Septic arthritis, also known as infectious arthritis, may represent a direct invasion of joint space by various microorganisms, most commonly caused by a variety of bacteria .However, viruses, mycobacteria, and fungi have been implicated. Reactive arthritis is a sterile inflammatory process that may result from an extra-articular infectious process. Bacteria are the most significant pathogens in septic arthritis because of their rapidly destructive nature. For this reason, the current discussion concentrates on the bacterial septic arthritides. Failure to recognize and to appropriately treat septic arthritis results in significant rates of morbidity and may even lead to death.
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 has become the most common and challenging type of septic arthritis 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]
Septic arthritis is also becoming increasingly common among people who are immunosuppressed and elderly persons. Of people with septic arthritis, 45% are older than 65 years; these groups are more likely to have various comorbid disease states. Fifty-six percent of patients with septic arthritis are male.
Septic arthritis due to bacterial infections is commonly classified as either gonococcal or nongonococcal.[1, 2, 4, 5, 6] Overall, although Neisseria gonorrhoeae remains the most common pathogen (75% of cases) among younger sexually active individuals,[7, 8] Staphylococcus aureus infection is the cause of the vast majority of cases of acute bacterial arthritis in adults and in children older than 2 years.[9] The increased incidence of this pathogen parallels the increase in presence of prosthetic joints and in the use of immunosuppressive agents. This pathogen is the cause in 80% of infected joints affected by rheumatoid arthritis.
Streptococcal species, such as Streptococcus viridans, S pneumoniae,[10, 11] and group B streptococci,[12] account for 20% of cases. Aerobic gram-negative rods are involved in 20-25% of cases. Most of these infections occur in people who are very young, who are very old,[13] who are diabetic, who are immunosuppressed, and who abuse intravenous drugs.[2]
Infection of the sternoclavicular and sacroiliac joints with Pseudomonas aeruginosa or Serratia species occurs almost exclusively in persons who abuse intravenous drugs. Persons with leukemia are predisposed to Aeromonas infections.[14]
Polymicrobial joint infections (5-10% of cases) and infection with anaerobic organisms (5% of cases) are usually a consequence of trauma or abdominal infection. The organism of Lyme disease (ie, Borrelia burgdorferi), a large 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 may produce nonsuppurative joint infection.[15]
Three major types of prosthetic joint infections exist: (1) those that occur early, within 3 months of implantation; (2) those that are delayed, within 3-24 months of implantation; and (3) those that occur later than 24 months following the implantation. Most cases of early prosthetic joint infection are caused by S aureus, whereas delayed infections are due to coagulase-negative S aureus (CoNS) and gram-negative aerobes. Both of these types are acquired in the operating room. Late cases of prosthetic joint infection are secondary to hematogenous spread from various infectious foci.[16]
See also Pediatric Septic Arthritis, Pediatric Septic Arthritis Surgery, and Septic Arthritis Surgery.
NextOrganisms may invade the joint by direct inoculation, by contiguous spread from infected periarticular tissue, or via the bloodstream (the most common route).[14]
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.
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 a joint infection. Some microorganisms have properties that promote their tropism to the synovium. S aureus readily binds to articular sialoprotein, fibronectin collage, 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.[15]
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:
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.
Prosthetic joint infections (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 the 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.[17] 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 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 cases of reactive arthritis may become chronic. Complications include dysfunctional joints, osteomyelitis, and sepsis.
Predictors of poor outcome in suppurative arthritis include the following:
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%.[18] S aureus is the most common cause of septic arthritis in all age groups. Among those aged 15-50 years, N gonorrhea runs a close second, especially among those who are sexually active.
Clinical Presentation
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