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.