistent arthritis (>6 months) and relapse.
  • Extra-articular features: Uveitis and cardiac conduction abnormalities are more common in HLA-B27-positive patients.
  • Not diagnostic: HLA-B27 testing alone cannot confirm or exclude ReA. Approximately 20–40% of ReA patients are HLA-B27-negative.

Proposed Mechanisms

  • Arthritogenic peptide hypothesis: HLA-B27 presents bacterial peptides (e.g., from Chlamydia or Salmonella) that cross-react with self-peptides on joint surfaces.
  • HLA-B27 misfolding: The HLA-B27 heavy chain tends to misfold in the endoplasmic reticulum, activating the unfolded protein response (UPR) and IL-23/IL-17 axis.
  • Altered intracellular killing: HLA-B27 transgenic models show impaired clearance of intracellular Chlamydia and Salmonella, potentially promoting persistent infection.

Testing for HLA-B27 in Australia

Available
HLA-B27 typing (flow cytometry or PCR)
MBS item 71156 — rebate available. Not routinely recommended for diagnosis of ReA, but useful for prognostication and when diagnostic uncertainty exists (e.g., differentiating from rheumatoid arthritis). Turnaround: 5–10 business days at most metropolitan pathology providers.
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Avoid reflexive HLA-B27 testing: HLA-B27 prevalence is 6–8% in Caucasian Australians and ~4% in Aboriginal Australians. A positive result in isolation does not confirm ReA, and a negative result does not exclude it. Testing is most useful in patients with incomplete clinical features where the pre-test probability is moderate (e.g., asymmetric oligoarthritis of lower limbs with history of preceding diarrhoea but no extra-articular features).

Clinical Presentation & Diagnostic Criteria

Typical Presentation

A previously well patient, typically aged 20–40 years, presents with acute-onset asymmetric oligoarthritis predominantly affecting the lower limbs — knees, ankles, and first metatarsophalangeal joint (MTP) are most commonly involved. There is often a history of preceding urethritis (1–4 weeks prior) or diarrhoeal illness (1–4 weeks prior), though the preceding infection may be subclinical.

Diagnostic Criteria

There is no universally accepted gold-standard diagnostic criterion for ReA. The diagnosis remains clinical and is one of exclusion. The following frameworks are commonly used:

Criterion Set Key Features
Berlin criteria (1979, modified) Asymmetric arthritis + evidence of preceding or concurrent infection + absence of other causes of arthritis. Does not require HLA-B27.
Classification of Spondyloarthropathies (Amor / ESSG) ReA is classified under spondyloarthropathy umbrella. Inflammatory arthritis + preceding infection = sufficient for classification.
BASDAI / ASAS criteria Primarily used for axial spondyloarthropathy; apply if sacroiliitis or axial symptoms are prominent.

Differential Diagnosis

  • Septic arthritis: Always exclude — aspirate synovial fluid urgently for cell count, Gram stain, and culture.
  • Crystal arthropathy: Gout and pseudogout — synovial fluid polarised microscopy.
  • Rheumatoid arthritis: Symmetric, small joints, RF/anti-CCP positive.
  • Psoriatic arthritis: Skin/nail psoriasis, dactylitis, enthesitis — overlap with ReA is significant.
  • Gonococcal arthritis: Disseminated N. gonorrhoeae — tenosynovitis, dermatitis, polyarthralgia; culture or NAAT positive.
  • Ankylosing spondylitis: Chronic axial involvement with sacroiliitis; may evolve from ReA in HLA-B27-positive individuals.
  • Viral arthritis: Parvovirus B19, rubella, hepatitis B — typically polyarticular and self-limiting.
🖼️ Reactive Arthritis — visual summary
Reactive Arthritis visual summary infographic

Investigations

Investigations in ReA serve three purposes: (1) excluding septic arthritis and other differentials, (2) identifying the triggering infection, and (3) assessing disease severity and chronicity.

Baseline Blood Tests

Essential
FBC, ESR, CRP, LFTs, UEC, urate
FBC may show leucocytosis and thrombocytosis. ESR and CRP are elevated in acute disease. Urate should be checked to exclude gout. All MBS-rebated at all pathology providers.
Available
Rheumatoid factor (RF) and anti-CCP antibodies
Usually negative in ReA. Positive results suggest rheumatoid arthritis or overlap. MBS-rebated.
Available
ANA, dsDNA
To exclude systemic lupus erythematosus if clinical features overlap. MBS-rebated.
Available
HLA-B27 typing
Prognostic value. MBS item 71156. Not required for diagnosis.

Infection Screening

Essential
Urogenital NAAT for Chlamydia trachomatis and Neisseria gonorrhoeae
First-void urine or urogenital swab. MBS-rebated. Perform in all patients regardless of symptom history.
Essential
Stool culture and multiplex GI PCR panel
For Salmonella, Campylobacter, Shigella, Yersinia, Clostridioides difficile. MBS-rebated. Request if any diarrhoeal history.
Available
HIV, syphilis (RPR/TPHA), hepatitis B & C serology
Consider as part of STI screen; relevant if risk factors present. MBS-rebated.

Synovial Fluid Analysis

Essential
Joint aspiration with synovial fluid analysis
Mandatory if septic arthritis is suspected. Send for cell count (inflammatory: 2,000–50,000/µL, predominantly neutrophils), Gram stain, culture, and crystal analysis. Monosodium urate and calcium pyrophosphate crystals should be absent. Available at all hospitals and many GP practice-based procedures.

Imaging

Available
Plain radiographs (affected joints, pelvis/AP for sacroiliac joints)
Often normal in acute disease. Periostitis, enthesophytes, and joint erosions may develop in chronic disease. Sacroiliac sclerosis and erosions suggest progression to axial disease. MBS-rebated.
Specialist
MRI of sacroiliac joints / affected joints
Detects bone marrow oedema (active sacroiliitis) before radiographic changes. Requested by rheumatology. MBS-rebated under specific indications.
Specialist
Musculoskeletal ultrasound
Enthesitis, synovitis, tenosynovitis detection. Increasingly used in rheumatology clinics. MBS-rebated item 55805 for specialist-requested MSK ultrasound.

Risk Stratification & Prognostic Factors

Identifying patients at risk of chronic disease is essential for guiding treatment intensity and follow-up frequency.

Favourable
Self-Limiting Course
HLA-B27 negative. Single episode. No extra-articular features beyond conjunctivitis. Enteric trigger with adequate treatment of source infection. Duration <6 weeks.
Setting: GP management with NSAIDs, 3–6 monthly review
Intermediate
Prolonged / Recurrent
HLA-B27 positive. Persistent oligoarthritis >6 weeks. Enthesitis and dactylitis. Urogenital trigger. Mild extra-articular features.
Setting: GP + rheumatology co-management; DMARD consideration
Unfavourable
Chronic / Destructive
HLA-B27 positive. Sacroiliitis or axial involvement. Recurrent anterior uveitis. Chronic skin lesions. Polyarticular involvement. >12 months duration. Functional impairment.
Setting: Rheumatology-led; DMARD or biologic therapy required

Poor Prognostic Factors

  • HLA-B27 positivity
  • Urogenital (vs enteric) trigger
  • Hip or shoulder involvement
  • Elevated ESR/CRP persisting >3 months
  • Dactylitis
  • Sacroiliitis on imaging
  • Inadequate initial response to NSAIDs
  • Recurrent episodes

Treatment & Prognosis

First-Line: NSAIDs

NSAIDs are the mainstay of symptomatic treatment for reactive arthritis. Use the lowest effective dose for the shortest duration necessary. In Australia, two NSAIDs are commonly prescribed:

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Naproxen
Naprosyn® · Generic · NSAID (propionic acid derivative)
Adult dose 500 mg PO BD with food; range 500–1000 mg/day in divided doses
Paediatric dose 5–7 mg/kg/dose PO BD (max 1000 mg/day)
Route Oral
Renal adjustment Avoid if eGFR <30 mL/min. Use with caution if eGFR 30–60. Monitor renal function.
Key adverse effects GI ulceration/bleeding, cardiovascular risk, renal impairment
PBS status ✔ PBS General Benefit
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Indomethacin
Indocid® · Generic · NSAID (indole acetic acid)
Adult dose 25–50 mg PO TDS with food; max 200 mg/day
Paediatric dose 1–2 mg/kg/day PO in 2–3 divided doses (max 150 mg/day)
Route Oral (also available PR)
Renal adjustment Avoid if eGFR <30 mL/min. Higher CNS side-effect profile than naproxen.
Key adverse effects Headache, dizziness, GI side effects; use PPI co-prescription for GI protection
PBS status ✔ PBS General Benefit
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GI protection: Co-prescribe a proton pump inhibitor (PPI) such as omeprazole 20 mg PO daily with NSAIDs in patients with risk factors for GI bleeding (age >65, prior peptic ulcer, concurrent anticoagulant or corticosteroid use, H. pylori infection). PPIs are PBS General Benefit.

Second-Line: Corticosteroids

  • Intra-articular corticosteroid injection: Triamcinolone acetonide 20–40 mg (knee) or 10–20 mg (ankle, MTP) — effective for persistent mono- or oligoarthritis despite NSAIDs. Perform under sterile conditions after excluding septic arthritis. PBS General Benefit (medical service).
  • Systemic corticosteroids: Prednisolone 15–25 mg PO daily, tapered over 4–6 weeks. Reserved for severe polyarticular disease or significant extra-articular features refractory to NSAIDs. Use lowest dose for shortest duration.
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Prednisolone
Solone® · Panafcortelone® · Generic · Systemic corticosteroid
Adult dose 15–25 mg PO daily, taper by 5 mg every 1–2 weeks
Paediatric dose 0.5–1 mg/kg/day PO (max 40 mg/day), taper as tolerated
Route Oral
Renal adjustment No dose adjustment; monitor fluid retention
Key adverse effects Hyperglycaemia, osteoporosis, adrenal suppression, weight gain, infection risk
PBS status ✔ PBS General Benefit

Third-Line: DMARDs (Chronic/Refractory Disease)

DMARDs are considered when arthritis persists beyond 6 weeks despite NSAIDs and corticosteroids, or in patients with frequent relapses. The evidence base for DMARDs in ReA is limited, primarily from small trials and observational studies.

💊
Sulfasalazine
Salazopyrin® · Generic · DMARD (aminosalicylate + sulfonamide)
Adult dose 500 mg PO daily for 1 week, then 500 mg BD, titrate to 1 g BD (max 3 g/day)
Paediatric dose Not routinely used in paediatric ReA
Route Oral
Monitoring FBC, LFTs, UEC at baseline, 2-weekly × 3 months, then monthly. Check G6PD before starting.
Key adverse effects Nausea, headache, rash, haemolysis (G6PD deficiency), hepatitis, agranulocytosis (rare)
PBS status ⚠ PBS Authority Required
💊
Methotrexate
Methoblastin® · Generic · DMARD (antifolate)
Adult dose 7.5–15 mg PO/SC once weekly with folic acid 5 mg on a non-methotrexate day
Route Oral or subcutaneous injection
Monitoring FBC, LFTs, UEC at baseline, 2-weekly × 2 months, then monthly. Chest X-ray at baseline.
Key adverse effects Hepatotoxicity, myelosuppression, pneumonitis, teratogenicity (PREGNANCY CONTRAINDICATED — both sexes must use contraception)
PBS status ⚠ PBS Authority Required

Antibiotics for Active Chlamydia Infection

Antibiotic therapy for the arthritis itself has NOT been shown to be beneficial in randomised controlled trials (including the STOP-REA and CLAIRTHRITIS trials). However, if there is evidence of active concurrent Chlamydia trachomatis infection (positive NAAT), treat the infection as per Australian STI management guidelines:

💊
Doxycycline
Doxy® · Generic · Tetracycline antibiotic
Adult dose 100 mg PO BD × 7 days (uncomplicated Chlamydia)
Paediatric dose 2.2 mg/kg/dose PO BD (max 100 mg/dose) × 7 days. Avoid in children <8 years unless no alternative.
Route Oral
Key adverse effects Photosensitivity, oesophageal ulceration (take upright with water), GI upset
PBS status ✔ PBS General Benefit
💊
Azithromycin
Zithromax® · Generic · Macrolide antibiotic
Adult dose 1 g PO STAT (single dose) for uncomplicated Chlamydia
Paediatric dose 20 mg/kg PO STAT (max 1 g) for Chlamydia
Route Oral
Key adverse effects GI upset, QT prolongation (rare), hepatotoxicity (rare)
PBS status ✔ PBS General Benefit
⚠️
Antibiotics for arthritis — no benefit: Multiple RCTs (including long-course rifampicin + doxycycline for Chlamydia-triggered ReA) have NOT demonstrated benefit for the joint disease. Prolonged antibiotic courses (≥3 months) carry significant risks including Clostridioides difficile infection, hepatotoxicity, and antimicrobial resistance. Do NOT prescribe prolonged antibiotics for reactive arthritis.

Prognosis

Self-Limiting (60–75%)

Complete remission within 6–12 months with NSAID therapy alone. Enteric-triggered ReA generally has a better prognosis than urogenital-triggered ReA. Most patients do not develop chronic disease.

Chronic Disease (15–20%)

Persistent arthritis >6 months. May evolve into undifferentiated spondyloarthropathy or, in HLA-B27-positive patients, ankylosing spondylitis. Requires long-term DMARD therapy and rheumatology follow-up.

Follow-Up

  • Review at 4–6 weeks post-diagnosis: assess NSAID response, symptom trajectory, and extra-articular features.
  • If improving: continue NSAIDs with plan to wean over 2–4 weeks as symptoms resolve.
  • If not improving at 6 weeks: refer rheumatology for DMARD consideration.
  • Ophthalmology review if anterior uveitis develops at any stage (urgent referral).
  • Sexual health screening and partner notification for Chlamydia-triggered ReA.

Special Populations

🤰 Pregnancy
NSAIDs
Avoid after 20 weeks gestation (risk of premature ductus arteriosus closure). Paracetamol is a safer analgesic option. If NSAIDs essential in first/second trimester, use lowest dose for shortest duration.
Methotrexate
CONTRAINDICATED in pregnancy and breastfeeding. Teratogenic. Both male and female patients must use reliable contraception and stop methotrexate ≥3 months before conception.
Sulfasalazine
Generally considered safe in pregnancy (Category A). Male fertility may be impaired (oligospermia) — reversible on cessation.
Azithromycin
Safe for Chlamydia treatment in pregnancy (Category B1). Single-dose 1 g PO preferred.
👶 Paediatrics
Epidemiology
Post-enteric ReA is the most common form in children, particularly following Salmonella or Yersinia infection. Post-Chlamydia ReA is rare in prepubertal children.
Treatment
NSAIDs first-line (naproxen 5–7 mg/kg/dose BD). Intra-articular corticosteroids for persistent monoarthritis. DMARDs rarely needed; seek paediatric rheumatology advice. Avoid doxycycline in children <8 years unless no alternative.
Prognosis
Generally excellent — most children achieve complete remission. Recurrence risk is lower than in adults.
👴 Elderly (>65 years)
NSAIDs
Use with extreme caution. Increased risk of GI bleeding, renal impairment, cardiovascular events, and drug interactions. Always co-prescribe PPI. Consider paracetamol or topical NSAIDs as alternatives.
Intra-articular corticosteroids
Preferred over systemic NSAIDs/steroids for localised disease. Safe and effective.
🫘 Renal Impairment
NSAIDs
AVOID if eGFR <30 mL/min. Use with caution if eGFR 30–60; monitor renal function. Consider intra-articular corticosteroids or paracetamol instead.
Sulfasalazine
No dose adjustment required; monitor renal function. Avoid in severe renal impairment.
Methotrexate
Dose reduce if eGFR <30. Contraindicated in severe renal impairment. Monitor closely.
🫁 Hepatic Impairment
Methotrexate
CONTRAINDICATED in significant hepatic impairment (Child-Pugh B/C). Avoid with alcohol excess. Monitor LFTs closely.
NSAIDs
Use with caution; increased risk of hepatotoxicity and fluid retention. Prefer naproxen over indomethacin.
🛡️ Immunocompromised
General
ReA may be more severe and chronic in immunocompromised patients (HIV, biologic therapy recipients). Exclude opportunistic infections before DMARD initiation. Consult immunology/infectious disease if diagnostic uncertainty.
DMARDs
Increased infection risk. Ensure all vaccinations are up to date before starting immunosuppressive therapy. Consider specialist guidance.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Reactive arthritis has particular significance in Aboriginal and Torres Strait Islander communities due to higher rates of both enteric infections and sexually transmitted infections, including Chlamydia trachomatis. The disproportionate burden of ReA reflects broader social determinants of health, including overcrowded housing, limited access to clean water and sanitation in remote communities, and barriers to healthcare access.

Key Considerations

Enteric infection burden
Aboriginal and Torres Strait Islander communities experience significantly higher rates of Salmonella, Shigella, and Campylobacter infection, particularly in remote Northern Territory, Western Australia, and Queensland communities. These infections are a leading trigger for post-enteric reactive arthritis. Environmental health programmes addressing water quality, food safety, and housing are essential prevention strategies.
Chlamydia prevalence
STI rates, including Chlamydia trachomatis, are 5–10× higher in Aboriginal and Torres Strait Islander populations compared with non-Indigenous Australians. Young people (15–29 years) are disproportionately affected. Culturally safe sexual health screening programmes are critical.
Rheumatology access
Specialist rheumatology services are predominantly available in metropolitan and major regional centres. Aboriginal and Torres Strait Islander patients in remote communities face significant travel barriers, cultural dislocation, and long wait times. Telehealth rheumatology consultations (MBS items 91822, 91823) are available and should be utilised to improve access.
Cultural safety
Engagement with Aboriginal Health Workers and Aboriginal Liaison Officers is essential. Communication should be culturally appropriate, use plain language, and involve family/community members as appropriate. Avoid medical jargon and ensure patients understand the link between the triggering infection and arthritis.
Medication access
PBS co-payments may be a barrier. Patients in remote areas may have difficulty accessing pharmacies. Ensure prescriptions can be dispensed through Aboriginal Community Controlled Health Organisation (ACCHO) pharmacies or remote area pharmacist programmes. Closing the Gap PBS co-payment measures reduce out-of-pocket costs for eligible patients.
Ophthalmology referral
Anterior uveitis may be harder to diagnose in settings with limited eye-care access. Train primary care providers in red-flag recognition. The Visiting Ophthalmologist Scheme and Indigenous Eye Health programmes (e.g., RANZCO) provide outreach services.

Recommended Actions

  • Incorporate enteric and STI screening into routine health assessments for Aboriginal and Torres Strait Islander patients (MBS 715 Health Assessment).
  • Ensure rheumatology referrals are facilitated through ACCHOs and Indigenous-specific care pathways where available.
  • Utilise telehealth for specialist consultations (MBS items 91822–91826).
  • Consider Closing the Gap PBS co-payment for medication access.
  • Engage Aboriginal Health Workers in patient education and follow-up coordination.
  • Advocate for improved environmental health infrastructure to reduce enteric infection burden.
📊 Reactive Arthritis — slide deck

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