Infections of Joints


Septic arthritis; infectious arthritis

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Related conditions

Prosthetic joint infections

1. Description of the problem

Infections of joints can arise from:

  • Hematogenous spread (in the course of bacteremia or fungemia): the most common route

  • Direct inoculation (surgical, injections of joints, or accidental trauma)

  • Contiguous spread (e.g., from adjacent osteomyelitis): rare

Infections of native joints

The most common agents are bacterial and include:

  • Gram-positive cocci:
    Staphylococcus aureus, streptococci — these are by far the most common causes

  • Gram-negative bacilli: enteric bacilli from urinary tract or intestinal or other infection; environmental gram-negative bacilli (e.g., Pseudomonas aeruginosa) after trauma

  • Gram-negative cocci: N. gonorrhoeae in patients with genital gonococcal infection; Neisseria meningitidis in patients with meningococcemia

Rarely, fungi or viruses (parvovirus, rubella, mumps, hepatitis B virus) can cause acute arthritis.

“Reactive” (sterile) arthritis, formerly known as Reiter’s syndrome, may occur following chlamydial genital infection or bacterial gastroenteritis caused by campylobacter, salmonella, and other agents.

Infections of prosthetic joints

The causative agents are similar to those that infect native joints except that organisms of low virulence (coagulase-negative staphylococci; diphtheroids) play a large role.

  • Gram-positive cocci:
    Staphylococcus aureus; coagulase-negative staphylococci

  • Gram-positive bacilli: Diphtheroids (especially in shoulder prostheses)

  • Gram-negative bacilli: Enteric and other organisms are infrequent causes of infections of prosthetic joints.

Clinical features
  • The clinical features of infections of native joints are usually straightforward with pain, swelling, warmth of the periarticular tissues and restriction of range of motion. These symptoms and signs may be subtle in patients with prosthetic joint infection.

  • Plain x-rays may show swelling of periarticular tissues.

  • In patients with a systemic noninfectious arthritic condition (e.g., rheumatoid arthritis), bacterial infection (rather than a flare-up of the underlying condition) is suggested by increased pain and swelling in one joint with little change in the inflammatory process in other joints.

Key management points
  • Determine that the infection involves the joint(s) and not a bursa or other periarticular tissues by clinical examination, imaging, and
    joint tap.

  • Distinguish infectious from gouty arthritis or pseudogout by analysis of joint fluid.

  • Note that Gram stains of joint fluid are positive in only about 50% of cases of bacterial arthritis, although cultures are positive (in the absence of antibiotics) in about 90%.

  • Obtain cultures of blood and other potential sources of infection (e.g., urine) if hematogenous infection is likely.

  • Obtain urine tests for Neisseria gonorrhoeae if gonococcal arthritis is a possibility.

  • Obtain urine test for chlamydia and stool cultures for bacterial pathogens if reactive arthritis is a possibility, even in the absence of genital or intestinal symptoms.

  • Ensure adequate drainagefor weight-bearing joints: unrelieved pressure causes necrosis of cartilage.

  • Hematogenous infection of joints should raise a question of endocarditis.

  • Infections of prosthetic joints may be cured without removal of the prosthesis if (1) the prosthesis was placed less than 3 months earlier (or infection is the result of hematogenous spread); (2) the symptoms have been present for not more than 3 weeks; and (3) the organism is susceptible to bactericidal antibiotics. Otherwise, removal of the prosthesis (in a one- or two-stage procedure) is usually needed for cure.

2. Emergency Management

  • Aspirate the jointfor diagnosis: order crystal search, Gram stain and culture for bacteria and fungi.

  • Base initial antibiotic choice on likely causes (see below).

  • There is no need to inject antibiotic into the joint: most antibiotics penetrate well from the bloodstream.

  • Ensure adequate drainage of weight-bearing joints to avoid damage to cartilage.

  • Search for and treat remote infection if the route of joint infection is hematogenous.

  • Consider the possibility of endocarditis (e.g., consider echocardiogram) if the route of infection is hematogenous.

  • Obtain orthopedic consultation for prosthetic joint infection.

3. Diagnosis

Joint tap usually confirms the diagnosis.

  • Distinguish gout or pseudogout from infection by crystal search of joint fluid.

  • If more than one joint is infected, consider hematogenous infection (including from endocarditis) OR a noninfectious rheumatological process OR reactive arthritis. In any event, tap a joint for confirmation of the presence or absence of infection.

  • The fluid of infected joints usually, but not always, contains at least 50,000 WBC/mm3.

  • Gram stains are negative in about 50% of cases of bacterial arthritis (and 75% of cases of gonococcal arthritis), but cultures are positive most of the time. However, a positive Gram stain provides a quick clue to the likely infecting organism.

  • Aspirates from infected prosthetic joints may contain few organisms; surgical exploration and cultures of synovium or sonication of the joint prosthesis may be necessary to identify the causative agent.

Normal lab values
  • Gram stains are negative in about 50% of cases of bacterial arthritis, but (in the absence of antibiotics) cultures are positive in about 90%.

  • The rate of positive Gram stains and cultures in gonococcal arthritis is about 25% and 50%, respectively.

Differential diagnosis

The differential diagnosis of bacterial arthritis includes:

  • Gout and pseudogout

  • Septic bursitis (olecranon and patellar)

  • Osteomyelitis adjacent to a joint masquerading as joint infection

  • Rheumatological diseases (e.g., rheumatoid arthritis); also sarcoidosis

  • “Reactive arthritis” (formerly known as Reiter’s syndrome)

  • Viral arthritis (esp. from parvovirus, rubella, mumps, and in the prodrome of hepatitis B)

  • Arthritis in the course of Lyme disease

Confirmatory tests

The confirmatory test is aspiration of joint fluid for WBC count, crystal search, and Gram stain and culture for bacteria (and fungi and possibly mycobacteria).

4. Specific Treatment

Antibiotic treatment

There are no randomized trials to guide therapy for infections of native joints. Treatment should be selected on the basis of Gram stains and cultures and clinical features (likely source of infection).

A wide variety of organisms can potentially infect the joint. The Gram stain can dictate the initial choice, e.g.:

  • Gram-positive cocci (staphylococci, streptococci): vancomycin

  • Gram-negative bacilli from a hematogenous source (likely enteric organisms): ceftriaxone or ceftazidime or piperacillin-tazobactam or ciprofloxacin

  • Gram-negative bacilli from an environmental source, such as trauma (Pseudomonas aeruginosa): ceftazidime or cefepime or ciprofloxacin

If neither the Gram stain nor the clinical setting indicates a likely causative organism, empirictreatment should cover for gram-positive cocci and gram-negative bacteria — for instance, vancomycin PLUS ceftazidime or cefepime or ciprofloxacin.

Cultures will usually become positive within a couple of days and antibiotic treatment can be adjusted according to culture and sensitivity results.

Relief of pressure:

In consultation with an orthopedist, ensure that the joint is adequately drained to avoid necrosis of cartilage. This may require repeated aspirations or indwelling catheter drainage.

Prosthetic joint infection

  • Will usually require
    removal and replacement of the prosthesis (one-stage or two-stage procedure)
    unless the infection has occurred within 3 months of insertion of the prosthesis (or is hematogenous), symptoms of infection have been present for < 3 weeks, the tissues around the joint are stable, and the infecting organism is susceptible to bactericidal antibiotics.

  • The addition of rifampin to another agent (e.g., a beta-lactam or a fluoroquinolone) may increase the likelihood of cure in patients in whom the prosthesis is retained.

Refractory cases

Refractoriness of the infection may be due to:

  • Misidentification of the infecting organism (repeat cultures): Consider the possibility of infection by a fungus or mycobacterium or resistant gram-negative organism or noninfectious arthritis.

  • Infection of a contiguous “feeding” focus, such as osteomyelitis: Consider imaging.

  • Prosthetic joint infection: Failure to respond to antibiotics usually signals need for removal of the prosthesis.

5. Disease monitoring, follow-up and disposition

Expected response to treatment

Most infections of native joints will respond with decreased pain and swelling and improved range of motion within a week of the initiation of appropriate antibiotics and good drainage. Antibiotic treatment will probably be necessary for 2-3 weeks in most cases. Once the joint inflammation has decreased markedly, antibiotics may be given by the oral route to complete the course of treatment.

Prosthetic joints in which the prosthesis is retained after debridement usually require antibiotic treatment for
much longer periods, 3-6 months.

A consultation with Physical Therapy or Rehabilitation Medicine should be obtained once the acute inflammation has subsided to help with muscle strength and joint stability.


Once the patient has been discharged from the hospital, follow-up visits to ensure resolution of the infection may be carried out for 1-2 weeks after the completion of antibiotic treatment.

Physical Therapy or rehabilitation may be indicated to help to restore muscle strength and joint stability.


The pathophysiology of bacterial (or fungal) arthritis differs according to the route of entry; that is:

  • Hematogenous (either in the course of a primary bacteremic illness, including endocarditis, or from another focus such as urinary tract or bowel): the hematogenous route is the most common route

  • Direct inoculation (e.g., after injection of steroid into a rheumatoid joint)

  • Contiguous spread (e.g., from osteomyelitis) — rare

Once infection has become established, cytokines are released and inflammatory products are liberated by phagocytic cells, producing inflammation of the synovium. There may be rapid and irreversible damage to cartilage.


The epidemiology is described above.


See above.

Special considerations for nursing and allied health professionals.


What's the evidence?

Gupta, MN, Sturrock, RD, Field, M. “Prospective comparative study of patients with culture proven and high suspicion of adult onset septic arthritis”. Ann Rheum Dis. vol. 62. 2003. pp. 327-331.

Margaretten, ME, Kohlwes, J, Moore, D, Bent, S. “Does this adult patient have septic arthritis?”. JAMA. vol. 297. 2007. pp. 1478-1488.

Zimmerli, W, Rampuz, A, Ochsner, PE. “Prosthetic-joint infections”. N Engl J Med. vol. 351. 2004. pp. 1645-1654.

Margaretten, ME, Kohlwes, J, Moore, D, Bent, S. “Does this adult patient have septic arthritis?”. JAMA. vol. 297. 2007. pp. 1478-1488.

Temmerman, OPP, Raijmakers, PGHM, Berkhof, J. “Accuracy of diagnostic imaging techniques in the diagnosis of aseptic loosening of the femoral component of a hip prosthesis”. J Bone Joint Surg (Br). vol. 87-B. 2005. pp. 781-785..

Trampuz, A, Piper, KE, Jacobson, M. “Sonication of removed hip and knee prostheses for diagnosis of infection”. N Engl J Med. vol. 357. 2007. pp. 654-663..

Leone, S, Borre, S, Monforte, A d’A. “Consensus document on controversial issues in the diagnosis and treatment of prosthetic joint infections”. Int J Infect Dis. vol. 1454. 2010. pp. S67-S77..

Zimmerli, W, Widmer, AF, Blatter, M. “Role of rifampin for treatment of orthopedic implant-related staphylococcal infections”. JAMA. vol. 279. 1998. pp. 1537-1541..