Septic Arthritis

Updated: Oct 13, 2021
  • Author: John L Brusch, MD, FACP; Chief Editor: Michael Stuart Bronze, MD  more...
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Septic arthritis (SA), also known as infectious arthritis, represents an invasion of a joint space by a wide range of microorganisms, most commonly bacteria. Various viruses, mycobacteria, and fungi are also causative. Because of their rapidly destructive nature, the current discussion will focus primarily on the bacterial septic arthritides. Even when expeditiously and appropriately treated, these pathogens characteristically result in significant rates of morbidity and mortality.

Reactive arthritis represents a sterile inflammatory process that is triggered by an extra-articular infection.

Approximately 20,000 cases of septic arthritis occur in the United States each year (7.8 cases per 100,000 person-years), with a similar incidence occurring in Europe. [1]  The incidence of arthritis due to disseminated gonococcal infection is 2.8 cases per 100,000 person-years. Because of the increasing use of prosthetic joints, infection associated with these devices is the most challenging type of SA encountered by most clinicians. [2] The incidence of prosthetic joint infection (PJI) among all prosthesis recipients ranges from 2% to 10%. These figures may be falsely low because surveillance is limited to the operative hospital, which may lead to underestimation of the rate of PJIs. [3]

Patients who have undergone treatment for infection of a native joint are at an increased risk for PJI after a total joint arthroplasty of that particular joint. [4]

Septic arthritis is increasingly common among persons older than 65 years, among immunosuppressed individuals, and among those with various  comorbiditiees such as diabetes. Fifty-six percent of patients with septic arthritis are male.

Gonococcal and nongonococcal bacterial/suppurative arthritis

Bacterial SA is commonly described as either gonococcal or nongonococcal. [1, 2, 5, 6, 7, 8]  Neisseria gonorrhoeae remains the most common pathogen (75% of cases) among younger sexually active individuals. [9, 10, 11] The increased incidence of S aureus parallels the rise of prosthetic joint implantation, intravenous drug abuse (IVDA), and the use of immunosuppressive agents. This pathogen causes 80% of infected joints affected by rheumatoid arthritis.

Streptococcal species, such as Streptococcus viridans, S pneumoniae, [12, 13] and group B streptococci [14] account for 20% of cases. Aerobic gram-negative rods are involved in 20-25% of cases. Most of these infections occur among very young and very old, [15]  patients with diabetes, immunosuppressed individuals, and people who use intravenous drugs. [16, 17]

Infection of the cartilaginous joints (sternoclavicular, sacroiliac, and pubic joints) with Pseudomonas aeruginosa or Serratia species occurs almost exclusively among people who abuse intravenous drugs. Individuals with leukemia are susceptible to Aeromonas infections. [18]

Polymicrobial joint infections (5-10% of cases) and infection with anaerobic organisms (5% of cases) are usually a consequence of trauma or abdominal infection. Individuals with multiple pathogens have a higher rate of previous native and prosthetic joint infections. The most common pathogens were coagulase-negative Staphylococcus (CoNS), MSSA, and enterococci. [4]

The organism that causes Lyme disease, Borrelia burgdorferi, commonly produces a septic arthritis picture. [17]  In some, the signs and symptoms of the acute infection persist despite successful eradication of the pathogen. This is due to ongoing inflammatory response that continues the synovial inflammation, vascular damage, and autoimmune processes that interfere with appropriate tissue repair.

Brucella may cause septic arthritis in areas where cattle are not vaccinated. The organism of Whipple disease, Mycoplasma species, and Ureaplasma species infrequently involve septic joints. [2]

A wide variety of viruses (eg, human immunodeficiency virus [HIV], lymphocytic choriomeningitis virus, hepatitis B virus, rubella virus), mycobacteria, fungi (eg, Histoplasma species, Sporothrix schenckii, Coccidioides immitis, Blastomyces species), and other pathogens produce nonsuppurative joint infections. [18]

Types of prosthetic joint infections

 There are three major categories of PJIs: those that develop within 3 months of implantation; those that appear within 3 to 24 months of implantation; and those that occur later than 24 months. Most cases of early prosthetic joint infection are caused by S aureus. The 3- to 24-month group are usually caused by coagulase-negative S aureus (CoNS) or gram-negative aerobes, both of which are acquired in the operating room. Late cases of prosthetic joint infection are secondary to hematogenous spread from a variety infectious foci. [19, 20]

Reactive arthritis represents a sterile inflammatory process that is triggered by a variety of extra articular infections. [21]

See also Pediatric Septic Arthritis, Pediatric Septic Arthritis Surgery, and Septic Arthritis Surgery.


Etiology and Pathophysiology

Organisms may invade the joint by direct inoculation, by contiguous spread from infected periarticular tissue, or via the bloodstream (the most common route). [8]

The normal joint has several protective components. Healthy synovial cells possess significant phagocytic activity, and synovial fluid normally has significant bactericidal activity. Rheumatoid arthritis and systemic lupus erythematosus hamper the defensive functions of synovial fluid and decrease chemotaxis and phagocytic function of polymorphonuclear leukocytes. Patients with deficiencies of the terminal components of complement are susceptible to neisserial bacteremia and joint infections.

Pathogenic invasion

Previously damaged joints, especially those damaged by rheumatoid arthritis, are the most susceptible to infection. The synovial membranes of these joints exhibit neovascularization and increased adhesion factors; both conditions increase the chance of bacteremia, resulting in joint infection. Some microorganisms have properties that promote their tropism to the synovium. S aureus readily binds to articular sialoprotein, fibronectin collagen, elastin, hyaluronic acid, and prosthetic material via specific tissue adhesion factors (microbial surface components recognizing adhesive matrix molecules [MSCRAMMs]). In adults, the arteriolar anastomosis between the epiphysis and the synovium permits the spread of osteomyelitis into the joint space.

The major consequence of bacterial invasion is damage to articular cartilage. This may be due to the particular organism's pathologic properties, such as the chondrocyte proteases of S aureus, as well as to the host's polymorphonuclear leukocytes response. The cells stimulate synthesis of cytokines and other inflammatory products, resulting in the hydrolysis of essential collagen and proteoglycans. Infection with N gonorrhoeae induces a relatively mild influx of white blood cells (WBCs) into the joint, explaining, in part, the minimal joint destruction observed with infection with this organism relative to destruction associated with S aureus infection.

As the destructive process continues, pannus formation begins, and cartilage erosion occurs at the lateral margins of the joint. Large effusions, which can occur in infections of the hip joint, impair the blood supply and result in aseptic necrosis of bone. These destructive processes are well advanced as early as 3 days into the course of untreated infection.

Viral infections may cause direct invasion (rubella) or production of antigen/antibody complexes. Such immunologic mechanisms occur in infections with hepatitis B, parvovirus B19, and lymphocytic choriomeningitis viruses.

Reactive/postexposure process

Reactive, or postexposure, arthritis is observed more commonly in patients with human lymphocyte antigen B27 (HLA-B27) histocompatibility antigens. Although various infections can cause reactive arthritis, gastrointestinal processes are by far the most common. Gastrointestinal pathogens associated with reactive arthritis include the following [21] :

  • Salmonella enteritidis

  • Salmonella typhimurium

  • Yersinia enterocolitica

  • Campylobacter jejuni

  • Clostridium difficile

  • Shigella sonnei

  • Entamoeba histolytica

  • Cryptosporidium

Genitourinary infections, especially those due to Chlamydia trachomatis, are the second most common cause of reactive arthritis. The arthritis of Lyme disease usually results from immunologic mechanisms, with a minority of cases due to direct invasion by an organism. A reactive/postexposure process may occur months after the gastrointestinal or genitourinary process has resolved.

COVID-19 infection has been increasingly implicated as a cause of reactive arthritis especially among patients with rheumatoid arthritis. [1, 22]

Local infection

 PJIs may be a consequence of local infection, such as intraoperative contamination (60-80% of cases), or of bacteremias (20-40% of cases). [2] The bacteremias may be spontaneous (ie, gingival disease) or secondary to various manipulations. Delayed wound healing is a major factor behind early prosthetic joint infection. Until the fascia has healed, the usual tissue barriers to infection of the implant are not present. Eventually, the implanted hardware becomes less susceptible to infection by hematogenous spread, because a pseudocapsule develops around it.

The biofilm of coagulase-negative S aureus (CoNS) protects the pathogen from the host's defenses, as well as from various antibiotics. Polymethylmethacrylate cement inhibits WBC and complement function.

Overall, the most common organisms of prosthetic joint infections are CoNS (22% of cases) and S aureus (22% of cases). Enteric gram-negative organisms account for 25% of isolates. [20] Streptococci, including S viridans, enterococci, and the beta-hemolytic streptococci, cause 21% of cases. Anaerobes are isolated from 10% of patients.

Other distinctive host and/or situation-pathogen associations have been described, including Pasteurella multocida, Capnocytophaga species (dog and cat bites), Eikenella corrodens, anaerobes (especially Fusobacterium nucleatum and streptococcal species [human bites]), Aeromonas hydrophila (myelogenous leukemia), P aeruginosa, Serratia species, Candida species (particularly common in persons who abuse intravenous drugs), Mycobacterium marinum (water exposure), S schenckii (gardening), and S pneumoniae (sickle cell anemia).

Unlike their causative role in sickle cell osteomyelitis, Salmonella species are not associated with the septic arthritis of sickle cell anemia. Ten to 30% of patients with brucellosis have lumbosacral spine involvement.



The primary morbidity of septic arthritis is significant dysfunction of the joint, even if treated properly. Fifty percent of adults with septic arthritis have significant sequelae of decreased range of motion or chronic pain after infection. [1] Thirty percent of reactive arthritis cases may become chronic. Complications include dysfunctional joints, osteomyelitis, and sepsis.

Predictors of poor outcome in suppurative arthritis include the following [23] :

  • Age older than 60 years
  • Infection of the hip or shoulder joints
  • Underlying rheumatoid arthritis
  • Positive findings on synovial fluid cultures after 7 days of appropriate therapy
  • Delay of 7 days or longer in instituting therapy

The mortality rate depends primarily on the causative organism. N gonorrhoeae septic arthritis carries an extremely low mortality rate, whereas that of S aureus can approach 50%. [22]  S aureus is the most common cause of septic arthritis in all age groups. Among those aged 15 to 50 years, N gonorrhea runs a close second, especially among those who are sexually active.