Sandbox:septic arthritis

## Overview

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Septic arthritis is the one of the most serious medical emergency of a patient present with one or more hot and swollen joints.[1]

Bacterial arthritis is the most rapidly destructive joint disease.[2] Septic arthritis is most common in patients with longstanding rheumatoid arthritis. Septic arthritis is a an important consideration in adults presenting with monoarticular arthritis in 80 to 90% of patients. It can involve any joint, but most commonly involves knee > hip > shoulder > ankle.[3] Other joints such as sacroiliac joint, sternoclacicular or costoclavicular joints may be involved in patient with history of intravenous drug abuse (IVDA), penetrating trauma, animal or human bites and local steroid injections.

## Defintion

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## Historical perspective

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## Classification

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### Classification Based on the Etiology

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Septic arthritis can be classified into 2 types based on the etiology:[4]

* Gonococcal septic arthritis
* Non-gonococcal septic arthritis

### Classification Based on the Presentation

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Septic arthritis can be classified into 2 types based on the involvement of number of joints involved during presentation:[5]

* Mono articular septic arthritis (MASA)
* Most common type of presentation
* Poly articular septic arthritis (PASA)
* Less common presentation (~15% of total septic arthritis cases)
* commonly caused by staphylococcus aureus and other non gonococcal infections such as streptococci and gram negative bacteria.

## Causes

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Septic arthritis is due to intra articular seeding of living microorganisms.[5] The most common etiological agent of all nongonococcal causes of septic arthritis in the United States is Staphylococcus aureus.[6] Gram-negative bacilli account for 10 to 20% of septic arthritis causes.[6] ~10% of patients with nongonococcal septic arthritis are due to polymicrobial cause of infections. Anaerobes are also can cause septic arthritis in few cases.

Most common cause of septic arthritis in children age < 2 years are Haemophilus influenzae (in immunized children), Staph. aureus, group A Streptococcal infections and Kingella kingae.[7]

The source of infection in most of the cases (~50%) often from the skin, lungs or bladder.

Causes of infection include

1. Hematogenous dissemination
2. Post operative wound infection such as after arthroscopic procedures
3. Intra articular steriod injections
4. Diagnostic punctures
5. Open traumatc injury to the joint

Common organisms

* Staphylococcus aureus
* Streptococcal pyogenous
* Streptococcal pneumonia
* Escherichia coli
* Staphylococcus epidermidis
* Borrelia burgdorferi

## Pathophysiology

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Presence of extreme vasularity and absence of limiting of basement membrane, promotes the easy access of infections into the synovial space.[8]

Hematogenous spread: Septic arthritis most commonly develop as a result of hematogenous spreading bacteria into the vascular synovial membrane.[9] Hematogenous spread is commonly associate with injection drug use, presence of indwelling catheters, and an underlying immunocompromised state such as HIV infection.

Direct inoculation: Direct inoculation of microorganisms may occur during deep penetrating injuries, intra-articular steroid injection, arthroscopy or prosthetic joint surgery, particularly in association with knee and hip arthroplasties and contiguous osteomyelitis rupturing into the joint.[10][11]

Bone infection such as osteomyelitis can spread by breaking through its outer cortex and then into the intracapsular region that lead to joint infection. This kind of spread is more common in children as the small capillaries can cross the epiphyseal growth plate and permit extension of infection into the epiphysis and joint space.[3][12]

Pathogenesis of septic arthritis depends on multiple factors and it mainly depends on the balance between virulence of the microbial pathogen and the host immune response against the pathogen.

### Non-gonococcal arthritis

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Staph. aureus is the most common pathogen non gonococcal pathogen that causes septic arthritis. The pathogenesis of septic arthritis by staphylococcus can be a better representation for pathogenesis of most non gonococcal arthritis.

Bacterial colonization and adherence into the synovium

Mechanism of infection transmission

Hematogenous spread: Septic arthritis most commonly develop as a result of hematogenous spreading bacteria into the vascular synovial membrane.[9] Hematogenous spread is commonly associate with injection drug use, presence of indwelling catheters, and an underlying immunocompromised state such as HIV infection.

Determinants of hematognous seeding:[9]

* Well vascularized synovium
* Absence of limiting basement membrne
* Recent joint surgery, induces the production of host-derived extracellular matrix proteins( e.g. collagen) that aids in post surgical healing process, can assist bacterial attachment and progression to infection
* Virulence of microorganism
* Susceptibility of synovial membrane for microorganism

Direct inoculation: Direct inoculation of microorganisms may occur during deep penetrating injuries, intra-articular steroid injection, arthroscopy or prosthetic joint surgery, particularly in association with knee and hip arthroplasties.[10][11]

Contiguous spread: Bone infection such as osteomyelitis can spread by breaking through its outer cortex and then into the intracapsular region that lead to joint infection.

Role of bacterial products in pathogenesis

Bacterial colonization and adherence into the synovium

Mechanism of transmission
Hematogenous spread: Septic arthritis most commonly develop as a result of hematogenous spreading bacteria into the vascular synovial membrane.[9] Hematogenous spread is commonly associate with injection drug use, presence of indwelling catheters, and an underlying immunocompromised state such as HIV infection.

Determinants of hematognous seeding:[9]

* Well vascularized synovium
* Absence of limiting basement membrne
* Recent joint surgery, induces the production of host-derived extracellular matrix proteins( e.g. collagen) that aids in post surgical healing process, can assist bacterial attachment and progression to infection
* Virulence of microorganism
* Susceptibility of synovial membrane for microorganism

Direct inoculation: Direct inoculation of microorganisms may occur during deep penetrating injuries, intra-articular steroid injection, arthroscopy or prosthetic joint surgery, particularly in association with knee and hip arthroplasties.[10][11]

Contiguous spread: Bone infection such as osteomyelitis can spread by breaking through its outer cortex and then into the intracapsular region that lead to joint infection.

Role of bacterial products in pathogenesis
Bacterial attachment proteins promote colonization and initiate the infectious process, a number of bacterial products activate the host immune response and increase tissue damage in cases of septic arthritis.

## Risk Factors

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### Common Risk Factors

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Most common risk factors that predisposes septic arthritis are rheumatoid arthritis, prosthetic joint or joint replacement and skin infections.[13][14][15][16]

Other common risk factors that predispose septic arthritis are as follows:[17][16][18][19][8]

Type of risk factor | Examples

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Host phagocytic defects |

* Complement deficiencies especially C7 and C8
* Inherited disorders of chemotaxis

Impaired host defense

mechanisms

* Age >80 years[20]
* Cancer
* Immunosuppressive drugs (e.g. azathioprine, methotrexate, or cyclophosphamide)
* Glucocorticosteroids

Direct penetration |

* Intravenous drug use
* Puncture wonds
* Intra articular steroid injection

Joint damage |

* Prosthetic joint surgery
* Degenerative joint diseases such as rheumatoid arthritis ( Prosthetic joint > Rheumatoid arthritis > Osteoarthritis)[16]

Other risk factors |

* Recent history of bacteremia
* Cirrhosis
* Chronic kidney disease
* Hypogammaglobulinemia
* Systemic lupus erythematosis
* Gout
* Psuedo gout[21]
* Charcot's arthropathy[22]

### Micrbiological Clue Based on Risk factors

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Type of risk factor | Examples

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Rheumatoid arthritis  |

* Staphylococcus aureus

Immunocompromised patients  |

* Staphylococcus aureus
* Streptococci
* Enteric gram-negative bacilli
* Listeria monocytogenes

Recent joint surgery  |

* Staphylococcus aureus

Intravenous drug use  |

* Staphylococcus aureus
* Pseudomonas aeruginosa

Diabetes mellitus  |

* Staphylococcus aureus
* Streptococcus agalactiae

Sexually active young adults

Menstruating females

* Neisseria gonorrhea

Animal bite (e.g.Cat or dog)  |

* Pasteurella multocida
* Capnocytophaga spp
* Anaerobes

Human bite  |

* Eikenella corrodens
* Viridans streptococci
* Anaerobes

Rat bite  |

* Streptobacillus moniliformis

Neonates and children age < 4 years  |

* Kingella kingae
* Gram-negative bacilli

Unvaccinated children  |

* Haemophilus influenza

Ingestion of unpasteurized dairy products  |

* Brucella spp

* Age >60 years
* Recent history of bacteremia
* Degenerative joint diseases such as rheumatoid arthritis ( Prosthetic joint > Rheumatoid arthritis > Osteoarthritis)[16]
* Corticosteroid therapy
* Diabetes mellitus
* Leukemia
* Cirrhosis
* Granulomatous diseases
* Hypogammaglobulinemia
* Intravenous substance abuse
* Chronic kidney disease
* Cytotoxic chemotherapy
* Alcoholism

* Recent history of joint aspiration or local corticosteroid joint injection.[23][9]
* History of Rhematoid arthritis[24]
* History of diabetes mellitus[18]

## Differential Diagnosis

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Differentiating gonococcal arthritis from non-gonococcal arthritis Characterestic | Gonococcal arthritis | Non gonococcal arthritis

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Patient profile |

* Mostly sexually active young adult

* Female > male

* Patient with history of rheumatoid arthritis or other systemic arthritis
* Immunocompromised patient
* Common in extremes of age such as in newborn or elderly

Initial presentation  |

* Migratory polyarthralgia is common
* Tenosynovitis in majority of patients
* Dermatitis in majority of patients

* Single hot, swollen and painful joint
* Polyarthralgia is very rare

* Tenosynovitis and dermatitis are very rare.

Polyarticular involvement  |

* Common (~40–70% of patients)
* Usually involves 2-3 joints

* Rare (~10–20% of patients).
* Mostly monoarticular involvement (>85%)

Recovery of bacteria  |

* Positive blood culture <10%
* Positive synovial fluid culture <50%

* Positive blood culture 50%
* Positive synovial fluid culture >90%

Response to antibiotics  |

* Within a few days outcome excellent

* Takes weeks
* Joint drainage must be adequate
* Outcome often poor

Mycobacterial and fungal arthritis both present with the slow onset of a chronic monoarthritis and they are more prone to weight bearing joints and spine.

Microorganism | Associated risk factors | Key clinical clues  | Most definitive tests

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Staphylococcus aureus |

* Rheumatioid arthritis[24]
* Diabetes mellitus[25]
* HIV patients[26]

* Healthy adult with skin lesions and previously hisoty of damaged joint (eg, rheumatoid arthritis) or prosthetic joint

Streptococcus pyogenes

Streptococcal pneumonia

* Autoimmune diseases[18]
* Chronic skin infections[25]
* Trauma

* Healthy adults with spleenic dysfunction

Groups B Streptococcal infection |

* Immunocompromised patients[27]
* Diabetes mellitus
* Malignancy
* Severe genitourinary or gastrointestinal infections

* Healthy adults with spleenic dysfunction

Neisseria gonorrhoeae |

* Complement deficiency
* Systemic lupus erythematosus
* Male homosexuality
* low socioeconomic status

* Healthy young and sexually active adult with
* Tenosynovitis
* Skin lesions such as vesicular pustules
* Complement deficiency (C5-9 deficiency)
* Culture negativity on synovial fluid analysis

Gram-negative bacilli

* Pseudomonas

* Escherichia coli

* History of intravenous drug abuse[6]
* Extremes of age
* Immunocompromised patients

* Immunocompromised patients
* Recent history gastrointestinal infections such as infectious diarrhea caused by Shigella, Salmonella, Campylobacter, or Yersinia

Haemophilus influenzae |

* Unimmunized children[28]

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Anaerobes |

* Diabetes mellitus
* Patients with prosthetic joints

* Immunocompromised hosts
* Recent history of gastrointestinal infection

Mycobacterium spp. |

* Recent history of travel to endemic areas

* Immunocompromised patients
* Recent history of travel to endemic areas (e.g. India, South Africa, Mexico etc.)
* Incidious onset of monoarthritis

* Synovial fluid analysis
* Histology
* Tissue culture

Fungal infection such as

* Blastomycosis
* Cryptococcus
* Coccidioidomycosis
* Sporotrichosis

* Immunocompromised patients

* Immunocompromised patients
* Incidious onset of monoarthritis

Mycoplasma hominis |

* Recent history of urinary tract procedure

* Immunocompromised patients
* Recent history of urinary tract procedure[29]

Viral arthritis  |

* Immunocompromised patient

* Polyarthritis

* Fever

* Rash

* Serology

## Epidemiology and Demographics

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* Incidence of septic arthritis approximately varies between 2 to 10 cases per 100,000 per year in the general population.[18]
* Incidence of septic arthritis in patients with history of rheumatoid arthritis and patients with joint prostheses is ~ 30–70 cases per 100,000 per year.[16]
* Incidence of septic arthritis in patients with joint prostheses is 40-68 cases per 100,000 per year.
* The case-fatality rate of septic arthritis is estimated to be 10-25%.[8]
* Even after survival from septic arthritis, 25-50% of the patients suffer from irreversible loss of joint function.[30][31]

Females are more at risk in getting gonorrheal arthritis and four fold risk compared to men, due to the asymptomatic nature of gonorrheal infection in women.

In children hip is most commonly involved.

PASA is more common in men when compared to women.[5]

Septic arthrtits can be affected by any age group, but most commonly affected are elderly and children <4 years.[32]

The first experimental model of septic arthritis mediated by staph. aureus is developed by Tarkowski and colleagues.[33]

# Natural history, Complications and Prognosis

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### Complications

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As the growth plate is in very close to the joint, direct extension of a joint infection to the growth plate can lead to reduced bone growth in children.[34][35]

### Prognosis

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Prognosis of septic arthritis depends on several factors.

Patients with history of chronic disease with concurrent septic arthritis can be misdiagnosed as acute flare of underlying chronic disease which often delays the treatment for septic arthritis. This diagnostic delay is an important prognostic factor contribute for the poor outcome of septic arthritis in rheumatoid arthritis, which carries a 30–50% case-fatality rate.[2] If septic arthritis involving multiple joints, case fatality rate will be >50%.[32]

Poor prognostic factors include age >50 years, history of rheumatoid arthritis as an underlying disease, staph. aureus is the causative agent.[5]

## Diagnosis

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Patients with history of chronic disease with concurrent septic arthritis can be misdiagnosed as acute flareup of underlying chronic disease which often delays the treatment for septic arthritis. So, patients with acute flare of one or two new inflamed joints with underlying chronic joint diseases or with another connective tissue disease, it should be assumed that the joint is septic until proven otherwise, should always rule out concurrent septic arthritis with appropriate diagnostic studies.[2]

In patients with acute effusion of unknown etiology, might have concurrent crystal-induced arthritis and septic arthritis. So, the synovial fluid should always be cultured and examined for crystals in the evaluation of an acute effusion.[36]

### History and Symptoms

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Abrupt onset of a single hot, swollen, and painful joint indicate non gonococcal arthritis.[8] It can involve any joint, but most commonly knee is the site of infection in 50% of cases of adults and elderly patients. Hip infection is the most common site in children.[18]

Disseminated gonococcal infection(DGI) often present initially with migratory polyarthralgias, tenosynovitis, dermatitis, and fever and less commonly, <50% of patients with DGI will present with purulent joint effusion, most often of the knee or wrist..[37] Often present with inflamed and tender tendons of the wrist, ankles, and small joints.

### Physical Examination

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### Appearance of the Patient

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Patient with septic arthritis usually appears toxic and with joint pain that involved

### Vital Signs

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* Low grade fever. Chills and spiking fever are very rare.
* Hyperthermia over the joint involved
* Tachycardia
* Tachypnea

### Skin

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* Warm over the joint

* Erythema over the around the joint that involved
* Disseminated gonococcal infection often present with skin lesions, typically multiple, painless macules and papules, most often found on the arms or legs or on the trunk.[2]

### HEENT

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### Neck

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### Lungs

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### Heart

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### Abdomen

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### Back

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### Genitourinary

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### Extremities

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Most commonly involves knee > hip > shoulder > ankle.[3] Other joints such as sacroiliac joint (~10%), sternoclacicular or costoclavicular joints may be involved in patient with history of intravenous drug abuse (IVDA), penetrating trauma, animal or human bites and local steroid injections.

* Swelling of the joint that involved
* Decreased range of motion
* Patient hold the hip in flexed and externally rotated position if SA involving hip.

### Neuromuscular

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### Laboratory Tests

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The definitive diagnosis of septic arthritis requires identification of bacteria in the synovial fluid by Gram’s stain or by culture.[2]

Clinical suspicion of joint sepsis should prompt for immediate synovial fluid aspiration. Septic arthritis should not be excluded even though the patient have low fever and normal WBC.

Diagnosis of septic arthritis depends maily on the arthrocentesis and isolation of the pathogen from aspirated joint fluid.[38]

If synovial fluid cannot be obtained with closed needle aspiration, the joint should be aspirated again with imaging guidance such as ultrasound guidance, computed tomography or fluoroscopic guidance.[2]

### Diagnostic Evaluation

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| Hot, swollen joint suspecting septic arthritis|

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| Joint aspiration
send synovial fluid for Gram stain, culture and cell count|

| If dry tap:
Do image guided joint apiration with ultrasound or CT|

| Inflammatory/Purulent joint fluid
Presence of PMN 50,000-150,000 cells and mostly neutrphils|

| Non-inflammatory fluid/Crystals
Suspect non bacterial arthritis|

| Gram positive cocci
Start empiric Vancomycin or Nafcicillin|

| Gram negative bacilli
Start empiric 3rd generation cephalosporins + aminoglycosides|

| Negative Gram stain|

| Follow-up with synovial fluid culture results|

| If culture positive
❑ Treat for septic arthritis
❑ Change antibiotics according to the culture results
❑ Joint drainage|

| If culture negative
❑ Assess for true or false positivity of Gram stain
❑ Assess for clinical response|

| Immunocompromised
start empiric Vancomycin and 3rd generation cephalosporins|

| Immunocompetent
start empiric varncomycin|

| Wait for culture results|

| If culture positive,
❑ Treat for septic arthritis
❑ Change antibiotics according to the culture results
❑ Joint drainage|

| If culture negative
Confirmed non bacterial arthritis and look for alternative diagnosis|

## Prevention

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Prevention of septic arthritis is possible by intensive treatment of risk factors such as old age patients having rheumatoid arthritis, diabetes mellitus, joint prostheses or joint surgery and skin infection.[16]

## Prognosis

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Prognosis of septic arthritis depends on several factors.

Patients with history of chronic disease with concurrent septic arthritis can be misdiagnosed as acute flareup of underlying chronic disease which often delays the treatment for septic arthritis. This diagnostic delay is an important prognostic factor contribute for the poor outcome of septic arthritis in rheumatoid arthritis, which carries a 30–50% case-fatality rate.[2]

Poor prognostic factors include age >50 years, history of rheumatoid arthritis as an underlying disease, staph. aureus is the causative agent.[5]

## References

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1. ↑ Mathews CJ, Weston VC, Jones A, Field M, Coakley G (2010). "Bacterial septic arthritis in adults". Lancet. 375 (9717): 846–55. doi:10.1016/S0140-6736(09)61595-6. PMID 20206778.CS1 maint: Multiple names: authors list (link)
2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Goldenberg DL (1998) Septic arthritis. Lancet 351 (9097):197-202. DOI:10.1016/S0140-6736(97)09522-6 PMID: 9449882
3. ↑ 3.0 3.1 3.2 Barton LL, Dunkle LM, Habib FH (1987) Septic arthritis in childhood. A 13-year review. Am J Dis Child 141 (8):898-900. PMID: 3498362
4. ↑ Shirtliff ME, Mader JT (2002) Acute septic arthritis. Clin Microbiol Rev 15 (4):527-44. PMID: 12364368
5. ↑ 5.0 5.1 5.2 5.3 5.4 Dubost JJ, Fis I, Denis P, Lopitaux R, Soubrier M, Ristori JM et al. (1993) Polyarticular septic arthritis. Medicine (Baltimore) 72 (5):296-310. PMID: 8412643
6. ↑ 6.0 6.1 6.2 Deesomchok U, Tumrasvin T (1990) Clinical study of culture-proven cases of non-gonococcal arthritis. J Med Assoc Thai 73 (11):615-23. PMID: 2283490
7. ↑ Yagupsky P, Bar-Ziv Y, Howard CB, Dagan R (1995) Epidemiology, etiology, and clinical features of septic arthritis in children younger than 24 months. Arch Pediatr Adolesc Med 149 (5):537-40. PMID: 7735407
8. ↑ 8.0 8.1 8.2 8.3 Goldenberg DL, Reed JI (1985) Bacterial arthritis. N Engl J Med 312 (12):764-71. DOI:10.1056/NEJM198503213121206 PMID: 3883171
9. ↑ 9.0 9.1 9.2 9.3 9.4 9.5 Klein RS (1988) Joint infection, with consideration of underlying disease and sources of bacteremia in hematogenous infection. Clin Geriatr Med 4 (2):375-94. PMID: 3288326
10. ↑ 10.0 10.1 10.2 Atcheson SG, Ward JR (1978) Acute hematogenous osteomyelitis progressing to septic synovitis and eventual pyarthrosis. The vascular pathway. Arthritis Rheum 21 (8):968-71. PMID: 737020
11. ↑ 11.0 11.1 11.2 Gray RG, Tenenbaum J, Gottlieb NL (1981) Local corticosteroid injection treatment in rheumatic disorders. Semin Arthritis Rheum 10 (4):231-54. PMID: 6787706
12. ↑ Buckholz JM (1987) The surgical management of osteomyelitis: with special reference to a surgical classification. J Foot Surg 26 (1 Suppl):S17-24. PMID: 3559051
13. ↑ Esterhai JL, Gelb I (1991) Adult septic arthritis. Orthop Clin North Am 22 (3):503-14. PMID: 1852426
14. ↑ Dubost JJ, Fis I, Soubrier M, Lopitaux R, Ristori JM, Bussière JL et al. (1994) [Septic arthritis in rheumatoid polyarthritis. 24 cases and review of the literature.] Rev Rhum Ed Fr 61 (3):153-65. PMID: 7920511
15. ↑ Gristina AG, Giridhar G, Gabriel BL, Naylor PT, Myrvik QN (1993) Cell biology and molecular mechanisms in artificial device infections. Int J Artif Organs 16 (11):755-63. PMID: 8150521
16. ↑ 16.0 16.1 16.2 16.3 16.4 16.5 Kaandorp CJ, Van Schaardenburg D, Krijnen P, Habbema JD, van de Laar MA (1995) Risk factors for septic arthritis in patients with joint disease. A prospective study. Arthritis Rheum 38 (12):1819-25. PMID: 8849354
17. ↑ Dickie AS (1986) Current concepts in the management of infections in bones and joints. Drugs 32 (5):458-75. PMID: 3792229
18. ↑ 18.0 18.1 18.2 18.3 18.4 Morgan DS, Fisher D, Merianos A, Currie BJ (1996) An 18 year clinical review of septic arthritis from tropical Australia. Epidemiol Infect 117 (3):423-8. PMID: 8972665
19. ↑ Rozadilla A, Nolla JM, Mateo L, del Blanco J, Valverde J, Roig D (1992) [Septic arthritis induced by pyogenic germs in patients without parenteral drug addiction. Analysis of 44 cases.] Med Clin (Barc) 98 (14):527-30. PMID: 1602850
20. ↑ Lagaay AM, van Asperen IA, Hijmans W (1992) The prevalence of morbidity in the oldest old, aged 85 and over: a population-based survey in Leiden, The Netherlands. Arch Gerontol Geriatr 15 (2):115-31. PMID: 15374369
21. ↑ Lurie DP, Musil G (1983) Staphylococcal septic arthritis presenting as acute flare of pseudogout: clinical, pathological and arthroscopic findings with a review of the literature. J Rheumatol 10 (3):503-6. PMID: 6887177
22. ↑ Rubinow A, Spark EC, Canoso JJ (1980) Septic arthritis in a Charcot joint. Clin Orthop Relat Res (147):203-6. PMID: 6989540
23. ↑ Hunter JA, Blyth TH (1999) A risk-benefit assessment of intra-articular corticosteroids in rheumatic disorders. Drug Saf 21 (5):353-65. PMID: 10554051
24. ↑ 24.0 24.1 Goldenberg DL, Cohen AS (1976) Acute infectious arthritis. A review of patients with nongonococcal joint infections (with emphasis on therapy and prognosis). Am J Med 60 (3):369-77. PMID: 769545
25. ↑ 25.0 25.1 Le Dantec L, Maury F, Flipo RM, Laskri S, Cortet B, Duquesnoy B et al. (1996) Peripheral pyogenic arthritis. A study of one hundred seventy-nine cases. Rev Rhum Engl Ed 63 (2):103-10. PMID: 8689280
26. ↑ Vassilopoulos D, Chalasani P, Jurado RL, Workowski K, Agudelo CA (1997) Musculoskeletal infections in patients with human immunodeficiency virus infection. Medicine (Baltimore) 76 (4):284-94. PMID: 9279334
27. ↑ Schattner A, Vosti KL (1998) Bacterial arthritis due to beta-hemolytic streptococci of serogroups A, B, C, F, and G. Analysis of 23 cases and a review of the literature. Medicine (Baltimore) 77 (2):122-39. PMID: 9556703
28. ↑ De Jonghe M, Glaesener G (1995) [Type B Haemophilus influenzae infections. Experience at the Pediatric Hospital of Luxembourg.] Bull Soc Sci Med Grand Duche Luxemb 132 (2):17-20. PMID: 7497542
29. ↑ Luttrell LM, Kanj SS, Corey GR, Lins RE, Spinner RJ, Mallon WJ et al. (1994) Mycoplasma hominis septic arthritis: two case reports and review. Clin Infect Dis 19 (6):1067-70. PMID: 7888535
30. ↑ Kaandorp CJ, Krijnen P, Moens HJ, Habbema JD, van Schaardenburg D (1997) The outcome of bacterial arthritis: a prospective community-based study. Arthritis Rheum 40 (5):884-92. <884::AID-ART15>3.0.CO;2-6 DOI:10.1002/1529-0131(199705)40:5<884::AID-ART15>3.0.CO;2-6 PMID: 9153550
31. ↑ Bengtson S, Knutson K (1991) The infected knee arthroplasty. A 6-year follow-up of 357 cases. Acta Orthop Scand 62 (4):301-11. PMID: 1882666
32. ↑ 32.0 32.1 Gupta MN, Sturrock RD, Field M (2001). "A prospective 2-year study of 75 patients with adult-onset septic arthritis". Rheumatology (Oxford). 40 (1): 24–30. PMID 11157138.CS1 maint: Multiple names: authors list (link)
33. ↑ Tarkowski A, Collins LV, Gjertsson I, Hultgren OH, Jonsson IM, Sakiniene E et al. (2001) Model systems: modeling human staphylococcal arthritis and sepsis in the mouse. Trends Microbiol 9 (7):321-6. PMID: 11435106
34. ↑ Knights EM (1982) Infectious arthritis. J Foot Surg 21 (3):229-33. PMID: 6749955
35. ↑ Nelson JD, Koontz WC (1966) Septic arthritis in infants and children: a review of 117 cases. Pediatrics 38 (6):966-71. PMID: 5297142
36. ↑ Ilahi OA, Swarna U, Hamill RJ, Young EJ, Tullos HS (1996). "Concomitant crystal and septic arthritis". Orthopedics. 19 (7): 613–7. PMID 8823821.CS1 maint: Multiple names: authors list (link)
37. ↑ O'Brien JP, Goldenberg DL, Rice PA (1983) Disseminated gonococcal infection: a prospective analysis of 49 patients and a review of pathophysiology and immune mechanisms. Medicine (Baltimore) 62 (6):395-406. PMID: 6415361
38. ↑ Bayer AS (1980) Gonococcal arthritis syndromes: an update on diagnosis and management. Postgrad Med 67 (3):200-4, 207-8. PMID: 7355135