Description

• Infection due to bacterial invasion of the joint space
• Systems affected: musculoskeletal
• Synonyms: suppurative arthritis; infectious arthritis; pyarthrosis; pyogenic arthritis; bacterial arthritis

Epidemiology

Gender differences:

• Gonococcal: female > male
• Nongonococcal: male > female

• May occur at any age; incidence is higher in very young and in the elderly.
• ~20,000 cases/year in U.S. (~8 cases per 100,000 person-years).
• Disseminated gonococcal infection is ~3/100,000 person-years

• 27% of patients presenting with monoarticular arthritis have nongonococcal septic arthritis (1).
• With increasing prevalence of prosthetic joints, infected hardware is now most common form of septic arthritis (ranging from ~2–10% of all joint recipients)

Etiology and Pathophysiology

• Multiple pathogens
• Nongonococcal:
  • Staphylococcus aureus (most common in adults)
    • Methicillin-resistant S. aureus risk increased in elderly, intravenous drug users (IVDU), postsurgical
  • Streptococcus spp. (second most common in adults)
  • Gram-negative rods (GNR): IVDU, trauma, extremes of age, immunosuppressed
• Neisseria gonorrhoeae (most common in young, sexually active adults)
• Other: rickettsial (e.g., Lyme), fungal, mycobacterial
• Risk by specific age (2):
  • <1 month: S. aureus, group B streptococcus (GBS), GNR
  • 1 month to 4 years: S. aureus, Streptococcus pneumoniae, Neisseria meningitidis
  • 16 to 40 years: N. meningitidis, S. aureus
  • >40 years: S. aureus
• Patients with native joint infection are at increased risk for infection of prosthesis (of same joint should it require replacement)
• Specific high-risk groups:
  • Rheumatoid arthritis (RA): S. aureus
  • IVDU: S. aureus, GNR, opportunistic pathogens
  • Neonates: GBS
  • Immunocompromised: gram-negative bacilli, fungi
  • Trauma patients with open injuries: mixed flora
• Pathogenesis:
  • Hematogenous spread (most common)
  • Direct inoculation by microorganisms secondary to trauma or iatrogenesis (e.g., joint surgery)
  • Adjacent spread (e.g., osteomyelitis)
• Pathophysiology:
  • Microorganisms initially enter through synovial membrane and spread to the synovial fluid.
  • Resulting inflammatory response releases cytokines and destructive proteases leading to systemic symptoms and joint damage.

Risk Factors

• Age >80 years
• Low socioeconomic status, alcoholism
• Cellulitis and skin ulcers
• Violation of joint capsule
  • Prior orthopedic surgery
  • Intra-articular steroid injection
  • Trauma
• History of previous joint disease
  • Inflammatory arthritis (RA: 10-fold increased risk)
  • Osteoarthritis
  • Crystal arthritides
• Systemic illness
  • Diabetes mellitus, liver disease, HIV, malignancy, end-stage renal disease/hemodialysis, immunosuppression, sickle cell anemia
• Risks for hematogenous spread
  • IVDU, severe sepsis/systemic infection

General Prevention

• Prompt treatment of skin and soft tissue infections.
• Control risk factors.
• Immunization (S. pneumoniae, N. meningitidis)

Commonly Associated Conditions

Pre-existing joint conditions, previous joint trauma or surgery, prosthetic joint