- Author: John L Brusch, MD, FACP; Chief Editor: Michael Stuart Bronze, MD more...
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. 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. 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.
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.
Gonococcal and nongonococcal bacterial/suppurative arthritis
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. 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, 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, who are diabetic, who are immunosuppressed, and who abuse intravenous drugs.
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.
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.
Types of prosthetic joint infections
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.
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).
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.
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). 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. 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. 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:
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%. 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.
Goldenberg DL, Cohen AS. Acute infectious arthritis. A review of patients with nongonococcal joint infections (with emphasis on therapy and prognosis). Am J Med. 1976 Mar. 60(3):369-77. [Medline].
Ross JJ, Shamsuddin H. Sternoclavicular septic arthritis: review of 180 cases. Medicine (Baltimore). 2004 May. 83(3):139-48. [Medline].
Yokoe DS, Avery TR, Platt R, Huang SS. Reporting surgical site infections following total hip and knee arthroplasty: impact of limiting surveillance to the operative hospital. Clin Infect Dis. 2013 Nov. 57(9):1282-8. [Medline].
Berbari EF, Marculescu C, Sia I, Lahr BD, Hanssen AD, Steckelberg JM, et al. Culture-negative prosthetic joint infection. Clin Infect Dis. 2007 Nov 1. 45(9):1113-9. [Medline].
Cucurull E, Espinoza LR. Gonococcal arthritis. Rheum Dis Clin North Am. 1998 May. 24(2):305-22. [Medline].
Broy SB, Schmid FR. A comparison of medical drainage (needle aspiration) and surgical drainage (arthrotomy or arthroscopy) in the initial treatment of infected joints. Clin Rheum Dis. 1986 Aug. 12(2):501-22. [Medline].
McGuire NM, Kauffman CA. Septic arthritis in the elderly. J Am Geriatr Soc. 1985 Mar. 33(3):170-4. [Medline].
Smith JW, Piercy EA. Infectious arthritis. Clin Infect Dis. 1995 Feb. 20(2):225-30; quiz 231. [Medline].
Baraboutis I, Skoutelis A. Streptococcus pneumoniae septic arthritis in adults. Clin Microbiol Infect. 2004 Dec. 10(12):1037-9. [Medline].
Raad J, Peacock JE Jr. Septic arthritis in the adult caused by Streptococcus pneumoniae: a report of 4 cases and review of the literature. Semin Arthritis Rheum. 2004 Oct. 34(2):559-69. [Medline].
Corvec S, Illiaquer M, Touchais S, et al. Clinical features of group B Streptococcus prosthetic joint infections and molecular characterization of isolates. J Clin Microbiol. 2011 Jan. 49(1):380-2. [Medline]. [Full Text].
Margaretten ME, Kohlwes J, Moore D, Bent S. Does this adult patient have septic arthritis?. JAMA. 2007 Apr 4. 297(13):1478-88. [Medline].
Rice PA. Gonococcal arthritis (disseminated gonococcal infection). Infect Dis Clin North Am. 2005 Dec. 19(4):853-61. [Medline].
Manadan AM, Block JA. Daily needle aspiration versus surgical lavage for the treatment of bacterial septic arthritis in adults. Am J Ther. 2004 Sep-Oct. 11(5):412-5. [Medline].
Zimmerli W, Trampuz A, Ochsner PE. Prosthetic-joint infections. N Engl J Med. 2004 Oct 14. 351(16):1645-54. [Medline].
Hsieh PH, Lee MS, Hsu KY, Chang YH, Shih HN, Ueng SW. Gram-negative prosthetic joint infections: risk factors and outcome of treatment. Clin Infect Dis. 2009 Oct 1. 49(7):1036-43. [Medline].
Kaandorp CJ, Krijnen P, Moens HJ, et al. The outcome of bacterial arthritis: a prospective community-based study. Arthritis Rheum. 1997 May. 40(5):884-92. [Medline].
Zimmermann B 3rd, Mikolich DJ, Ho G Jr. Septic bursitis. Semin Arthritis Rheum. 1995 Jun. 24(6):391-410. [Medline].
Garcia-De La Torre I. Advances in the management of septic arthritis. Rheum Dis Clin North Am. 2003 Feb. 29(1):61-75. [Medline].
Wilson ML, Winn W. Laboratory diagnosis of bone, joint, soft-tissue, and skin infections. Clin Infect Dis. 2008 Feb 1. 46(3):453-7. [Medline].
Osmon DR, Berbari EF, Berendt AR, Lew D, Zimmerli W, Steckelberg JM, et al. Executive summary: diagnosis and management of prosthetic joint infection: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis. 2013 Jan. 56(1):1-10. [Medline].
Schäfer P, Fink B, Sandow D, Margull A, Berger I, Frommelt L. Prolonged bacterial culture to identify late periprosthetic joint infection: a promising strategy. Clin Infect Dis. 2008 Dec 1. 47(11):1403-9. [Medline].
Goldenberg DL. Septic arthritis and other infections of rheumatological significance. Rheum Clin NA. 1991. 17:149. [Medline].
Wise CM, Morris CR, Wasilauskas BL, et al. Gonococcal arthritis in an era of increasing penicillin resistance. Presentations and outcomes in 41 recent cases (1985-1991). Arch Intern Med. 1994 Dec 12-26. 154(23):2690-5. [Medline].
Palestro CJ. FDG-PET in musculoskeletal infections. Semin Nucl Med. 2013 Sep. 43(5):367-76. [Medline].
Sharff KA, Richards EP, Townes JM. Clinical management of septic arthritis. Curr Rheumatol Rep. 2013 Jun. 15(6):332. [Medline].
Centers for Disease Control and Prevention (CDC). Cephalosporin susceptibility among Neisseria gonorrhoeae isolates--United States, 2000-2010. MMWR Morb Mortal Wkly Rep. 2011 Jul 8. 60(26):873-7. [Medline].
Kaandorp CJ, Dinant HJ, van de Laar MA, et al. Incidence and sources of native and prosthetic joint infection: a community based prospective survey. Ann Rheum Dis. 1997 Aug. 56(8):470-5. [Medline].
Koeppe J, Johnson S, Morroni J, Siracusa-Rick C, Armon C. Suppressive antibiotic therapy for retained infected prosthetic joints: case series and review of the literature. Infect Dis Clin Pract. 2008. 16(4):224-9. [Full Text].
Berbari EF, Osmon DR, Carr A, et al. Dental procedures as risk factors for prosthetic hip or knee infection: a hospital-based prospective case-control study. Clin Infect Dis. 2010 Jan 1. 50(1):8-16. [Medline].
Martínez-Pastor JC, Muñoz-Mahamud E, Vilchez F, García-Ramiro S, Bori G, Sierra J, et al. Outcome of acute prosthetic joint infections due to gram-negative bacilli treated with open debridement and retention of the prosthesis. Antimicrob Agents Chemother. 2009 Nov. 53(11):4772-7. [Medline]. [Full Text].
Suprax [package insert]. Lupin Pharmaceuticals, Inc: Baltimore, Md. 2008. Available at [Full Text].
Centers for Disease Control and Prevention. Availability of cefixime 400 mg tablets--United States, April 2008. MMWR Morb Mortal Wkly Rep. 2008 Apr 25. 57(16):435. [Medline].
Bono KT, Samora JB, Klingele KE. Septic Arthritis in Infants Younger Than 3 Months: A Retrospective Review. Orthopedics. 2015 Sep 1. 38 (9):e787-93. [Medline].
|Virus||Clinical Features of Viral Septic Arthritis|
|Parvovirus B19||Occurs in adult women with erythema infectiosum, often an itchy rash|
|Hepatitis A||Muscle aches and rash in 10% of cases|
|Hepatitis B||Onset in the preicteric phase; usually resolves as jaundice develops; chronic arthritis possible in patients with chronic hepatitis B infection|
|Hepatitis C||History similar to hepatitis B joint infection|
|Rubella (natural infection and vaccine related)||Onset is possible before, during, or after the appearance of the rash; usually resolves in a few weeks; may recur and, more commonly, may persist|
|Human immunodeficiency virus [HIV] (2 types occur, both with noninflammatory, sterile joint fluid)||Develops over several days, and severe knee or ankle pain is characteristic; excellent response to nonsteroidal anti-inflammatory agents (NSAIDS)|
|Sudden onset of severe pain in the shoulders and elbows, closely resembling an acute gouty attack; Opiates often necessary to control pain|
|Mumps||Occurs in adult men 2 weeks after the presentation of parotitis|