Septic arthritis in adults

Authors:
Don L Goldenberg, MD
Daniel J Sexton, MD
Section Editor:
Stephen B Calderwood, MD
Deputy 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: Mar 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 clindamycin (300 to 450 mg orally every 6 to 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 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].

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
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four or five key questions a patient might have about a given condition. These articles
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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 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.)

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