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Acute
infectious arthritis is a joint infection that evolves over hours
or days. The infection resides in synovial or periarticular tissues
and is usually bacterial—in younger adults, frequently Neisseria gonorrhoeae. However,
nongonococcal bacterial infections can also occur and can rapidly
destroy joint structures. Symptoms include rapid onset of pain,
effusion, and restriction of both active and passive range of motion, usually
within a single joint. Diagnosis requires synovial fluid analysis
and culture. Treatment is IV antibiotics and drainage
of pus from joints.
Acute infectious arthritis may occur in children. About 50% of children with joint infection are < 3 yr. However, routine childhood vaccination for Haemophilus influenzae and Streptococcus pneumoniae is decreasing the incidence in this age group.
Risk factors are listed in Table 1: Infections of Joints and Bones: Risk Factors for Infectious Arthritis . Risk is substantially increased in patients with RA and other disorders causing chronic joint damage, a past history of joint infection, IV drug abuse, or a prosthetic joint (see Infections of Joints and Bones: Prosthetic Joint Infectious Arthritis). RA patients are at particular risk of bacterial arthritis (prevalence 0.3 to 3.0%; annual incidence 0.5%). Most children who develop infectious arthritis do not have identified risk factors.
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Table 1
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Risk Factors for Infectious Arthritis
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Advanced age (50% of adults are > 60 yr)
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Alcoholism
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Anemia
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Arthrocentesis or joint surgery
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Bacteremia
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Cancer
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Chronic medical illness (eg, lung or liver disease)
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Diabetes
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Hemodialysis
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Hemophilia
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History of previous joint infection
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Immunodeficiency, including HIV
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Immunosuppressive therapy, including corticosteroids
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IV drug abuse
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Prosthetic joint implant
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RA
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Risk factors for sexually transmitted diseases (eg, multiple sex partners, absence of barrier precautions)
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Sickle cell disease
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Skin infections
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SLE
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Etiology
Infectious organisms reach joints by direct penetration (eg, trauma, surgery, arthrocentesis, bites), extension from an adjacent infection (eg, osteomyelitis, a soft-tissue abscess, an infected wound), or hematogenous spread from a remote site of infection.
Common organisms are listed in Table 2: Infections of Joints and Bones: Organisms That Commonly Cause Acute Infectious Arthritis . In adults, most cases result from bacteria and are classified as gonococcal or nongonococcal. In adults overall, Staphylococcus aureus tends to be the most frequent cause of infectious arthritis. Methicillin resistance has become more common among community isolates of S.
aureus. In young adults and adolescents, Neisseria
gonorrhoeae is the most common cause and results when N. gonorrhoeae spreads from infected mucosal surfaces (cervix, urethra, rectum, pharynx) via the bloodstream. Affected patients often have simultaneous genital infections with Chlamydia trachomatis (see Sexually Transmitted Diseases (STD): Chlamydial, Mycoplasmal, and Ureaplasmal Infections). Streptococcus species are also frequent causes, particularly in patients with polyarticular infections.
Pathophysiology
Infecting organisms multiply in the synovial fluid and synovial lining. Some bacteria (eg, S. aureus) produce virulence factors (adhesins), which allow bacteria to penetrate, remain within, and infect joint tissues. Other bacterial products (eg, endotoxin from gram-negative organisms, cell wall fragments, exotoxins from gram-positive organisms, immune complexes formed by bacterial antigens and host antibodies) augment the inflammatory reaction.
PMNs migrate into the joint and phagocytose the infecting organisms. Phagocytosis of bacteria also results in PMN autolysis with release of lysosomal enzymes into the joint, which damage synovia, ligaments, and cartilage. Therefore, PMNs are both the major host defense system and the cause of joint damage. Articular cartilage can be destroyed within hours or days. Inflammatory synovitis may occasionally persist even after the infection has been eradicated by antibiotics. Particularly in gonococcal cases, persistent antigen debris from bacteria or infection may alter cartilage, causing it to become antigenic, and—together with the adjuvant effects of bacterial components—immune-mediated, “sterile” chronic inflammatory synovitis results.
Symptoms and Signs
Over a few hours to a few days, patients develop moderate to severe joint pain, warmth, tenderness, effusion, restricted active and passive motion, and sometimes redness. Systemic symptoms may be minimal or absent. Infants and children may present with limited spontaneous movement of a limb (pseudoparalysis), irritability, feeding disturbances, and a high, low-grade, or no fever.
Gonococcal arthritis:
Gonococcal arthritis can cause a distinctive dermatitis-polyarthritis-tenosynovitis syndrome. Classic manifestations are fever (for 5 to 7 days); shaking chills; multiple skin lesions (petechiae, papules, pustules, hemorrhagic vesicles or bullae, necrotic lesions) on mucosal surfaces and on the skin of the trunk, hands, or lower extremities; and migratory arthralgias, arthritis, and tenosynovitis, which evolves into persistent inflammatory arthritis in one or more joints, most often the small joints of the hands, wrists, elbows, knees, and ankles, and rarely the axial skeletal joints. Symptoms of the original mucosal infection (eg, urethritis, cervicitis) may not be present.
Nongonococcal
bacterial arthritis:
Nongonococcal bacterial arthritis causes progressive moderate to severe joint pain that is markedly worsened by movement or palpation. Most infected joints are swollen, red, and warm. Fever is absent or low grade in up to 50% of patients; 20% of patients report a shaking chill. Virulent organisms (eg, S. aureus or Pseudomonas
aeruginosa) generally cause a more fulminant arthritis, whereas less virulent organisms (eg, coagulase-negative staphylococci or Propionibacterium acnes) cause a less fulminant arthritis. In 80% of adults, nongonococcal bacterial arthritis is monarticular and usually occurs in a peripheral joint: knee, hip, shoulder, wrist, ankle, or elbow. In children, ≥ 90% is monarticular: knee (39%), hip (26%), and ankle (13%). Polyarticular involvement is somewhat more common among patients who are immunosuppressed or have an underlying chronic arthritis (eg, RA, osteoarthritis). In IV drug users and patients with indwelling vascular catheters, axial joints are often involved (eg, sternoclavicular, costochondral, hip, shoulder, vertebrae, symphysis pubis, sacroiliac joints).
Infectious arthritis
secondary to bite wounds:
Infection due to human, dog, or cat bites usually develops within 48 h. Rat bites cause systemic symptoms such as fever, rash, and joint pain or true arthritis with regional adenopathy within about 2 to 10 days.
Viral infectious
arthritis:
Viral infectious arthritis sometimes causes symptoms similar to acute nongonococcal bacterial arthritis and is more likely than bacterial to be polyarticular.
Borrelia
burgdorferi arthritis:
Patients with B. burgdorferi arthritis may have other symptoms of Lyme disease (see Spirochetes: Symptoms and Signs) or present only with acute monarthritis or oligoarthritis.
Diagnosis
Infectious arthritis is suspected in patients with acute monarticular arthritis and in patients with other combinations of symptoms characteristic of particular infectious arthritis syndromes (eg, migratory polyarthritis, tenosynovitis and skin lesions typical of disseminated gonococcal infection; erythema migrans or other symptoms and signs of Lyme disease—see Spirochetes: Symptoms and Signs). Even mild monarticular joint symptoms should arouse suspicion in patients with risk factors (eg, RA), a prosthetic joint, or an extra-articular infection capable of spreading to a joint (eg, genital gonococcal infection, bacteremia, any anaerobic infection).
General arthritis:
Synovial
fluid examination is the cornerstone of diagnosis. Fluid is examined grossly and sent for cell count and differential, Gram stain, aerobic and anaerobic culture, and crystals. Foul-smelling synovial fluid suggests anaerobic infection. Fluid from an acutely infected joint usually reveals a WBC count > 20,000/μL (often > 100,000/μL) consisting of > 95% PMNs. WBC counts tend to be higher in nongonococcal bacterial than in gonococcal infectious arthritis. WBC counts may also be lower in early or partially treated infections. Gram stain reveals organisms in only 50 to 75% of joints with acute bacterial arthritis, most often with staphylococci. If positive, Gram stain is usually relatively specific, but cultures are definitive. The presence of crystals does not exclude infectious arthritis. Sometimes synovial fluid analysis cannot differentiate between infectious and other inflammatory synovial fluid. If differentiation is impossible by clinical means or synovial fluid examination, infectious arthritis is assumed, pending culture results.
Blood tests, such as blood cultures, CBC, and ESR (or C-reactive protein), are usually obtained. However, normal results do not exclude infection. Likewise, WBC count, ESR, or C-reactive protein may be increased in noninfectious as well as infectious joint inflammation.
Plain x‑rays of the involved joint are not diagnostic of acute infection but can exclude other conditions under consideration (eg, fractures). Abnormalities in early acute bacterial arthritis are limited to soft-tissue swelling and signs of synovial effusions. After 10 to 14 days of untreated bacterial infection, destructive changes of joint space narrowing (reflecting cartilage destruction) and erosions or foci of subchondral osteomyelitis may appear. Gas visible within the joints suggests infection with Escherichia coli or anaerobes.
MRI is considered if the joint is not easily accessible for examination and aspiration (eg, an axial joint). MRI or ultrasound can identify sites of effusion or abscess that can be aspirated or drained for both diagnosis and therapy. MRI can provide early suggestion of associated osteomyelitis. Bone scans using technetium-99m can be falsely negative in infectious arthritis. Also, because they show increased uptake with increased blood flow in inflamed synovial membranes and in metabolically active bone, they can be falsely positive in noninfectious inflammatory arthritis. Nuclear imaging and MRI do not distinguish infection from crystal-induced arthritis.
Gonococcal arthritis:
If gonococcal arthritis is suspected, blood and synovial fluid samples should be immediately plated on nonselective chocolate agar, and specimens from the urethra, endocervix, rectum, and pharynx should be plated on selective Thayer-Martin medium. Genital chlamydial cultures are also done. Blood cultures are positive in 60 to 75% of cases during the first week and may be the only method by which to identify the organism; cultures from joints with early tenosynovitis or arthritis are often negative. Synovial fluid cultures from joints with frank purulent arthritis are usually positive, and fluid from skin lesions may be positive. If disseminated gonococcal infection is suspected based on clinical criteria, it is assumed to be present even if all gonococcal cultures are negative. Clinical response to antibiotics (anticipated within 5 to 7 days) can help confirm the diagnosis.
Prognosis
Acute nongonococcal bacterial arthritis can destroy articular cartilage, permanently damaging the joint within hours or days. Gonococcal arthritis does not usually damage joints permanently. Factors that increase susceptibility to infectious arthritis may also increase disease severity. In patients with RA, functional outcome is particularly poor, and the mortality rate is increased.
Treatment
Antibiotic therapy:
Initial antibiotic selection is directed at the most likely pathogens. The regimen is adjusted based on the results of culture and susceptibility testing.
Gonococcal arthritis is treated with ceftriaxone 1 g IV once/day until at least 24 h after symptoms and signs resolve, followed by cefixime 400 mg po bid for 7 days. Joint drainage and debridement may be unnecessary. Coexisting genital infection with C. trachomatis is also treated, often with doxycycline 100 mg bid for 7 days, and sexual contacts of the patient are treated as necessary (see Human Immunodeficiency Virus (HIV): Treatment).
If nongonococcal gram-positive infection is suspected by Gram stain in an adult, the empiric choice is one of the following: a semisynthetic penicillin (eg, nafcillin 2 g IV q 4 h), a cephalosporin (eg, cefazolin 2 g IV q 8 h), or vancomycin 1 g IV q 12 h (if methicillin resistance is common among local community isolates of S. aureus). If gram-negative infection is suspected, empiric treatment includes a parenteral 3rd-generation cephalosporin with antipseudomonal activity (eg, ceftazidime 2 g IV q 8 h) and, if infection is severe, an aminoglycoside.
Parenteral antibiotics are continued until clinical improvement is clear (usually 2 to 4 wk), and oral antibiotics should be given at high doses for another 2 to 6 wk according to the clinical response. Infections caused by streptococci and Haemophilus are usually eradicated after 2 wk of oral antibiotics after IV treatment. Staphylococcal infections require at least 3 wk and often 6 wk or longer, especially in patients with prior arthritis.
Other therapies:
In addition to antibiotics, acute nongonococcal bacterial arthritis requires large-bore needle aspiration of intra-articular pus at least once/day, or tidal irrigation lavage, arthroscopic lavage, or arthrotomy for debridement. Infected RA joints should generally undergo even earlier and more aggressive surgical debridement and drainage. For gonococcal arthritis with persistent effusion, pus is aspirated and drainage may need to be repeated as necessary. Acute bacterial arthritis requires joint splinting for the first few days to reduce pain, followed by passive and active range-of-motion exercises to limit contractures, with muscle strengthening as soon as tolerated. NSAIDs can help decrease pain and inflammation.
Viral arthritis
and arthritis secondary to bite wounds:
Viral arthritis is treated supportively. Bite wounds are treated with antibiotics and surgical drainage as necessary (see Bites and Stings: Treatment).
Last full review/revision February 2008 by Steven Schmitt, MD
Content last modified February 2008
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