eMedicine Specialties > Infectious Diseases > Bone and Joint Infections

Septic Arthritis

Author: John L Brusch, MD, FACP, Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance
Contributor Information and Disclosures

Updated: Aug 25, 2008

Introduction

Background

Septic arthritis, also known as infectious arthritis, may represent a direct invasion of joint space by various microorganisms, including bacteria, viruses, mycobacteria, and fungi. Reactive arthritis, a sterile inflammatory process, may be the consequence of an infectious process located elsewhere in the body. Although any infectious agent may cause arthritis, bacterial pathogens are the most significant because of their rapidly destructive nature. For this reason, the current discussion concentrates on bacterial septic arthritides. Failure to recognize and to appropriately treat septic arthritis results in significant rates of morbidity and may even lead to death.

Because of the increasing use of prosthetic joints, infection associated with these devices may be the most common and challenging type of septic arthritis encountered by most clinicians.¹

Approximately 20,000 cases of septic arthritis occur in the United States each year. The 2 major classes of bacterial/suppurative arthritis are gonococcal and nongonococcal.^1,2,3,4 Overall, although Neisseria gonorrhoeae remains the most common pathogen (75% of cases) among younger sexually active individuals,^5,6 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.⁷ This pathogen is the cause in 80% of infected joints affected by rheumatoid arthritis.

Streptococcal species, such as Streptococcus viridans, Streptococcus pneumoniae ,^8,9 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,¹⁰ who are immunosuppressed, and who abuse intravenous drugs.¹ 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.¹¹

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, 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.¹²

Three major types of prosthetic joint infections (PJIs) exist: those that occur early, within 3 months of implantation; those that are delayed, within 3-24 months of implantation; and those that occur later than 24 months following the implantation. Most cases of early PJI are caused by S aureus, while 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 PJI are secondary to hematogenous spread from various infectious foci.¹³

Pathophysiology

Organisms may invade the joint by direct inoculation, by contiguous spread from infected periarticular tissue, or via the bloodstream (the most common route).¹¹

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.

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 pathological 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 WBCs into the joint, explaining, in part, the minimal joint destruction observed with infection with this organism compared 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 immunological mechanisms occur in infections with hepatitis B, parvovirus B19, and lymphocytic choriomeningitis viruses.¹²

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:

• 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 immunological mechanisms, with a minority of cases due to direct invasion by an organism.

PJIs may be a consequence of local infection, such as intraoperative contamination (60-80% of cases), or of bacteremias (20-40% of cases).¹ The latter type may be spontaneous (ie, gingival disease) or secondary to various manipulations. Delayed wound healing is a major factor behind early PJI. 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 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 PJIs 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.

Frequency

United States

Approximately 20,000 cases of septic arthritis occur each year in the United States (7.8 cases per 100,000 person-years).⁴ The incidence of arthritis due to disseminated gonococcal infection is 2.8 cases per 100,000 person-years. Septic arthritis is becoming increasingly common among people who are immunosuppressed and elderly persons; these groups are more likely to have various comorbid disease states. The incidence of PJI among all prosthesis recipients ranges from 2-10%.

International

The incidence of septic arthritis in Europe is identical to that in the United States.

Mortality/Morbidity

The primary morbidity of septic arthritis is significant dysfunction of the joint, even if treated properly. The mortality rate depends primarily on the causative organism. N gonorrhoeae septic arthritis carries an extremely low mortality rate, while that of S aureus can approach 50%.¹⁴

Race

Septic arthritis has no recognized racial predisposition.

Sex

Fifty-six percent of patients with septic arthritis are male.

Age

Forty-five percent of people with septic arthritis are older than 65 years.

Clinical

History

Because joint infections are uncommon, be especially attentive to features of the patient's history that may indicate an infectious process instead of a primary rheumatologic or orthopedic process.³

• Pay attention to the following symptoms:
  • Acuteness of onset of the joint pain
  • Whether the pain is superimposed on chronic pain
  • Previous history of joint disease or trauma, whether accidental or iatrogenic (eg, infection complicates 0.4% of arthrocenteses)
  • Whether the process is monoarticular or polyarticular and which joints are involved
  • The presence of extra-articular symptoms
  • Whether the patient has had vascular invasion due to catheterizations or intravenous drug abuse
• Obtain a thorough history regarding the possible presence of sexually transmitted diseases (STDs) or exposure to ticks (Lyme disease). The increase of group B streptococcal joint infections is associated with the increased prevalence of diabetes and increasing life expectancy.
• Numerous conditions that adversely affect the host's defenses (eg, liver disease, diabetes mellitus, lymphoma, solid tumors, complement deficiencies [C7, C8], immunosuppressive drugs, hypogammaglobulinemia) are increasingly observed in patients with septic arthritis. Determine the possible contribution of these diseases to the clinical presentation.
• The most important historical feature is the existence of underlying joint disease, especially rheumatoid arthritis. In addition, the possibility of recent injury to the joint or penetrating or blunt trauma must be explored. Ask the patient about needle aspiration of the joint or injections of corticosteroids into the joint. Elicit a history of diarrheal disease. Patients with an infected joint typically present with the triad of fever (40-60% of cases), pain (75% of cases), and impaired range of motion. These symptoms may evolve over a few days to a few weeks. Fever usually is low-grade (<102°F), with rigors present in only 20% of cases. Spiking fevers and chills are much more common with crystalline arthritis.
• Months after infection onset, 60% of patients with untreated Lyme disease develop swelling and pain, chiefly affecting the large joints. Usually, Lyme disease affects 1-2 joints at a time, with the knee involved most commonly. The distinguishing pattern is attacks extending from a few weeks to months and separated by periods of complete remission. The rate of recurrence lessens by about 15% per year. A small percentage of individuals develop chronic arthritis (ie, inflammation of a joint lasting ³ 1 y). This type of relapsing course almost always precedes the chronic stage of Lyme arthritis.
• Compared with patients with infections of native joints, most patients with PJI exhibit a prolonged low-grade course with gradually increasing pain.
  • Usually, no significant fever or swelling occurs (delayed PJI). However, individuals with early PJI present with an acute illness characterized by high-grade fever, focal swelling, and redness. Cellulitis and draining sinus tracts often develop.
  • Because late PJI is usually secondary to bacteremia, the clinical picture is often dominated by the source of the bloodstream infection.
  • The nature of the invading organism, the type of tissue infected, and the route of infection determine presentation. Thus, a high index of suspicion is needed for identification of bacteremic and delayed PJI. Because of its many pathogenic mechanisms, S aureus is usually associated with a fulminant course, as opposed to the indolent course of CONS that dominates delayed PJI. Relatively devitalized tissues (eg, wound hematomas) are conducive to rapid bacterial replication and a more acute course. Bacteremic spread allows infection with fewer organisms and leads to a more muted course.
• Reactive arthritis usually begins several weeks after the underlying infection has resolved. Few concurrent systemic symptoms occur.
• Symptoms of tuberculous arthritis are quite indolent; the diagnosis may be delayed for several years. Usually, the purified protein derivative (PPD) results are negative, and no signs, past or present, of pulmonary tuberculous exist.

Clinical Features of Viral Septic Arthritis

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Physical

The most commonly involved joint is the knee (50% of cases), followed by the hip (20%), shoulder (8%), ankle (7%), and wrists (7%). The elbow, interphalangeal, sternoclavicular, and sacroiliac joints each make up 1-4% of cases. A thorough inspection of all joints for signs of erythema, swelling (90% of cases), warmth, and tenderness is essential for diagnosing infection. Infected joints usually exhibit an obvious effusion, which is associated with marked limitation of both active and passive ranges of motion. Frequently, these findings are apparent but may be diminished or poorly localized in cases of infection of the spine, hip, and shoulder joints.¹²

Signs and symptoms of infection may be muted in people who are elderly, who are immunocompromised (especially those with rheumatoid arthritis), and who abuse intravenous drugs.

• The pattern of joint involvement is an extremely important diagnostic feature. Of cases of nongonococcal suppurative arthritis, 85-90% are monoarticular. If the disease affects more than one joint, S aureus is most commonly implicated. Polyarticular arthritis is usually observed in gonococcal disease, various viral infections, Lyme disease, reactive arthritis, and various noninfectious processes.
• Group B streptococci most commonly infect the sacroiliac and sternoclavicular joints.
• Gonococcal musculoskeletal involvement may present in one of two ways.
  • Fever, arthralgias of multiple joints, and multiple skin lesions (dermatitis-arthritis syndrome) characterize disease that develops soon after the gonococcus disseminates from the cervix, urethra, or pharynx. Usually, this disease exhibits no clinical direct joint findings, but the process is one of tenosynovitis of asymmetric distribution. Typically, hand joints are involved most often, as well as those of the knee, wrist, ankle, and elbow. Skin lesions are multiple but seldom number more than 12, while lesions associated with meningococcemia may number more than 100. The lesions evolve over a few days from papular to pustular or vesicular to necrotic. This course may recur for several months. Findings on cultures of blood and mucosal surfaces are often positive; findings on cultures of joint fluid are usually negative. Sixty percent of disseminated gonococcal infections are of this type.
  • Monoarticular arthritis without associated systemic symptoms, tenosynovitis, or skin lesions characterizes disease that begins later after gonococcal dissemination than does dermatitis arthritis syndrome.⁶ Dermatitis-arthritis syndrome may or may not precede this phase. In a joint infected by the Lyme organism, swelling may be disproportionate to the level of pain. Baker cysts are a frequent feature of this type of infectious arthritis. Because the pain of an infected hip joint may not be localized directly and swelling of the joint is inconspicuous, perform specific maneuvers, such as the Fabere maneuver. Infection of the sacroiliac joint often presents as buttock, hip, or anterior thigh pain. Direct pressure usually elicits tenderness in the joint. Alternatively, hyperextension of the hip and leg while the patient is lying down (ie, Gaenslen maneuver) elicits pain in a suppurative sacroiliac joint.
• Septic bursitis most commonly involves the olecranon and prepatellar bursae. Swelling and pain are present. However, an infected bursa does not limit the range of motion of the underlying joint the way an actual joint infection does.¹⁵
• Physical findings are usually minimal in an infection of the prosthetic joint, and swelling is usually slight. The most distinctive finding is a draining sinus presumed to originate in the underlying infected prosthetic joint.
• Most cases of reactive arthritis involve a few large joints in an asymmetric fashion.
• Viral arthritis usually exhibits symmetric involvement of the smaller joints, especially the hands, with a concurrent rash.
• The joints of tuberculous arthritis can appear to be boggy on palpation.

Causes

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), S aureus, CONS, gram-negative bacteria (prosthetic joints), 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.

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