Septic arthritis in adults

Authors:Don L Goldenberg, MDDaniel J Sexton, MDSection Editor:Stephen B Calderwood, MDDeputy

Editor:Elinor L Baron, MD, DTMH

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Jul 2018. | This topic last updated: Sep 15, 2017.

INTRODUCTION — Septic arthritis refers to infection in a joint; it is usually caused by bacteria but can be
caused by fungi or mycobacteria. Septic arthritis due to bacterial infection is often a destructive form of
acute arthritis.

The predisposing factors, pathogenesis, clinical manifestations, diagnosis, and treatment of

nongonococcal bacterial arthritis are reviewed here. Issues related to prosthetic joint infections, gonococcal
arthritis, and fungal and mycobacterial arthritis are discussed separately. (See "Prosthetic joint infection:
Epidemiology, clinical manifestations, and diagnosis" and "Prosthetic joint infection: Treatment" and
"Disseminated gonococcal infection" and "Skeletal tuberculosis".)

EPIDEMIOLOGY

Prevalence — The prevalence of bacterial arthritis as the diagnosis among adults presenting with one or
more acutely painful joints has been estimated to range from 8 to 27 percent; the lower figure is based on a
series of 100 patients presenting to an urban hospital emergency department; the latter figure is based on a
study of 75 patients presenting emergently in Taiwan [1,2]. These series included some patients with
prosthetic joints and a small minority in whom the final diagnosis was gonococcal septic arthritis.

Predisposing factors — Predisposing factors for septic arthritis were identified in a systematic review that
included more than 6200 patients with acutely painful joints; 10 percent had septic arthritis [3].
Predisposing factors include [3-5]:

●Age >80 years

●Diabetes mellitus

●Rheumatoid arthritis

●Presence of prosthetic joint

●Recent joint surgery

●Skin infection

●Intravenous drug abuse, alcoholism

●Prior intraarticular corticosteroid injection

Each of these factors appears to have a modest impact on the risk of septic arthritis; however,
combinations of independent risk factors substantially increase risk. As an example, acute joint pain in the
presence of a joint prosthesis and concurrent evidence of skin infection is associated with a positive
likelihood ratio of 15 (95% CI 8.1-28) [3]. (See "Glossary of common biostatistical and epidemiological
terms", section on 'Likelihood ratio'.)

Bacteremia is more likely to localize in a joint with preexisting arthritis, particularly if associated with
synovitis. As an example, a prospective community-based study of 154 patients with bacterial arthritis
found that 40 percent had preexisting joint disease, usually either rheumatoid arthritis (RA) or osteoarthritis
[6]. Patients with RA appear to be especially prone to bacterial arthritis; the risk may also be increased in
gout, pseudogout, osteoarthritis, and Charcot arthropathy [7,8]. Patients with RA may have additional
predisposing factors, such as prior intraarticular steroid injections, maintenance immunosuppressive
medications, and anti-tumor necrosis factor therapy [9-12]. (See "Tumor necrosis factor-alpha inhibitors
and mycobacterial infections".)

MECHANISM OF INFECTION — In most cases, bacterial arthritis arises from hematogenous spread to the
joint. Bacterial arthritis can also arise as a result of a bite or other trauma, direct inoculation of bacteria
during joint surgery, or, in rare cases, following extension of preexisting bony infection through the cortex
into the joint space [7,8,13]. In a retrospective review including 191 cases of septic arthritis, 72 percent
were thought to have arisen hematogenously [13]. Common predisposing factors for hematogenous
dissemination include injection drug use, presence of indwelling catheters, and an underlying
immunocompromised state such as HIV infection. Neonates and older adults are at highest risk [14].

In some cases, bacterial arthritis is the presenting sign of infective endocarditis [15]. This is most likely to
occur in patients who use injection drugs. Endocarditis should also be suspected when septic arthritis due
to Staphylococcus aureus, enterococci, or streptococci occurs in a patient without an obvious predisposing
cause. (See "Clinical manifestations and evaluation of adults with suspected native valve endocarditis".)

Patients with hematogenously induced bacterial arthritis may present with joint abnormalities in the
absence of documented bacteremia. These patients presumably acquired their infection from a transient or
self-limited bacteremia. It is unknown why only a small percentage of patients with bacteremia develop
septic arthritis. For example, the incidence of pneumococcal septic arthritis in patients with pneumococcal
bacteremia is extremely low (ranging from 0.5 to 0.7 percent in three different case series) [16].

Bacterial arthritis can occur in conjunction with bacterial meningitis. In a prospective cohort study including
nearly 700 adults with bacterial meningitis, arthritis was diagnosed in 7 percent of cases [17]. Joint fluid
cultures were positive in 6 of 23 patients (26 percent) in whom aspiration was performed. Arthritis was most
frequent in patients with meningococcal meningitis (12 percent).

Bacterial arthritis can also occur by other mechanisms. Sternoclavicular joint arthritis is a rare complication
of subclavian vein catheterization [18]. Septic arthritis of the hip can result in rare cases from femoral
venipuncture or ruptured colonic diverticular disease, in which the infection dissects via the retroperitoneal
space into the posterior thigh and hip joint, presenting as a seemingly spontaneous-onset polymicrobial
septic arthritis [19,20].

PATHOGENESIS — Bacteria entering the joint produce an acute inflammatory cell response in the synovial
membrane. Because synovial tissue has no limiting basement plate, bacterial organisms can quickly gain
access to the synovial fluid, creating acute-onset joint inflammation with purulence. Following onset of
infection, there is marked hyperplasia of the lining cells in the synovial membrane within seven days. In
addition, inflammatory cells release cytokines and proteases that cause cartilage degradation and inhibit
cartilage synthesis. Pressure necrosis from large synovial effusions may result in further cartilage and bone
loss.

Bacterial DNA and bacterial toxins may have a deleterious effect on joint structures. As an example,
extracts of unmethylated bacterial DNA from S. aureus or Escherichia coli produced arthritis in a murine
model that lasted up to 14 days [21]. Bacterial superantigens, such as staphylococcal toxic shock
syndrome toxin (TSST)-1 and staphylococcal enterotoxins may induce a potent inflammatory response that
damages joint cartilage. Animals infected with strains of S. aureus expressing TSST-1 and enterotoxin, for
example, developed severe arthritis, while those infected with strains in which these toxins were absent
had no or only mild joint inflammation. Moreover, vaccination with recombinant forms of staphylococcal
enterotoxin protected mice against severe arthritis due to enterotoxin containing staphylococci [22]. (See
"Staphylococcal toxic shock syndrome", section on 'pathogenesis'.)

The presence of surface components on organisms such as S. aureus may be important in the
pathogenesis of septic arthritis. Adhesins, called "microbial surface components recognizing adhesive
matrix molecules" (MSCRAMMs), mediate adherence of staphylococci to intraarticular proteins, such as
fibronectin, laminin, elastin, collagen, hyaluronic acid, and to prosthetic joint materials. There is increasing
experimental and clinical evidence that the presence or absence of genes encoding certain MSCRAMMs
affects whether or not individual strains of S. aureus cause septic arthritis [23]. A fibrinogen-binding
adhesion (FbsA) was a virulence factor in an animal model of septic arthritis following the intravenous
injection of Streptococcus agalactiae [24]. In contrast, the absence of pili-mediated adherence factors in
organisms such as Kingella kingae seem to be paradoxically associated with a tendency to develop joint,
bone, or endocardial infections [25].

Microbiology  —  Many pathogens are capable of causing nongonococcal bacterial arthritis (table 1). The
incidence of causative organisms varies by age and geographic location. S. aureus (including methicillin-
resistant S. aureus [MRSA]) is the most common bacterium infecting adult joints [4,8,26]. Other gram-
positive organisms such as streptococci are also frequent causes of septic arthritis. Septic arthritis due to
gram-negative bacilli is generally observed in the setting of trauma, intravenous drug users, neonates, older
adults, and in association with underlying immunosuppression.

Streptococcus pneumoniae cause a small but important percentage of cases of septic arthritis in adults.
One review of 190 cases of pneumococcal septic arthritis noted that the majority of cases were
monoarticular but that polyarticular involvement occurred in 36 percent [16]. Only one-half of the patients
had another clinically apparent focus of pneumococcal infection.

Septic arthritis is usually monomicrobial. Polymicrobial infections are less common and usually occur in the
setting of penetrating trauma involving the joint space, direct extension from the bowel as mentioned
above, or via hematogenous seeding in patients with polymicrobial bacteremia.

CLINICAL MANIFESTATIONS  —  Patients with nongonococcal bacterial arthritis usually present acutely
with a single swollen and painful joint (ie, monoarticular arthritis) [27]. Joint pain, swelling, warmth, and
restricted movement are reported by a majority of patients. These symptoms were noted at presentation in
80 percent of patients with septic arthritis [3].

A majority of patients with bacterial arthritis are febrile; chills and spiking fevers are unusual [3]. Older adult
patients with septic arthritis are less likely to present with fever. There may be evidence of an associated
skin, urinary tract, or respiratory infection, which should provide a clue to the likely infecting organism (table
1).

The knee is involved in more than 50 percent of cases; wrists, ankles, and hips are also commonly affected
[7]. Infection of the symphysis pubis is uncommon. In one review of 100 cases of infections of the pubic
symphysis, four major underlying factors were identified including patients who had undergone female
incontinence surgery (24 percent), who were athletes (19 percent), who had pelvic malignancy (17 percent),
or who used injection drugs (15 percent) [28]. (See "Pelvic osteomyelitis and other infections of the bony
pelvis in adults".)

Oligoarticular or polyarticular infection occurs in approximately 20 percent of septic joint infections, usually
involving two or three joints. Polyarticular septic arthritis is most likely to occur in patients with rheumatoid
arthritis or other systemic connective tissue disease and in patients with overwhelming sepsis [29].

Injection drug users have a predilection to develop bacterial arthritis in axial joints, such as the
sternoclavicular [30] or sternomanubrial joint. Injection drug users may also develop bacterial arthritis as a
consequence of infective endocarditis [15]. Endocarditis should also be suspected when septic arthritis due
to S. aureus, enterococci, or streptococci occurs in a patient without an obvious predisposing cause. (See
"Clinical manifestations and evaluation of adults with suspected native valve endocarditis".)

DIAGNOSIS — The definitive diagnostic test is identification of bacteria in the synovial fluid. In the setting
of suspected joint infection, synovial fluid aspiration should be performed (prior to administration of
antibiotics); fluid should be sent for Gram stain and culture, leukocyte count with differential, and
assessment for crystals (table 2 and algorithm 1). (See "Synovial fluid analysis".)

If synovial fluid cannot be obtained with closed needle aspiration, the joint should be aspirated under
computed tomography (CT) or fluoroscopic or ultrasound guidance. Certain joints, such as the hip or
sacroiliac joint, may require surgical arthrotomy for diagnostic aspiration.

The following results are typically obtained from synovial fluid analysis in patients with bacterial arthritis [8]:

●Synovial fluid is usually purulent, with typical leukocyte count of 50,000 to 150,000 cells/mm3 (most of
which are neutrophils). The likelihood of septic arthritis increases with increasing synovial fluid leukocyte
count [4]. High synovial fluid white blood cell counts can also occur in noninfectious conditions, so it is
important to interpret the results of synovial fluid testing in the overall clinical context. (See 'Differential
diagnosis' below.)

●Gram stain is positive in many but not all cases; the sensitivity is 30 to 50 percent [3]. False-positive
results may occur since precipitated crystal violet and mucin in the synovial fluid can mimic gram-positive
cocci. (See "Synovial fluid analysis".)

●Culture is positive in the majority of patients with nongonococcal bacterial arthritis. Negative cultures may
occur in the setting of recent antimicrobial therapy or infection with a fastidious organism.

Blood cultures are positive in approximately 50 percent of cases; thus, blood cultures should be obtained in
the setting of suspected bacterial arthritis (even if fever is absent). Other laboratory findings, such as an
increased white blood cell count and an elevated erythrocyte sedimentation rate, are common but
nonspecific.

Inflammatory markers (C-reactive protein [CRP] level and erythrocyte sedimentation rate) are frequently
elevated in the setting of septic arthritis [31]; they are also elevated in most forms of nonseptic acute
arthritis. In the absence of underlying inflammatory arthritis, serial inflammatory marker measurements may
be useful to guide duration of therapy. Measurement of synovial fluid CRP does not offer a significant
advantage over serum CRP; there is a strong correlation between serum and synovial CRP levels [32].

Radiographs of the infected joint should be obtained; associated osteomyelitis or concurrent joint disease
may be present in rare cases. In addition, a baseline radiograph is often useful for comparison purposes
should the response to therapy be delayed or poor. Scintigraphy, CT scanning, or magnetic resonance
imaging (MRI) can detect effusions and inflammation in joints that are difficult to examine, especially in the
hip and sacroiliac joints [33].

In the setting of septic arthritis due to S. aureus, echocardiography to evaluate for infective endocarditis is
warranted for patients with known valvular heart disease and/or polyarticular involvement, in the absence
of a clear source of infection. Echocardiography need not be pursued for patients with negative blood
cultures, no clinical stigmata of infective endocarditis or other sites of metastatic infection, and clear source
of infection (such as cellulitis, recent injection, recent surgery, or penetrating trauma). (See "Clinical
manifestations and evaluation of adults with suspected native valve endocarditis".)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of septic arthritis includes (table 3):

●Other causes of infection:

•Gonococcal arthritis – Gonococcal arthritis typically presents acutely in sexually active individuals with
fever, chills, skin lesions, polyarthralgias, and tenosynovitis, evolving into a persistent monoarthritis or
oligoarthritis. The diagnosis is established via identification of Neisseria gonorrhoeae with synovial fluid
nucleic acid amplification testing (NAAT) or culture (which requires processing on plates of chocolate agar
or Thayer-Martin medium); the organism cannot be cultured on routine culture media. (See "Disseminated
gonococcal infection".)

•Lyme disease – Lyme disease should be suspected in patients with an acute monoarthritis in the setting of
epidemiologic exposure in an endemic area; erythema migrans rash, fever, and migratory arthralgias may
occur weeks or months prior. The diagnosis is established via serologic testing. (See "Diagnosis of Lyme
disease".)

•Tuberculous arthritis – Tuberculous arthritis should be suspected in patients with indolent presentation of
persistent culture-negative oligoarthritis or monoarthritis, in the setting of relevant epidemiologic exposure.
The sensitivity of synovial fluid Ziehl-Neelsen stain for detection of acid-fast bacilli is low; the diagnosis is
established via synovial membrane histopathology and culture. (See "Skeletal tuberculosis", section on
'Arthritis'.)

•Fungal arthritis – Fungal arthritis should be suspected in patients with indolent presentation of persistent
culture-negative oligoarthritis or monoarthritis, in the setting of relevant epidemiologic exposure; it is most
common in the setting of immunosuppression. Fungal causes of arthritis include sporotrichosis,
coccidioidomycosis, candidiasis and others. The diagnosis is established via fungal stain and culture of
synovial fluid or via synovial membrane histopathology and culture. (See related topics.)

•Viral causes of arthritis – Viral causes of arthritis typically present with polyarthritis; they include dengue
fever, chikungunya, Zika virus, parvovirus, and rubella. A number of other viruses including enterovirus,
adenovirus, and alphaviruses may also cause arthritis (see "Specific viruses that cause arthritis"). (See
related topics.)

●Inflammatory arthritis:

•Crystal-induced arthritis (gout or pseudogout) – Manifestations of crystal-induced arthritis may include

monoarthritis and leukocytosis. Clinical clues suggestive of gout include involvement of the first
metatarsophalangeal joint, prior self-limited attacks of arthritis, and presence of tophi. If the knee or wrist
are involved, radiographs may demonstrate chondrocalcinosis, which would be more consistent with
pseudogout. The diagnosis can be established by synovial fluid analysis demonstrating monosodium urate
crystals of gout or calcium pyrophosphate dihydrate (CPPD) crystals of pseudogout. Concurrent crystal-
induced and bacterial arthritis can occur. (See "Clinical manifestations and diagnosis of gout" and "Clinical
manifestations and diagnosis of calcium pyrophosphate crystal deposition (CPPD) disease".)

•Reactive arthritis or spondyloarthritis – Chronic inflammatory joint disease can present with a new swollen
joint, simulating bacterial arthritis. This is especially common in the seronegative spondyloarthropathies
such as reactive arthritis. Most patients with reactive arthritis have recent genitourinary or gastrointestinal
signs or symptoms, conjunctivitis, or skin or mucus membrane lesions. Occasionally, patients with
ankylosing spondylitis present with acute-onset hip arthritis that mimics septic arthritis. (See "Reactive
arthritis" and "Diagnosis and differential diagnosis of axial spondyloarthritis (ankylosing spondylitis and
nonradiographic axial spondyloarthritis) in adults".)

•Rheumatoid arthritis (RA) – RA is typically a symmetrical, chronic polyarthritis; however, acute or subacute
exacerbation of one or a few joints can occur. The diagnosis may be difficult to establish because the
clinical findings may be somewhat atypical; many patients with RA present indolently (rather than acutely)
with bacterial arthritis, often with little fever or leukocytosis. Conversely, RA itself may present with a
"pseudoseptic arthritis" picture, including an explosive acute synovitis with a marked synovial fluid
leukocytosis. Thus, Gram stain and culture of synovial fluid are essential when evaluating the new onset of
synovitis in these patients. The diagnosis of RA is established via clinical criteria summarized separately.
(See "Diagnosis and differential diagnosis of rheumatoid arthritis".)

●Acute traumatic arthritis – Acute traumatic arthritis usually causes bloody synovial fluid and is generally
associated with a history of significant trauma to the joint. (See "Hemarthrosis", section on 'Traumatic'.)

TREATMENT  —  Treatment of acute bacterial arthritis requires antibiotic therapy and joint drainage
(algorithm 2) [34].

Initial antibiotic approach  —  No randomized controlled studies have evaluated antibiotic regimens for
bacterial arthritis. The initial choice of antimicrobial regimens is based on coverage of the most likely
organisms to cause infection, the Gram stain, the clinical presentation, and data from case series.

●If the initial Gram stain of the synovial fluid demonstrates gram-positive cocci, empiric treatment with
vancomycin (15 to 20 mg/kg/dose intravenously [IV] every 8 to 12 hours) should be administered [35]. Most
patients with normal renal function can be started on 15 mg/kg/dose (usual maximum 2 g per dose initially)
every 12 hours.

•Septic arthritis due to methicillin-susceptible S. aureus should be treated with a beta-lactam agent such as
cefazolin (2 g IV every 8 hours), nafcillin or oxacillin (2 g IV every 4 hours), or flucloxacillin (2 g IV every 6
hours). Patients who are allergic to penicillins can be treated with vancomycin.

•Septic arthritis due to methicillin-resistant S. aureus (MRSA) should be treated with vancomycin; if this is
not feasible due to allergy or drug intolerance, reasonable alternative agents include daptomycin (6 mg/kg/
day IV), linezolid (600 mg orally or intravenously twice daily), or clindamycin (600 mg orally or intravenously
three times daily) [35].

●If the initial Gram stain of the synovial fluid demonstrates gram-negative bacilli, treatment with a third-
generation cephalosporin should be administered. Options include:

•Ceftriaxone (2 g IV once daily)

•Cefotaxime (2 g IV every 8 hours)

•Ceftazidime (1 to 2 g intravenously every 8 hours)

In the setting of clinical suspicion for Pseudomonas aeruginosa (eg, in patients who inject illicit drugs),
ceftazidime should be given with an aminoglycoside such as gentamicin (3 to 5 mg/kg per day in two or
three divided doses); the regimen may be streamlined to a single agent once antimicrobial susceptibility
data are available. In cephalosporin-allergic patients, initial treatment with ciprofloxacin (400 mg IV every 12
hours or 500 to 750 mg orally twice daily) may be administered (in addition to an aminoglycoside).

In patients with penicillin allergy, alternative empiric regimens include aztreonam (2 g every 8 hours) or
gentamicin (3 to 5 mg/kg per day in two to three divided doses). The regimen may be tailored to
antimicrobial susceptibility data when available.

● If the initial Gram stain is negative and the patient is immunocompetent, treatment with vancomycin
should be administered. If the initial Gram stain is negative and the patient is immunocompromised,
treatment with vancomycin plus a third-generation cephalosporin should be administered. The same
regimen is appropriate in the setting of traumatic bacterial arthritis and for injection drug users [36].

The initial antibiotic regimen should be tailored to culture and susceptibility results when available. As an
example, vancomycin should be discontinued in patients with staphylococcal or streptococcal infections
that are susceptible to beta-lactam therapy.

There is no role for intraarticular antibiotics; parenteral and oral antibiotic therapy produce adequate drug
levels in joint fluid. Furthermore, direct instillation of antibiotics into a joint may induce an inflammatory
response [8].

Duration of antibiotic therapy  —  There have been no controlled trials examining the duration of
antimicrobial therapy in bacterial arthritis; treatment recommendations are based on case series. We
typically administer parenteral antibiotics for at least 14 days followed by oral therapy for an additional 14
days.

The choice of oral therapy for subsequent therapy depends upon the pathogen:

●Suitable choices for patients with methicillin-sensitive S. aureus include dicloxacillin (500 mg orally every 6
hours) or cephalexin (500 mg orally every 6 hours). Patients who are allergic to penicillins can be treated
with clindamycin (600 mg orally every 8 hours).

●Suitable choices with methicillin-resistant S. aureus include clindamycin, trimethoprim-sulfamethoxazole,

doxycycline (or minocycline), and linezolid (or tedizolid) (table 4). We do not favor use of other agents with
activity against MRSA that have not been studied for treatment of septic arthritis.

Patients with infections due to organisms that are susceptible to oral agents with high bioavailability (such
as a fluoroquinolone) can be successfully treated with a short course (4 to 7 days) of parenteral therapy
followed by 14 to 21 days of oral therapy. Compliance and response to therapy should be monitored
carefully in such cases.

Longer courses of outpatient parenteral antibiotic therapy (eg, three to four weeks) may be necessary to
cure infections due to difficult-to-treat pathogens such as P. aeruginosa or Enterobacter spp. In addition, a
longer course of parenteral therapy (four weeks) is warranted in the setting of concomitant bacteremia and
arthritis associated with S. aureus.

Joint drainage — No randomized controlled studies have evaluated joint drainage procedures in adults for
bacterial arthritis; recommendations are based on small retrospective studies. The approach depends on
the joint affected and the duration of infection.

In general, joint drainage should be performed in the setting of septic arthritis as this condition represents a
closed abscess collection. Options for drainage include needle aspiration (single or multiple), arthroscopic
drainage, or arthrotomy (open surgical drainage). If adequate drainage cannot be obtained by needle
aspiration, either arthroscopy or open drainage is necessary. [37]. Adequacy of needle aspiration is best
assessed using clinical criteria, including improvement in temperature, white cell count, joint swelling, and
pain. Improvement in joint swelling is easier to assess in the knee than in the hip or shoulder.

In most cases, initial surgical drainage is warranted for hips, shoulders, and prosthetic joint infections.
Surgical drainage should also be undertaken for any joint that is not improving clinically after serial needle
aspiration or if needle drainage is inadequate to remove the fluid [7,8,38]. In general, if daily needle
aspiration is not adequate for joint decompression after three to five days, surgical drainage may be
warranted.

For knee, shoulder, and wrist infections, arthroscopy is often preferred because of easier irrigation and
better visualization of the joint [39-41]. A multicenter study of 46 cases of septic arthritis of the knee treated
by arthroscopic drainage showed a bacteriologic cure rate of 78 percent [39]. A retrospective study of 76
patients with septic arthritis (62 knee, 10 shoulder, 5 ankle joints, and 1 hip joint) evaluated initial
arthroscopic management [40]. Outcomes were dependent on the stage of infection, with more severe
infections more likely to require repeated arthroscopic irrigations.

For hip infections, initial open surgical drainage may be necessary. Although arthrotomy has been
considered standard treatment, a retrospective study involving six patients with septic hips found that
arthroscopic treatment with large-volume irrigation was effective [42]. Further clinical studies will be needed
to determine the best approach.

If joint drainage is manage initially via needle aspiration(s), serial synovial fluid analyses should demonstrate
that the fluid has become sterile and that the total leukocyte count is decreasing. If not, more definitive joint
drainage and/or an alteration in the antimicrobial regimen may be warranted. Infected knees often continue
to accumulate synovial fluid and require daily aspiration for 7 to 10 days. Attention should also be paid to
joint position and rapid mobilization to prevent contractures and promote optimal nutrition to the articular
cartilage.

PROGNOSIS  —  It is difficult to predict the functional outcome of individual patients during and at the
conclusion of treatment. The outcome is directly related to host factors, such as prior joint damage, the
virulence of the infecting organism, and duration of infection prior to initiation of therapy.

As an example, in one study including 121 adults and 31 children with bacterial arthritis, a poor joint
outcome (as defined by the need for amputation, arthrodesis, prosthetic surgery, or severe functional
deterioration) occurred in one-third of the patients [6]. Adverse prognostic factors included older age,
preexisting joint disease, and an infected joint containing synthetic material.

Inflammation and joint destruction may continue even in the setting of a sterile joint, despite effective
antimicrobial therapy [43]. This may be due to the persistence of bacterial DNA within the joint, which has
been shown to induce arthritis in an animal model of septic arthritis [21].

The pathogen may also have an important influence on the outcome of treatment. In the series of patients
with pneumococcal bacterial arthritis, for example, 95 percent of adults and 90 percent of children had a
return to baseline joint function or only mild limitation of joint motion following the completion of therapy
[16]. These results are in contrast with other studies of S. aureus bacterial arthritis that report 46 to 50
percent with poor joint outcomes following therapy [8,44].

Mortality due to bacterial arthritis depends on the presence of comorbid conditions such as advanced age,
coexistent renal or cardiac disease, and immunosuppression. The mortality rates in most series have
ranged from 10 to 15 percent [6]. Polyarticular septic arthritis, particularly when it is due to S. aureus or
occurs in the presence of rheumatoid arthritis, has an extremely poor prognosis, with mortality rates as
high as 50 percent [29]. Mortality due to septic pneumococcal arthritis was reported as 19 percent in one
series.

SOCIETY GUIDELINE LINKS  —  Links to society and government-sponsored guidelines from selected
countries and regions around the world are provided separately. (See "Society guideline links: Septic
arthritis in adults".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics"
and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to
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detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who
want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail
these topics to your patients. (You can also locate patient education articles on a variety of subjects by
searching on "patient info" and the keyword(s) of interest.)

●Basics topic (see "Patient education: Septic arthritis (The Basics)")

●Beyond the Basics topics (see "Patient education: Arthritis (Beyond the Basics)" and "Patient education:
Joint infection (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

●Septic arthritis due to nongonococcal bacterial infection is often a destructive form of acute arthritis. In
most cases, bacterial arthritis arises from hematogenous spread to the joint. Bacterial arthritis can also
arise as a result of a bite or other trauma, direct inoculation of bacteria during joint surgery, or, in rare cases,
following extension of preexisting bony infection through the cortex into the joint space. (See 'Mechanism
of infection' above.)

●Bacteremia is more likely to localize in a joint with preexisting arthritis, particularly if associated with
synovitis. Patients with rheumatoid arthritis appear to be especially prone to bacterial arthritis; the risk may
also be increased in gout, pseudogout, osteoarthritis, and Charcot arthropathy. (See 'Predisposing factors'
above.)

●Many pathogens are capable of causing bacterial arthritis (table 1). Organisms such as Staphylococcus
aureus and streptococci have a higher propensity to cause joint infections than gram-negative bacilli, which
typically cause infections following trauma or in patients with severe underlying immunosuppression. (See
'Microbiology' above.)

●Patients with bacterial arthritis usually present acutely with a single swollen and painful joint (ie,
monoarticular arthritis). The knee is involved in more than 50 percent of cases; wrists, ankles, and hips are
also commonly affected. (See 'Clinical manifestations' above.)

●The definitive diagnostic test is identification of bacteria in the synovial fluid. In the setting of suspected
joint infection, synovial fluid aspiration should be performed (prior to administration of antibiotics); fluid
should be sent for Gram stain and culture, leukocyte count with differential, and assessment for crystals
(table 2 and algorithm 1). (See 'Diagnosis' above.)

●Treatment of acute bacterial arthritis consists of antibiotic therapy and joint drainage (algorithm 2). The
initial choice of antibiotics for treatment of septic arthritis is based on the Gram stain. The initial regimen
should be tailored to culture and susceptibility results when available. The typical duration of therapy is
three to four weeks. (See 'Initial antibiotic approach' above and 'Joint drainage' above.)

●If the initial Gram stain of the synovial fluid shows gram-positive cocci, we suggest treatment with
vancomycin (Grade 2B). If the initial Gram stain of the synovial fluid shows gram-negative bacilli, we
suggest treatment with a third-generation cephalosporin (Grade 2B). (See 'Treatment' above.)

●If the initial Gram stain is negative and the patient is immunocompetent, we suggest treatment with
vancomycin (Grade 2C). If the initial Gram stain is negative and the patient is immunocompromised, we
suggest treatment with vancomycin plus a third-generation cephalosporin (Grade 2C).(See 'Initial antibiotic
approach' above.)

●In general, we recommend joint drainage in the setting of septic arthritis (Grade 1B), as this condition
represents a closed abscess collection. Options for drainage include needle aspiration (single or multiple),
arthroscopic drainage, or arthrotomy (open surgical drainage). (See 'Joint drainage' above.)