Septic arthritis in adults

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Apr 2017. | This topic last updated: Dec 15, 2016.

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 (TNF) 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 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".)

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 non-radiographic 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].

Antibiotic therapy 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 in this setting, the Gram stain, the clinical presentation, and data from case series.

If the initial Gram stain of the synovial fluid shows gram-positive cocci, treatment
with vancomycin (30 mg/kg per 24 hours in two equally divided doses, not to exceed 2 g per 24 hours
unless concentrations in serum are inappropriately low) should be administered [35].

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 intravenously [IV]), linezolid (600 mg by mouth [PO] or IV twice daily),
or clindamycin (600 mg PO or IV three times daily) [35].

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

Ceftriaxone (2 g intravenously once daily) or

Cefotaxime (2 g IV every eight hours) or

Ceftazidime (1 to 2 g intravenously every eight 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 eight 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 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 (if possible) for an additional 14 days. However, selected
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
patients.

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 therapy (four weeks) is warranted in the setting of 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 [16].

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 5 th to 6th grade
reading level, and they answer the four or five key questions a patient might have about a given condition. These
articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond
the Basics patient education pieces are longer, more sophisticated, and more 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 S. 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 'Antibiotic therapy' 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).

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.)