Septic arthritis represents acute bacterial infection of a joint, with rapid neutrophil influx, cytokine release, and proteolytic enzyme activity causing irreversible cartilage destruction within days if untreated. Pathogens reach joints through hematogenous seeding (most common), direct inoculation from trauma or surgery, or contiguous spread from adjacent osteomyelitis. Annual incidence is 4-10 per 100,000 in the general population, increasing to 30-70 per 100,000 in patients with rheumatoid arthritis or prosthetic joints.
Pathogen distribution varies by age and host factors: Staphylococcus aureus accounts for 40-50% across age groups (with rising MRSA proportion), streptococci for 20-25%, gram-negative bacilli increasing in elderly and immunocompromised. Neisseria gonorrhoeae causes the disseminated gonococcal infection syndrome in sexually active young adults with characteristic migratory polyarthralgia, tenosynovitis, and pustular skin lesions. Children show age-specific patterns with Kingella kingae predominant in those under 4 years. Rare but important pathogens include Brucella in endemic areas, Mycobacterium tuberculosis in chronic monoarthritis, and fungi in immunocompromised hosts.
Diagnostic evaluation centers on emergent joint aspiration with synovial fluid analysis showing characteristically high leukocyte count (typically >50,000/μL with >75% neutrophils), positive gram stain or culture, and absence of crystals on polarized microscopy. Blood cultures, complete blood count, and inflammatory markers (CRP, ESR) support but do not exclude diagnosis. Imaging (ultrasound, MRI) helps assess deep joints and identify complications. Treatment requires emergent surgical drainage (arthroscopic preferred for accessible joints, open arthrotomy for hip and complex cases), parenteral empiric antimicrobial therapy guided by gram stain and clinical context (typically vancomycin plus ceftriaxone), and transition to pathogen-directed therapy with total duration of 2-4 weeks.