Infectious Arthritis¶
Chapter 135 | Part 5: Infectious Diseases
KEY CLINICAL POINTS¶
- Common pathogens include Staphylococcus aureus, Neisseria gonorrhoeae, Mycobacterium tuberculosis, and fungi (e.g., Candida, Aspergillus).
- Acute bacterial arthritis typically involves a single joint with synovial fluid cell counts >100,000/ µ L (90% neutrophils).
- Differential diagnosis includes crystal-induced arthritis, reactive arthritis, and autoimmune conditions like rheumatoid arthritis.
- Diagnosis relies on synovial fluid analysis (Gram stain, culture, NAATs), imaging, and clinical context.
- Treatment requires antibiotics, joint drainage, and tailored therapy based on pathogen susceptibility.
1. DEFINITION & OVERVIEW¶
Infectious arthritis is a joint infection caused by bacteria, fungi, viruses, or parasites. It presents as acute or chronic inflammation with potential for cartilage destruction. Early diagnosis and treatment are critical to prevent joint damage.
Table 135-1 Differential Diagnosis of Arthritis Syndromes¶
| ACUTE MONARTICULAR ARTHRITIS | CHRONIC MONARTICULAR ARTHRITIS | POLYARTICULAR ARTHRITIS |
|---|---|---|
| Staphylococcus aureus | Mycobacterium tuberculosis | Neisseria meningitidis |
| Streptococcus pneumoniae | Nontuberculous mycobacteria | N. gonorrhoeae |
| Gram-negative bacilli | Borrelia burgdorferi | Nongonococcal bacterial arthritis |
| Neisseria gonorrhoeae | Treponema pallidum | Bacterial endocarditis |
| Candida spp. | Coccidioides immitis | Candida spp. |
| Crystal-induced arthritis | Blastomyces dermatitidis | Poncet’s disease |
| Fracture | Aspergillus spp. | Hepatitis B virus |
| Hemarthrosis | Cryptococcus neoformans | Parvovirus B19 |
| Foreign body | Nocardia spp. | HIV |
| Osteoarthritis | Brucella spp. | Human T-lymphotropic virus type 1 |
| Ischemic necrosis | Legg-Calvé-Perthes disease | Rubella virus |
| Monoarticular rheumatoid arthritis | Osteoarthritis | Arthropod-borne viruses |
| Sickle cell disease flare | Serum sickness | Sarcoidosis |
1.1 Pathogenesis¶
Bacteria enter joints via hematogenous spread, contiguous infection, or direct inoculation. Neutrophils and bacteria invade synovium, leading to cartilage degradation within 48 hours. Pathogens include S. aureus, N. gonorrhoeae, mycobacteria, and fungi.
1.2 Microbiology¶
Common pathogens: S. aureus (most common), N. gonorrhoeae, M. tuberculosis, gram-negative bacilli, and fungi. Viruses (e.g., HIV, hepatitis B) and spirochetes (e.g., B. burgdorferi) also cause arthritis.
2. EPIDEMIOLOGY¶
Infectious arthritis occurs in 0.5–2% of total joint replacements. Risk factors include IV drug use, diabetes, immunosuppression, and prior joint surgery. Acute bacterial arthritis is most common in children and young adults, while mycobacterial infections are more prevalent in immunocompromised hosts.
2.1 Demographics¶
Acute bacterial arthritis peaks in children <5 years (S. aureus, GBS) and young adults (N. gonorrhoeae). Chronic infections (e.g., tuberculosis) are more common in older adults and immunocompromised patients.
2.2 Risk Factors¶
IV drug use, diabetes, hemodialysis, rheumatoid arthritis, and immunosuppressive therapy increase risk. HIV-positive patients are prone to fungal and mycobacterial arthritis.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
Pathogens include bacteria (S. aureus, N. gonorrhoeae), fungi (Candida, Aspergillus), viruses (HIV, hepatitis B), and spirochetes (B. burgdorferi). Infection leads to synovial inflammation, neutrophil infiltration, and cartilage destruction. Biofilm formation in prosthetic joints complicates treatment.
3.1 Bacterial Mechanisms¶
S. aureus adheres to cartilage via surface adhesins and endotoxins. Gram-negative bacilli (e.g., Pseudomonas) cause pseudomonal arthritis. Mycobacteria (e.g., M. tuberculosis) form granulomas.
3.2 Viral and Fungal Pathogenesis¶
Viruses (e.g., HIV) impair immune response, allowing opportunistic infections. Fungi (e.g., Histoplasma) cause granulomatous inflammation. Sporotrichosis spreads via direct inoculation.
4. CLINICAL FEATURES¶
Acute presentation includes joint pain, swelling, erythema, and fever. Chronic infections (e.g., tuberculosis) present with low-grade fever and insidious joint involvement. Complications include joint destruction, deformity, and septic arthritis in immunocompromised patients.
4.1 Acute vs. Chronic¶
Acute: Sudden onset with severe pain and effusion. Chronic: Gradual onset with low-grade fever and joint destruction (e.g., tuberculous arthritis).
4.2 Systemic Symptoms¶
Fever (38.3–38.9°C), leukocytosis, and elevated ESR/C-reactive protein. HIV-associated arthritis may present with arthralgia without fever.
5. DIFFERENTIAL DIAGNOSIS¶
Distinguish infectious arthritis from crystal-induced arthritis (gout/pseudogout), reactive arthritis, rheumatoid arthritis, and autoimmune conditions. Consider viral arthritis (e.g., HIV, hepatitis B) and parasitic infections (e.g., schistosomiasis).
5.1 Crystal-Induced Arthritis¶
Gout (monosodium urate crystals) and pseudogout (calcium pyrophosphate crystals) mimic septic arthritis. Synovial fluid analysis confirms crystal presence.
5.2 Reactive Arthritis¶
Post-infectious arthritis following Chlamydia, Salmonella, or Yersinia. Features include asymmetric oligoarthritis and extraarticular manifestations (e.g., conjunctivitis).
6. INVESTIGATIONS & DIAGNOSIS¶
Diagnosis requires synovial fluid analysis (Gram stain, culture, NAATs), imaging (X-ray, MRI, ultrasound), and clinical evaluation. Cell counts >100,000/ µ L with >90% neutrophils suggest bacterial infection.
6.1 Synovial Fluid Analysis¶
Turbid, purulent fluid with >100,000 cells/ µ L (90% neutrophils) indicates bacterial infection. Crystal detection confirms gout/pseudogout. Procalcitonin may aid in differentiating bacterial vs. viral etiology.
6.2 Imaging¶
X-ray shows joint space narrowing, erosions, or effusion. MRI/CT detects early changes in hip, sacroiliac, or spinal infections. Ultrasound guides aspiration.
7. MANAGEMENT & TREATMENT¶
Prompt antibiotic therapy, joint drainage, and pathogen-specific treatment are critical. Prosthetic joint infections require prosthesis removal and long-term antibiotics. HIV-associated arthritis may need antiretroviral therapy.
7.1 Antibiotic Therapy¶
Ceftriaxone (1g IV) for gonococcal arthritis. Vancomycin (15–20 mg/kg) for MRSA. Fluoroquinolones (e.g., ciprofloxacin) for gram-negative infections. Rifampin + quinolone for prosthetic joint infections.
7.2 Drainage and Surgery¶
Needle aspiration or arthroscopy for accessible joints. Arthrotomy or reimplantation for prosthetic infections. Debridement of infected tissue and synovectomy may be required.
8. PROGNOSIS & COMPLICATIONS¶
Early treatment prevents joint destruction. Complications include chronic arthritis, deformity, and septic arthritis in immunocompromised patients. Prosthetic joint infections have high recurrence rates without prosthesis removal.
8.1 Long-Term Outcomes¶
Prompt treatment leads to full recovery in 60–70% of cases. Chronic infections (e.g., tuberculosis) may require 6–9 months of antituberculous therapy.
8.2 Complications¶
Joint destruction, osteoarthritis, and disability. Prosthetic joint infections may necessitate amputation if salvage is not possible.
9. SPECIAL CONSIDERATIONS¶
Pregnancy: Avoid certain antibiotics (e.g., fluoroquinolones). Pediatrics: Monitor for septic arthritis in children with fever and joint pain. HIV patients require antiretroviral therapy and antifungal agents for opportunistic infections.
9.1 Immunocompromised Patients¶
Higher risk of fungal and mycobacterial infections. Prophylaxis for opportunistic pathogens (e.g., Pneumocystis, Cryptococcus).
9.2 Prosthetic Joint Infections¶
Require prosthesis removal and long-term antibiotics. Rifampin + quinolone regimen reduces recurrence. Avoid dental procedures without prophylaxis.
10. KEY POINTS & CLINICAL PEARLS¶
- Synovial fluid analysis is critical for diagnosis.
- Early antibiotics and drainage prevent joint destruction.
- Prosthetic infections require prosthesis removal.
- HIV-associated arthritis needs antiretroviral therapy.
- Use NAATs for rapid detection of pathogens in culture-negative cases.