A. Characteristics

1. Most rapidly destructive form of arthritis
   1. Gonococcal and meningococcal
   2. Non-gonococcal - usually immunocompromised and/or pre-existing arthritis or joint damage
   3. Staphylococcus aureus is most common form of non-gonococcal arthritis
2. Gonococcal and Meningococcal [3]
   1. Reactive Arthritis (see below) - may be weeks or months post-infection
   2. Disseminated Infection - organisms may be cultured from joint (localized septic arthritis)
   3. Disseminated gonococcal infection may cause arthritis-dermatitis syndrome (ADS)
   4. ADS resembles systemic vasculitis with macules, petechiae, purulent vessicles and arthritis, and usually includes positive blood cultures
   5. Meningococcal form even if vaccination has been received
   6. Disseminated gonococcal infection may cause localized septic arthritis or
3. Non-Gonococcal
   1. Immunocompromised Host (mainly HIV) - atypical organisms
   2. Normal Host - streptococci and staphylococci
   3. Lyme Arthritis
4. Reactive Arthritis
   1. Acute, asymmetric arthritis
   2. Usually follows chlamydial (or ureaplasma) urethritis or infectious gastroenteritis
   3. Typically within 6 weeks of infection
   4. Mainly affects joints of legs (knees > ankles > feet)
   5. Enthesitis (inflammation of tendinous insertion on bone) is common; mainly of Achilles'
   6. Reiter's syndrome is related, also includes conjucntivitis with urethritis

B. Predisposing Factors for Non-Gonococcal Arthritis

1. Abnormal Joint
   1. Rheumatoid Arthritis
   2. Crystal Induced Arthritis
   3. Severe Osteoarthritis
   4. Joint Trauma
   5. Charcot Joint
   6. Hemarthrosis (especially in hemophiliacs)
   7. Prosthetic Joint - hip or knee
   8. Joint surgery
2. Systemic Factors
   1. Advancing Age
   2. Intravenous Drug Abuse (often with endocarditis)
   3. Skin infection overlying joint
   4. Sickle Cell Disease
3. Immunodeficiency / Immunosuppression
   1. Glucocorticoid therapy
   2. Diabetes mellitus
   3. HIV1 infection

C. Joints Involved

1. Knee 55%
2. Hip 11%
3. Ankle 8%
4. Shoulder 8%
5. Wrist 7%
6. Elbow 6%
7. Other
8. >1 Joint 12%

D. Organisms (non-gonococcal)

1. S. aureus ~50%
2. Group A Strep ~15%
3. Gram Negative Rods ~15%
4. S. pneumoniae ~ 5%
5. Polymicrobial ~ 5%
6. Mycobacterium
7. Fungi (usually in immunosuppressed hosts)

E. Diagnosis [1]

1. Presence of risk factors above, especially in acute monoarthritis, increase likelihood
2. Physical Exam
   1. Joint pain: 85%
   2. Joint swelling: 78%
   3. Fever: 57%
   4. Diaphoresis: 27%
   5. Rigors: 19%
3. In essentially all cases, an acute monoarthritis should be aspirated to rule out infection
4. Analysis of Joint Fluid Aspirate
   1. Rapid Gram-stain and culture should be performed
   2. If neutrophils predominate with >50K/µL leukocyte counts, consider empiric antibiotics
5. Gram Stain
   1. ~75% sensitivity for gram positive cocci
   2. ~50% sensitivity for gram negative rods
6. Leukocyte (WBC) Joint Fluid Count
   1. Usually >25K/µL with >90% neutrophils
   2. Rheumatoid Arthritis and Crystal Disease occassionally have such high cell counts
   3. WBC <25K/µL: 0.32X likelihood of septic arthritis
   4. WBC >25K/µL: 2.9X likelihood of septic arthritis
   5. WBC >50K/µL: 7.7X likelihood of septic arthritis
   6. WBC >100K/µL: 28X likelihood of septic arthritis
   7. Neutrophils >90%: 3.4 likelihood of septic arthritis
   8. Neutrophils <90%: 0.34 likelihood of septic arthritis
7. Culture
   1. ~100% sensitivity for non-gonococcal
   2. ~30% sensitive for GC
   3. Atypical organisms should be sought including fungi, mycobacteria
8. Lactate Dehydrogenase - low or normal usually rules out bacterial disease

F. Differential Diagnosis

1. Mycobacterial or fungal arthritis - usually insidious (slow) onset
2. Viral arthritis - usually with rash, usually polyarthritis
3. HIV Infection - often with reactive arthritis, sterile acute synovitis
4. Hemearthrosis - especially with trauma, coagulopathy, blood-thinners
5. Lyme Disease
6. Reactive Arthritis - compenents of Reiter's syndrome
7. Rheumatoid Arthritis
8. Crystal Disease - gout, pseudogout

F. Treatment

1. Depends on organism and host
2. Antibiotics
   1. Usually begin with oxacillin (nafcillin) or vancomycin
   2. Add gentamicin initially until culture results back
   3. Consider broader bacterial and atypical coverage in immunocompromised hosts
   4. Ceftriaxone or Cefotaxime for gonococcus or meningococcus
3. Open versus closed joint aspiration
4. In general, joint should be drained daily until accumulation (nearly) ceases
5. Indications for surgery
   1. Continued accumulation of fluid
   2. Continued bacteremia
   3. Difficult to get-at joints (such as hip, sternoclavicular)
   4. Prosthetic joints - usually requires removal of prosthesis
   5. Coexistant osteomyelitis
   6. Fungal or other atypical infection
6. NSAID Therapy can decrease pain and inflammation (better than acetaminophen)

G. Septic Bursitis [3]

1. Most commonly occurs in olecranon or pre-patellar bursa
   1. Trauma is major risk factor
   2. Alcoholism
   3. Diabetes mellitus
   4. Typically occurs in middle-aged men involved in manual labor
2. Etiology of Bursitis
   1. Infectious agents - through breaks in skin
   2. Inflammatory Disease - rheumatoid arthritis, gout, pseudogout, spondylitis
3. Organisms
   1. S. aureus 80%
   2. Group A Streptococci (ß-hemolytic) ~5%
   3. Staphylococcus epidermidis ~5%
   4. Variety of other bacteria (gram positive and negative)
   5. Atypical bacteria, fungi, algea
4. Symptoms of Septic Bursitis
   1. Bursal warmth ~100%
   2. Bursal tenderness ~100%
   3. Prebursal cellulitis ~80%
   4. Skin Lesion ~55%
   5. Fever ~40%
5. Laboratory Findings
   1. Bursal Fluid White Count usually ~50-150K/µL (>80% neutrophils)
   2. Gram Stain demonstrating organisms in ~20% of cases
   3. Bursal fluid glucose usually <35mg/dL
6. Associated Diseases
   1. Septic Arthritis and Osteomyelitis
   2. Toxic Shock Syndrome (usually staphylococcal)
   3. Polymicrobial Infection - especially in patients with chronic disease, diabetes
   4. Necrotizing Fasciitis
7. Treatment
   1. Intravenous antibiotics are almost always indicated
   2. Gram positive coverage usually sufficient except in immunocompromised host
   3. Broader spectrum coverage (eg. Unasyn®, Timentin®) recommended in complicated host
   4. Repeated drainage of bursal area (usually without irrigation) is required
   5. Failure of bursal cell counts to drop with treatment suggests surgical evaluation
   6. A minimum of 4-7 days intravenous antibiotics recommended, followed by oral therapy
   7. Total duration of therapy depends on response and comorbid conditions
   8. A minimum of 2 weeks total therpay is recommended

References

1. Margaretten ME, Kohlwes J, Moore D, Bent S. 2007. JAMA. 297(13):1478
2. Goldenberg DL. 1998. Lancet. 351(9097):197
3. Davis BT and Pasternack MS. 2007. NEJM. 356(25):2631 (Case Record)
4. Enzenauer RJ and Pluss JL. 1996. Am J Med. 100(4):479