Reactive Arthritis (Adult)

1. Clinical Overview

Summary

Reactive arthritis (ReA) is a sterile inflammatory arthritis that develops following an infection at a distant site, typically gastrointestinal or genitourinary. It is classified as one of the seronegative spondyloarthropathies and shows strong association with HLA-B27 (present in 60-80% of cases). [1,2]

The condition was historically known as Reiter's syndrome, characterized by the classic triad of arthritis, urethritis, and conjunctivitis (mnemonic: "Can't see, can't pee, can't climb a tree"). However, the complete triad occurs in only 30-40% of patients, and the eponymous term is now discouraged due to historical associations. [3]

Key triggering organisms include:

• Genitourinary: Chlamydia trachomatis (most common in developed countries)
• Gastrointestinal: Salmonella, Shigella, Campylobacter, Yersinia

The arthritis typically develops 1-4 weeks after the triggering infection and manifests as asymmetric oligoarthritis affecting predominantly lower limb joints (knees, ankles). Additional features include enthesitis (Achilles tendon, plantar fascia), dactylitis ("sausage digits"), and extra-articular manifestations including keratoderma blennorrhagica (hyperkeratotic pustular rash on soles/palms) and circinate balanitis (painless annular lesions on glans penis). [4,5]

Key Facts

• Classification: Seronegative spondyloarthropathy (SpA)
• Triggers: Post-enteric (Campylobacter, Salmonella, Shigella, Yersinia) or post-STI (Chlamydia)
• HLA-B27: Positive in 60-80%; associated with more severe and chronic disease
• Triad: Arthritis + Urethritis + Conjunctivitis (only 30-40% complete)
• Pattern: Asymmetric oligoarthritis, lower limb predominant
• Timing: 1-4 weeks post-infection
• Prognosis: Self-limiting in 60-70% (3-12 months); chronic in 15-30%
• Treatment: NSAIDs first-line; DMARDs for chronic disease
• Red Flags: Anterior uveitis, septic arthritis differential

Clinical Pearls

"Sterile Joint, Distant Infection": The arthritis is sterile — no organisms are cultured from synovial fluid, distinguishing it from septic arthritis.

"Can't See, Can't Pee, Can't Climb a Tree": Classic mnemonic for the Reiter's triad, though the complete triad is present in only 1/3 of patients.

"HLA-B27: Severity Predictor": HLA-B27 positivity correlates with chronic disease, recurrence, and progression to axial spondyloarthritis.

"Treat Chlamydia, Not Arthritis": Antibiotic treatment of underlying Chlamydia prevents transmission but does NOT shorten the arthritis duration.

"Keratoderma Mimics Psoriasis": The hyperkeratotic skin lesions on soles/palms are clinically and histologically indistinguishable from pustular psoriasis.

"Lower Limb Loves Reactive": Unlike rheumatoid arthritis (upper limb predominant), reactive arthritis preferentially affects knees, ankles, and feet.

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2. Epidemiology

Incidence and Prevalence

Demographics

Triggering Infections

Genitourinary Triggers

Gastrointestinal Triggers

Other Reported Triggers (Rare)

• Respiratory: Chlamydia pneumoniae, Mycoplasma pneumoniae
• Genitourinary: Chlamydia trachomatis serovars L1-L3 (lymphogranuloma venereum)

Exam Detail: MRCP/FRACP Exam Point: Questions often test knowledge of which organisms cause post-enteric vs. post-STI reactive arthritis. Remember the "Big 4" gastrointestinal triggers (Salmonella, Shigella, Campylobacter, Yersinia) and Chlamydia as the dominant STI trigger. E. coli and Staphylococcus are NOT typical triggers and should prompt consideration of septic arthritis instead.

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3. Aetiology and Pathophysiology

Genetic Susceptibility

HLA-B27 Association

[8,9]

HLA-B27 Structure:

• Class I major histocompatibility complex (MHC) molecule
• Presents intracellular peptides to CD8+ T cells
• Heavy chain encoded by HLA-B gene on chromosome 6p21.3
• Over 170 HLA-B27 subtypes; HLA-B27:05 most common in Caucasians

Pathogenic Mechanisms of HLA-B27 (Competing Hypotheses)

Exam Detail: 1. Arthritogenic Peptide Hypothesis

• HLA-B27 presents bacterial peptides that mimic self-antigens
• Molecular mimicry between bacterial and host proteins
• Cross-reactive T-cell responses target joint tissues
• Evidence: Peptides from Chlamydia, Salmonella, Yersinia bind HLA-B27

2. Misfolding and Endoplasmic Reticulum (ER) Stress

• HLA-B27 heavy chains misfold and form homodimers
• Accumulation triggers unfolded protein response (UPR)
• ER stress activates IL-23/IL-17 inflammatory pathway
• Independent of peptide presentation function

3. HLA-B27 Homodimers and Innate Immunity

• Cell surface HLA-B27 homodimers activate innate immune receptors
• Bind killer immunoglobulin-like receptors (KIR) on NK cells and T cells
• Promote survival of CD4+ T cells producing IL-17
• IL-17 drives synovial inflammation

4. Bacterial Persistence

• Intracellular bacteria (especially Chlamydia) persist in synovium
• HLA-B27+ cells may fail to clear intracellular pathogens efficiently
• Chronic antigen stimulation maintains inflammation
• Evidence: Bacterial DNA detected in synovium months post-infection

[10,11]

Immunopathogenesis

The Molecular Cascade

Triggering Infection (GI or GU)
         ↓
Bacterial Antigens Disseminate
         ↓
HLA-B27+ Antigen Presenting Cells Activated
         ↓
CD4+ Th17 Cell Activation (IL-23 pathway)
         ↓
IL-17, IL-22, TNF-α Production
         ↓
Synovial Inflammation + Entheseal Inflammation
         ↓
Clinical Arthritis + Enthesitis + Extra-articular Features

Key Cytokines: [12]

• IL-23: Central to Th17 differentiation
• IL-17A/F: Recruit neutrophils, induce synovial inflammation
• IL-22: Epithelial inflammation, skin manifestations
• TNF-α: Pro-inflammatory; target of biologic therapy

Why Joints? (Tropism for Synovium and Entheses)

1. Bacterial Antigen Deposition: Bacterial lipopolysaccharide (LPS) and DNA detected in synovial fluid [13]
2. Entheseal Mechanical Stress: Repetitive microtrauma at entheses (Achilles, plantar fascia) creates inflammatory niche
3. Rich Blood Supply: Synovium highly vascularized, facilitating immune cell infiltration
4. Expression of Adhesion Molecules: Synovial endothelium upregulates ICAM-1, VCAM-1

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4. Clinical Presentation

Timeline

Classic Triad (Reiter's Syndrome)

[3,14]

Articular Features

Distribution and Pattern

Examination Findings

• Warm, swollen, tender joints
• Joint effusions (especially knees)
• Reduced range of motion
• Dactylitis: "Sausage digit" — diffuse swelling of entire digit (toe > finger)
• Enthesitis: Tender Achilles insertion, plantar fascia insertion (heel pain)

Exam Detail: OSCE/PACES Examination Tip: When examining a patient with oligoarthritis, specifically assess:

1. Symmetry: Asymmetric pattern suggests seronegative SpA (ReA, PsA) over RA
2. Distribution: Lower limb predominance in ReA vs. small hand joints in RA
3. Entheses: Palpate Achilles tendon insertion and plantar fascia — tenderness indicates enthesitis (hallmark of SpA)
4. Dactylitis: Inspect digits for uniform "sausage" swelling (not just joint swelling)
5. Spine: Ask about inflammatory back pain, assess spinal mobility (Schober's test, lateral flexion)

Extra-articular Features

Ocular Manifestations

[15]

⚠️ RED FLAG: Anterior uveitis is a sight-threatening emergency. Symptoms: severe eye pain, photophobia, blurred vision, ciliary flush (redness around cornea). Requires same-day ophthalmology review.

Mucocutaneous Manifestations

[4,5]

Exam Detail: Viva Question: "How do you differentiate keratoderma blennorrhagica from psoriasis?"

Model Answer:

• Clinically indistinguishable: Both show hyperkeratotic plaques on soles/palms
• Histology: Nearly identical (parakeratosis, acanthosis, neutrophilic infiltrate)
• Differentiation relies on context:
  • "Keratoderma: Associated with arthritis, urethritis, post-infectious history"
  • "Psoriasis: May have psoriatic arthritis (but DIP joint involvement, nail pitting more typical); chronic course; family history"
• Key Point: Reactive arthritis and psoriatic arthritis are both seronegative spondyloarthropathies with overlapping features; consider entire clinical picture

Genitourinary Features

Note: "Sterile urethritis" is characteristic — Gram stain shows neutrophils but no organisms; standard bacterial culture negative (unless Chlamydia testing performed).

Cardiac Manifestations (Rare, Chronic Disease)

• Aortitis: Ascending aorta inflammation
• Aortic Regurgitation: Leaflet thickening, incompetence
• Conduction Defects: AV block (1st-degree most common)
• Pericarditis: Rare

[16]

Frequency: less than 5% overall; more common in chronic HLA-B27+ disease with axial involvement

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5. Differential Diagnosis

Key Differentials by Presentation

Acute Oligoarthritis

Seronegative Spondyloarthropathy Differential

[2,17]

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6. Investigations

Initial Assessment

Blood Tests

Note: HLA-B27 is NOT diagnostic — present in 6-8% of healthy Caucasian population. It supports the diagnosis in the appropriate clinical context but is neither sensitive nor specific enough to diagnose in isolation. [8]

Infection Screening

Key Point: Infection may have cleared by the time arthritis develops (1-4 weeks later). Negative microbiology does NOT exclude reactive arthritis; diagnosis is clinical supported by serology or history. [6,7]

Synovial Fluid Analysis

Indication: Monoarthritis or dominant large joint effusion → mandatory to exclude septic arthritis

[13,18]

⚠️ RED FLAG: If clinical suspicion of septic arthritis (fever, severe pain, systemically unwell, risk factors), treat empirically with IV antibiotics while awaiting culture results. Do NOT delay treatment.

Imaging

Plain Radiographs

Indication: Baseline assessment; exclude other pathology

Findings (in acute phase):

• Often normal in early disease
• Soft tissue swelling around affected joints
• Joint effusions

Findings (in chronic/recurrent disease):

• Enthesophytes: Bony spurs at tendon insertions (Achilles, plantar fascia)
• Periostitis: Periosteal new bone formation (calcaneus, metatarsals)
• Sacroiliitis: Unilateral or asymmetric bilateral (less common than AS)
• Erosions: Marginal erosions (especially feet)
• Ankylosis: Rare; late complication

Ultrasound

Advantages: Real-time assessment; no radiation; detects early changes

Findings:

• Joint effusions: Anechoic/hypoechoic fluid
• Synovial hypertrophy: Thickened, hypoechoic synovium
• Power Doppler signal: Active inflammation (hyperaemia)
• Enthesitis: Hypoechoic thickening, bony erosions, calcifications at entheses
• Dactylitis: Diffuse tenosynovitis and soft tissue oedema

MRI

Indication: Suspected sacroiliitis, axial involvement, or chronic disease assessment

Findings:

• Bone marrow oedema: STIR/T2 high signal in subchondral bone
• Synovitis: Enhanced synovium on post-contrast T1
• Enthesitis: High signal at tendon insertions
• Sacroiliitis: Bone marrow oedema, erosions, sclerosis, ankylosis

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7. Management

General Principles

1. Symptomatic Treatment: NSAIDs first-line for arthritis and enthesitis
2. Treat Underlying Infection: Antibiotics for active Chlamydia (does NOT shorten arthritis)
3. DMARDs for Chronic Disease: Sulfasalazine or methotrexate if symptoms > 3-6 months
4. Biologic Therapy: Anti-TNF for refractory disease
5. Multidisciplinary Approach: Rheumatology, sexual health, ophthalmology, physiotherapy

Management Algorithm

┌───────────────────────────────────────────────────────────────────────┐
│                   REACTIVE ARTHRITIS MANAGEMENT                       │
├───────────────────────────────────────────────────────────────────────┤
│                                                                       │
│  ACUTE PHASE (0-3 months)                                             │
│  ┌─────────────────────────────────────────────────────────────────┐ │
│  │ 1. SYMPTOMATIC TREATMENT                                        │ │
│  │    • NSAIDs (Naproxen 500mg BD or Indomethacin 25-50mg TDS)    │ │
│  │    • Intra-articular corticosteroid injection (large joints)   │ │
│  │    • Short-course oral prednisolone (if severe, 20-40mg daily) │ │
│  │                                                                 │ │
│  │ 2. TREAT INFECTION                                              │ │
│  │    • Chlamydia: Doxycycline 100mg BD × 7 days OR               │ │
│  │                  Azithromycin 1g stat                          │ │
│  │    • Partner notification and treatment                        │ │
│  │    • GI pathogens: Usually supportive (antibiotics if severe)  │ │
│  │                                                                 │ │
│  │ 3. PHYSIOTHERAPY                                                │ │
│  │    • Range-of-motion exercises                                 │ │
│  │    • Strengthening (once acute inflammation settles)           │ │
│  └─────────────────────────────────────────────────────────────────┘ │
│                                                                       │
│  PERSISTENT/CHRONIC PHASE (> 3-6 months)                               │
│  ┌─────────────────────────────────────────────────────────────────┐ │
│  │ 4. DMARDs                                                       │ │
│  │    • FIRST-LINE: Sulfasalazine 500mg daily → 2-3g daily        │ │
│  │    • ALTERNATIVE: Methotrexate 15-25mg weekly (if SSZ fails)   │ │
│  │                                                                 │ │
│  │ 5. BIOLOGICS (Refractory Disease)                               │ │
│  │    • Anti-TNF: Etanercept, Adalimumab, Infliximab              │ │
│  │    • IL-17 inhibitors: Secukinumab, Ixekizumab (emerging)      │ │
│  └─────────────────────────────────────────────────────────────────┘ │
│                                                                       │
│  EXTRA-ARTICULAR COMPLICATIONS                                        │
│  ┌─────────────────────────────────────────────────────────────────┐ │
│  │ • ANTERIOR UVEITIS: **Urgent ophthalmology** referral          │ │
│  │   → Topical corticosteroids (prednisolone 1% hourly)           │ │
│  │   → Cycloplegic (cyclopentolate 1%)                            │ │
│  │   → Consider systemic steroids if severe                       │ │
│  │                                                                 │ │
│  │ • ENTHESITIS: Local corticosteroid injection, physiotherapy    │ │
│  └─────────────────────────────────────────────────────────────────┘ │
└───────────────────────────────────────────────────────────────────────┘

Pharmacotherapy

NSAIDs

First-line for symptomatic relief

Contraindications: Active peptic ulcer, severe renal impairment (eGFR less than 30), heart failure, high CV risk

Precautions: PPI co-prescription if GI risk factors; monitor renal function and BP

[19]

Corticosteroids

Note: Avoid long-term systemic steroids; transition to DMARDs if chronic disease.

DMARDs (Disease-Modifying Anti-Rheumatic Drugs)

Indication: Persistent symptoms > 3-6 months despite NSAIDs; chronic/recurrent disease

Evidence: Limited high-quality RCT evidence for DMARDs in reactive arthritis specifically; extrapolated from other seronegative SpA (psoriatic arthritis, ankylosing spondylitis). [20]

Biologic Therapy

Indication: Severe, refractory disease despite NSAIDs and ≥1 DMARD

Pre-biologic Screening: TB (quantiferon/T-SPOT, CXR), hepatitis B/C, HIV, baseline CXR

[21]

Antibiotic Therapy for Chlamydia

Indication: Proven or suspected Chlamydia trachomatis infection

Key Points:

• Treating Chlamydia does NOT shorten arthritis duration (arthritis is sterile) [22]
• Purpose: Eradicate infection, prevent transmission, prevent re-infection
• Partner notification and treatment mandatory
• Test of cure not routinely needed (unless pregnant, ongoing symptoms, or poor adherence)

Controversial: Prolonged antibiotics (3-6 months) for chronic reactive arthritis

• Evidence: Limited; one RCT (Lauhio et al.) showed benefit of 3-month doxycycline + rifampicin, but not replicated [23]
• Current Consensus: NOT recommended routinely; consider only in research settings

Non-Pharmacological Management

Physiotherapy

Enthesitis-Specific: Eccentric strengthening for Achilles tendinopathy, plantar fascia stretching

Patient Education and Self-Management

• Prognosis: Reassure most cases self-limiting (3-12 months)
• Activity Modification: Avoid high-impact activities during acute inflammation
• Sexual Health: Safe sex practices, partner treatment
• Eye Symptoms: Seek urgent care if eye pain, redness, photophobia

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8. Complications

Musculoskeletal Complications

Ocular Complications

Cardiac Complications (Rare)

• Aortitis: Ascending aorta inflammation
• Aortic Regurgitation: 2-5% in chronic HLA-B27+ disease with axial involvement
• Conduction Defects: AV block, bundle branch block

Monitoring: Echocardiography if chronic disease, murmurs, or symptoms suggestive of aortic regurgitation

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9. Prognosis and Outcomes

Acute Episode

Long-Term Outcomes

Favourable Prognostic Factors:

• HLA-B27 negative
• Post-enteric (vs. post-STI) trigger
• Mild initial disease
• Isolated peripheral arthritis (no axial involvement)
• Complete resolution of triggering infection

Poor Prognostic Factors:

• HLA-B27 positive (especially HLA-B27:05 homozygous)
• Severe initial disease (polyarthritis, high CRP)
• Hip involvement
• Recurrent infections (especially untreated Chlamydia)
• Early axial symptoms (inflammatory back pain, sacroiliitis)

[9,24]

Functional Outcomes

• Return to Normal Activity: 70-80% by 12 months
• Residual Symptoms: 20-30% have intermittent joint pain or stiffness
• Work Disability: less than 5% in uncomplicated cases; up to 20-30% if chronic/severe

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10. Prevention

Primary Prevention

No specific prophylaxis available; general infection prevention:

• Food Hygiene: Prevent Salmonella, Campylobacter, Yersinia (proper food handling, cooking)
• Safe Sex Practices: Prevent Chlamydia (barrier contraception, regular STI screening)
• Hand Hygiene: Prevent Shigella transmission

Secondary Prevention (Preventing Recurrence)

1. Eradicate Chlamydia: Complete antibiotic course, partner treatment, test of cure if indicated
2. Avoid Re-Infection: Safe sex, treat partners
3. Prompt Treatment of New Infections: Early antibiotics for GI/GU infections (controversial efficacy)
4. HLA-B27+ Patients: Close monitoring for recurrence and axial progression

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11. Examination Focus (MRCP/FRACP PACES, Viva)

Clinical Case Scenario

Station: History Taking or Brief Clinical Consultation

Scenario: 28-year-old man presents with 3-week history of painful, swollen right knee and left ankle. He mentions he had diarrhoea 4 weeks ago after a barbecue. He also has burning on urination and red, gritty eyes.

Viva Questions and Model Answers

Q1: "What is your differential diagnosis?"

Model Answer:

"The combination of oligoarthritis, urethritis, and conjunctivitis following a gastrointestinal infection is highly suggestive of reactive arthritis.

My differential diagnosis includes:

1. Reactive Arthritis — most likely given the classic triad and temporal relationship to GI infection
2. Septic Arthritis — must exclude in any acute monoarthritis; would expect fever, severe pain, single joint
3. Gonococcal Arthritis — sexually active age group; can cause arthritis-dermatitis syndrome with migratory polyarthralgia
4. Gout/Pseudogout — possible in monoarthritis (knee) but wouldn't explain urethritis or conjunctivitis
5. Other Seronegative Spondyloarthropathies — psoriatic arthritis (ask about skin/nails), early ankylosing spondylitis (ask about back pain)

I would investigate with joint aspiration (exclude septic arthritis), inflammatory markers, RF/anti-CCP (seronegative status), HLA-B27, and infection screening (stool culture, Chlamydia NAAT)."

Q2: "What organisms cause reactive arthritis?"

Model Answer:

"Reactive arthritis is triggered by gastrointestinal or genitourinary infections:

Gastrointestinal triggers (post-enteric):

• Salmonella species (non-typhoidal)
• Shigella flexneri
• Campylobacter jejuni
• Yersinia enterocolitica

Genitourinary trigger (post-STI):

• Chlamydia trachomatis — the most common trigger in developed countries

The arthritis develops 1-4 weeks after the infection. Importantly, the joint is sterile — no organisms are cultured from synovial fluid, distinguishing it from septic or gonococcal arthritis."

Q3: "What is the significance of HLA-B27 in reactive arthritis?"

Model Answer:

"HLA-B27 is a class I MHC molecule present in 6-8% of the general Caucasian population but found in 60-80% of patients with reactive arthritis.

Clinical Significance:

1. Risk Stratification: HLA-B27+ individuals have a 20-25% risk of developing reactive arthritis after a triggering infection, compared to 1-3% in HLA-B27 negative individuals.

2. Disease Severity: HLA-B27+ patients tend to have:

   • More severe disease
   • Higher likelihood of chronic arthritis (30-50% vs. 10-15%)
   • Greater risk of axial involvement (sacroiliitis, inflammatory back pain)
   • Higher recurrence rates (50% vs. 15%)

3. Prognosis: HLA-B27 positivity predicts progression to ankylosing spondylitis in 5-10% of cases.

4. Diagnostic Value: HLA-B27 is NOT diagnostic in isolation — it supports the diagnosis in the appropriate clinical context but lacks sufficient sensitivity and specificity to diagnose alone.

It's part of the seronegative spondyloarthropathy family, which includes ankylosing spondylitis, psoriatic arthritis, and IBD-associated arthritis."

Q4: "How would you manage this patient?"

Model Answer:

"My management follows a stepwise approach:

Immediate (Acute Phase):

1. Exclude Septic Arthritis: Joint aspiration of the knee — send for Gram stain, culture, crystals, cell count
2. Symptomatic Treatment: NSAIDs first-line (e.g., naproxen 500mg BD or indomethacin 25-50mg TDS)
3. Intra-articular Steroid: If large joint effusion and septic arthritis excluded (e.g., triamcinolone 40mg in knee)
4. Treat Underlying Infection:
   • Chlamydia: Doxycycline 100mg BD for 7 days (or azithromycin 1g stat)
   • Partner notification and treatment
   • Note: This eradicates infection but does NOT shorten arthritis duration
5. Ophthalmology Referral: If symptoms suggest anterior uveitis (pain, photophobia) rather than simple conjunctivitis

Short-Term (Weeks):

6. Physiotherapy: Range-of-motion exercises, strengthening once acute inflammation settles
7. Patient Education: Reassure most cases resolve in 3-12 months; safe sex; eye symptom red flags

If Chronic (> 3-6 months):

8. DMARDs: Sulfasalazine 500mg → 2-3g daily (first-line) or methotrexate 15-25mg weekly
9. Biologics: Anti-TNF (etanercept, adalimumab) if refractory to DMARDs

Follow-Up:

• Monitor CRP, functional status
• Watch for axial symptoms (inflammatory back pain)
• Screen for recurrent uveitis
• Long-term HLA-B27+ patients: consider echocardiography if chronic (aortic regurgitation risk)"

Q5: "The patient asks if antibiotics will cure his arthritis. What do you tell him?"

Model Answer:

"I would explain: 'The antibiotics are important to clear the infection and prevent it spreading to your partner, but unfortunately they won't shorten how long your joint pain lasts.

This is because your arthritis is a reaction to the infection — your immune system is reacting to the bacteria, but the bacteria themselves are not in your joints. We call this "reactive arthritis" or "sterile arthritis".

However, treating the Chlamydia is still crucial because:

1. It prevents you from passing it to sexual partners
2. It prevents re-infection, which could trigger another episode of arthritis
3. Untreated Chlamydia can cause other complications

The good news is that in most people (60-70%), the arthritis resolves on its own over 3 to 12 months. We'll treat your symptoms with anti-inflammatory medications in the meantime.'"

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12. Patient/Layperson Explanation

What is Reactive Arthritis?

Reactive arthritis is joint inflammation (pain, swelling, stiffness) that happens after an infection in another part of your body — usually your gut (from food poisoning) or your urinary system (from a sexually transmitted infection like chlamydia).

The infection triggers your immune system to "overreact", causing inflammation in your joints even though the bacteria are not actually in the joints themselves. This is why it's called "reactive" arthritis.

What Are the Symptoms?

The most common symptoms are:

• Joint pain and swelling — usually in your knees, ankles, or feet; often worse in the morning or after rest
• Eye redness — red, gritty eyes (like having sand in your eyes); sometimes more serious eye pain and light sensitivity
• Burning when urinating or discharge
• Heel pain or sausage-like swelling of toes or fingers
• Sometimes a rash on the soles of your feet or palms

The symptoms usually start 1 to 4 weeks after the infection.

What Causes It?

The most common triggers are:

• Food poisoning bacteria like Salmonella, Campylobacter, or Shigella
• Sexually transmitted infections, especially chlamydia

Some people have a gene called HLA-B27 that makes them more likely to get reactive arthritis after an infection.

Is It Serious?

For most people, reactive arthritis gets better on its own within 3 to 12 months. However:

• About 1 in 5 people may have symptoms lasting longer or coming back
• If you have the HLA-B27 gene, you may have more severe symptoms or a longer illness
• Rarely, it can cause permanent joint damage or serious eye problems (if not treated)

How is It Treated?

1. Anti-inflammatory tablets (NSAIDs) like ibuprofen or naproxen to reduce pain and swelling
2. Antibiotics to clear the infection (e.g., chlamydia) — this won't cure the arthritis but prevents spread to partners
3. Steroid injections into swollen joints if needed
4. Physiotherapy to keep your joints moving
5. Stronger medications (DMARDs or biologics) if symptoms last more than 6 months

Will I Need Antibiotics?

If the trigger was chlamydia, you'll be given antibiotics (usually doxycycline or azithromycin). Your sexual partner(s) will also need treatment.

Important: The antibiotics clear the infection but do not shorten the arthritis — the joint inflammation takes time to settle on its own.

Can I Prevent It?

• Practice safe sex to avoid chlamydia
• Wash hands and cook food properly to avoid food poisoning
• If you've had reactive arthritis before, treating new infections early might reduce the risk of it coming back (though this is not proven)

When Should I Seek Urgent Help?

See a doctor urgently if you have:

• Severe eye pain, blurred vision, or sensitivity to light — this could be a serious eye complication (uveitis)
• Fever and very painful, hot, swollen joint — this could be a different type of infection in the joint (septic arthritis)

What is the Long-Term Outlook?

• Most people recover fully within a year
• About 15-30% have symptoms that last longer or come back
• Regular follow-up with your doctor is recommended, especially if you have the HLA-B27 gene

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13. Evidence and Guidelines

Key Guidelines

1. British Society for Rheumatology (BSR)

   • BSR and British Health Professionals in Rheumatology guideline for the treatment of axial spondyloarthritis (including ankylosing spondylitis) with biologics (2017) [25]
   • Reactive arthritis managed as peripheral spondyloarthritis; escalation to biologics if refractory

2. European League Against Rheumatism (EULAR)

   • EULAR recommendations for the management of psoriatic arthritis with pharmacological therapies (2019) [26]
   • Extrapolated to other seronegative SpA including reactive arthritis

3. British Association for Sexual Health and HIV (BASHH)

   • UK National Guideline for the Management of Pelvic Inflammatory Disease (2018)
   • Covers treatment of Chlamydia in reactive arthritis context

Landmark Studies

No large-scale RCTs specific to reactive arthritis due to heterogeneity and self-limiting nature. Evidence extrapolated from:

• Seronegative spondyloarthropathy trials (AS, PsA)
• Observational cohort studies
• Case series

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14. References

Primary Resources

1. Selmi C, Gershwin ME. Diagnosis and classification of reactive arthritis. Autoimmun Rev. 2014;13(4-5):546-549. doi:10.1016/j.autrev.2014.01.005

2. Barber CE, Kim J, Inman RD, Esdaile JM, James MT. Antibiotics for treatment of reactive arthritis: a systematic review and metaanalysis. J Rheumatol. 2013;40(6):916-928. doi:10.3899/jrheum.121192

3. Keat AC, Thomas BJ, Taylor-Robinson D. Chlamydial infection in the aetiology of arthritis. Br Med Bull. 1983;39(2):168-174. doi:10.1093/oxfordjournals.bmb.a071807

4. Leirisalo-Repo M. Reactive arthritis. Scand J Rheumatol. 2005;34(4):251-259. doi:10.1080/03009740510026706

5. Hannu T. Reactive arthritis. Best Pract Res Clin Rheumatol. 2011;25(3):347-357. doi:10.1016/j.berh.2011.01.018

6. Carter JD, Hudson AP. Reactive arthritis: clinical aspects and medical management. Rheum Dis Clin North Am. 2009;35(1):21-44. doi:10.1016/j.rdc.2009.03.010

7. Hannu T, Mattila L, Rautelin H, et al. Campylobacter-triggered reactive arthritis: a population-based study. Rheumatology (Oxford). 2002;41(3):312-318. doi:10.1093/rheumatology/41.3.312

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