Reprinted from www.antimicrobe.org
Septic Arthritis - Causes
Septic arthritis is a medical and surgical emergency that can lead to rapid destruction of the joint and irreversible loss of function. It is caused by invasion of the microorganisms into the synovial space. Bacteria are the most common cause of joint of infection although other pathogens such as viruses, fungi and mycobacteria may also be responsible.
Bacteria enter the joint through several mechanisms including direct inoculation, penetrating trauma, surgical incision including arthroscopy, spread from a contiguous focus of soft tissue infection or hematogenous seeding from a distant focus. Hematogenous seeding is the most common route. Negative prognostic factors include older age, delay in onset of treatment, pre-existing arthritis, immunosuppressive therapy, resistant organisms and multiple joint involvements. Septic arthritis results in loss of function in 25% to 50% of patients despite appropriate therapy. Table 1 lists the microbiology of bacterial arthritis in relationship to patient’s age.
Table 1 Microbiology of Bacterial Septic Arthritis Related to Age of Patient.
Organism
Children
(6 mo. to 5 yrs.)
Young adult
Adult
Elderly
Staphylococcus aureus
10% - 20%
15% - 20%
60% - 70%
45% - 65%
Streptococci
5% - 10%
1% - 5%
15% - 20%
10% - 15%
Gram-negative bacteria
1% - 5%
Rare
10% - 15%
15% - 35%
Haemophilus influenzae
30% - 50%
1% - 5%
1% - 5%
Rare
Neisseria gonorrhoeae
1% - 5%
60% - 80%
1% - 5%
Rare
Adapted from Gorbach SL et al (Eds), Infectious Diseases, 2nd Edition, 1998
RISK FACTORS
Degenerative joint disease, rheumatoid arthritis, and corticosteroid therapy are the most common predisposing conditions. Total joint arthroplasties are susceptible to intraoperative or hematogenous seeding which can result in subsequent prosthetic infection. While patients infected with HIV demonstrate a higher prevalence of septic arthritis or osteomyelitis than does the general population this may be due to intravenous drug abuse and multiple transfusions in this patient population.
NON GONOCOCCAL BACTERIAL SEPTIC ARTHRITIS
In adults non gonococcal acute septic arthritis occurs with an incidence of 0.034% to 0.13%. One to two percent of patients with total joint arthroplasty may develop septic complications. 90% of cases are mono-articular with knee being involved in 50% of these cases. Staphylococcus aureus and streptococci remain the predominant organism although certain other unusual organisms may be seen in specific clinical settings (Table 2). In addition, certain microorganisms may be associated with reactive arthritis (Table 3). Several unusual organisms such as Kingella spp., A. actinomycetemcomitans, M. catarrhalis and P. multocida have been implicated in osteoarticular infections.
Table 2. Septic Arthritis Complicating a Clinical Setting
Clinical Setting |
Risk Factors |
Pathogen |
Frequency of Pathogen |
Special Points |
Rheumatoid Arthritis
|
Disabling arthritis Skin lesions Infected rheumatoid nodule TNF suppression therapy |
Staphylococcus aureus Streptococcus pyogenes (Salmonella, M. catarrhalis, Listeria –with TNF suppression Therapy) |
40-60% 10-20% |
Patient education Early diagnosis Surgical debridement and antibiotics Special caution with TNF suppression therapy |
Advanced Age |
Diabetes mellitus, Urinary tract infection, Biliary tract infection, Diverticulitis |
Staphylococcus aureus Gram negatives bacilli |
30-40% 10-20% |
Poor outcome if treatment started after 7 days of symptoms |
Bacterial Endocarditis |
Septic immobilization Reactive immune arthritis Intravenous drug use |
Staphylococcus aureus Streptococcus pyogenes Pseudomonas aeruginosa |
10-30% 40-60% 5-10% |
Adverse affects of antibiotics Duration 4- 6 weeks |
Prosthetic Joints |
Dental procedures SLE Immunosuppression DM, hemophilia, UTI, Skin Infection Previous Joint infection Joint replacement < 2 yrs |
Staphylococcus species Streptococcus species Gram negative bacilli |
40-60% 10-30% 10-15% |
Antibiotic prophylaxis indicated |
Immunosuppression, AIDS and Stem cell transplantation |
Immunosuppression Decreased humoral and cell mediated immunity |
Stenotrophomonas Salmonella Agrobacterium Fungi Atypical mycobacteria |
Rare |
Nonpathgenic and unusual organisms |
Whipple’s Disease |
|
Tropheryma whippelii |
Rare |
|
Hypogammaglobinemia |
Decreased humoral immunity |
Ureaplasma |
Rare |
|
Hemoglobinopathy |
Microinfracts in intestinal wall. |
Salmonella Staphylococcus aureus |
Rare |
Osteomyelitis more common than septic arthritis |
Human and Animal Bites |
Inoculation of indigenous mouth flora |
Pasteurella multocida, Eikenella corrodens Streptobacillus moniliformis |
Rare |
Septic arthritis in proximity to site of injury. Knuckle osteo with clenched fist injury. |
Intravenous drug use |
Endocarditis Discitis |
Staphylococcus aureus Pseudomonas aeruginosa Candida species |
60-80% Rare Rare |
Seen in sacroiliac, strenocostal and strenclavicular clavicular joints |
Plant Thorns |
Puncture wound Foreign body |
Pantoea agglomerans, Sporotrichosis, Atypical mycobacteria, Nocardia, Clostridium sordellii, actinomycosis |
Rare |
Image joint for foreign body |
Resident in endemic area with known or suspected tick exposure |
|
Borrelia burgdorferi |
|
|
Exposure to aquatic environment |
|
M. marinum |
|
Small joints of hand |
Positive Tuberculin skin test. Resident in endemic area |
|
M. tuberculosis
|
|
Axial skeleton and large joint |
Table 3. Microorganisms Associated with Reactive Arthritis
Chlamydia trachomatis |
Shigella flexneri |
Salmonella enteriditis |
Salmonella typhimurium |
Yersinia enteocolitica |
Yersinia pseudotuberculosis |
Campylobacter jejuni |
PATHOPHYSIOLOGY
Bacterial invasion of the highly vascular synovium results in bacterial trapping and multiplication in the subsynovium. The host responds with acute inflammatory reaction and phagocytosis by the polymorphonuclear leucocytes. Toxins and enzymes are released by bacterial and stimulated T-cells leading to destruction of the articular cartilage. Revascularization, synovial proliferation and granulation tissue develop. Synovial fluid white blood cell count can exceed over 50,000/mm3 and increased intracavitary of pressure from accumulation of the purulent fluid resulting in necrosis of the synovium and cartilage. Pro-inflammatory cytokines such as interluken-1 and tumor necrosis factor α also contribute to joint injury.