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Septic Arthritis
Updated: Dec 06, 2018
Author: John L Brusch, MD, FACP; Chief Editor: Michael Stuart Bronze, MD more...

OVERVIEW

Background
Septic arthritis, also known as infectious arthritis, may represent a direct invasion of joint
space by various microorganisms, most commonly caused by bacteria. However, viruses,
mycobacteria, and fungi have been implicated. Reactive arthritis is a sterile inflammatory
process that may result from an extra-articular infectious process. Bacteria are the most
significant pathogens in septic arthritis because of their rapidly destructive nature. For this
reason, the current discussion concentrates on the bacterial septic arthritides. Failure to
recognize and to appropriately treat septic arthritis results in significant rates of morbidity
and may even lead to death.

Approximately 20,000 cases of septic arthritis occur in the United States each year (7.8
cases per 100,000 person-years), with a similar incidence occurring in Europe. [1] The
incidence of arthritis due to disseminated gonococcal infection is 2.8 cases per 100,000
person-years.

Because of the increasing use of prosthetic joints, infection associated with these devices
has become the most common and challenging type of septic arthritis encountered by
most clinicians. [2] The incidence of prosthetic joint infection (PJI) among all prosthesis
recipients ranges from 2% to 10%. These figures may be falsely low because surveillance
is limited to the operative hospital, which may lead to underestimation of the rate of PJIs.
[3]

Septic arthritis is also becoming increasingly common among people who are
immunosuppressed and elderly persons. Of people with septic arthritis, 45% are older
than 65 years; these groups are more likely to have various comorbid disease states.
Fifty-six percent of patients with septic arthritis are male.

Gonococcal and nongonococcal bacterial/suppurative arthritis

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 Septic arthritis due to bacterial infections is commonly classified as either gonococcal or
nongonococcal. [1, 2, 4, 5, 6] Overall, although Neisseria gonorrhoeae remains the most
common pathogen (75% of cases) among younger sexually active individuals, [7, 8]
Staphylococcus aureus infection is the cause of the vast majority of cases of acute
bacterial arthritis in adults and in children older than 2 years. [9] The increased incidence
of this pathogen parallels the increase in presence of prosthetic joints and in the use of
immunosuppressive agents. This pathogen is the cause in 80% of infected joints affected
by rheumatoid arthritis.

Streptococcal species, such as Streptococcus viridans, S pneumoniae, [10, 11] and group
B streptococci, [12] account for 20% of cases. Aerobic gram-negative rods are involved in
20-25% of cases. Most of these infections occur in people who are very young, who are
very old, [13] who are diabetic, who are immunosuppressed, and who abuse intravenous
drugs. [2]

Infection of the sternoclavicular and sacroiliac joints with Pseudomonas aeruginosa or

Serratia species occurs almost exclusively in persons who abuse intravenous drugs.
Persons with leukemia are predisposed to Aeromonas infections. [14]

Polymicrobial joint infections (5-10% of cases) and infection with anaerobic organisms
(5% of cases) are usually a consequence of trauma or abdominal infection. The organism
of Lyme disease (ie, Borrelia burgdorferi), a large variety of viruses (eg, human
immunodeficiency virus [HIV], lymphocytic choriomeningitis virus, hepatitis B virus, rubella
virus), mycobacteria, fungi (eg, Histoplasma species, Sporothrix schenckii, Coccidioides
immitis, Blastomyces species), and other pathogens may produce nonsuppurative joint
infection. [15]

Types of prosthetic joint infections

Three major types of prosthetic joint infections exist: (1) those that occur early, within 3
months of implantation; (2) those that are delayed, within 3-24 months of implantation;
and (3) those that occur later than 24 months following the implantation. Most cases of
early prosthetic joint infection are caused by S aureus, whereas delayed infections are
due to coagulase-negative S aureus (CoNS) and gram-negative aerobes. Both of these
types are acquired in the operating room. Late cases of prosthetic joint infection are
secondary to hematogenous spread from various infectious foci. [16]

See also Pediatric Septic Arthritis, Pediatric Septic Arthritis Surgery, and Septic Arthritis
Surgery.

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 Etiology and Pathophysiology
Organisms may invade the joint by direct inoculation, by contiguous spread from infected
periarticular tissue, or via the bloodstream (the most common route). [14]

The normal joint has several protective components. Healthy synovial cells possess
significant phagocytic activity, and synovial fluid normally has significant bactericidal
activity. Rheumatoid arthritis and systemic lupus erythematosus hamper the defensive
functions of synovial fluid and decrease chemotaxis and phagocytic function of
polymorphonuclear leukocytes. Patients with deficiencies of the terminal components of
complement are susceptible to neisserial bacteremia and joint infections.

Pathogenic invasion

Previously damaged joints, especially those damaged by rheumatoid arthritis, are the
most susceptible to infection. The synovial membranes of these joints exhibit
neovascularization and increased adhesion factors; both conditions increase the chance
of bacteremia, resulting in a joint infection. Some microorganisms have properties that
promote their tropism to the synovium. S aureus readily binds to articular sialoprotein,
fibronectin collage, elastin, hyaluronic acid, and prosthetic material via specific tissue
adhesion factors (microbial surface components recognizing adhesive matrix molecules
[MSCRAMMs]). In adults, the arteriolar anastomosis between the epiphysis and the
synovium permits the spread of osteomyelitis into the joint space.

The major consequence of bacterial invasion is damage to articular cartilage. This may be
due to the particular organism's pathologic properties, such as the chondrocyte proteases
of S aureus, as well as to the host's polymorphonuclear leukocytes response. The cells
stimulate synthesis of cytokines and other inflammatory products, resulting in the
hydrolysis of essential collagen and proteoglycans. Infection with N gonorrhoeae induces
a relatively mild influx of white blood cells (WBCs) into the joint, explaining, in part, the
minimal joint destruction observed with infection with this organism relative to destruction
associated with S aureus infection.

As the destructive process continues, pannus formation begins, and cartilage erosion
occurs at the lateral margins of the joint. Large effusions, which can occur in infections of
the hip joint, impair the blood supply and result in aseptic necrosis of bone. These
destructive processes are well advanced as early as 3 days into the course of untreated
infection.

Viral infections may cause direct invasion (rubella) or production of antigen/antibody

complexes. Such immunologic mechanisms occur in infections with hepatitis B, parvovirus
B19, and lymphocytic choriomeningitis viruses. [15]

Reactive/postexposure process

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 Reactive, or postexposure, arthritis is observed more commonly in patients with human
lymphocyte antigen B27 (HLA-B27) histocompatibility antigens. Although various
infections can cause reactive arthritis, gastrointestinal processes are by far the most
common. Gastrointestinal pathogens associated with reactive arthritis include the
following:

Salmonella enteritidis

Salmonella typhimurium

Yersinia enterocolitica

Campylobacter jejuni

Clostridium difficile

Shigella sonnei

Entamoeba histolytica

Cryptosporidium

Genitourinary infections, especially those due to Chlamydia trachomatis, are the second
most common cause of reactive arthritis. The arthritis of Lyme disease usually results
from immunologic mechanisms, with a minority of cases due to direct invasion by an
organism.

A reactive/postexposure process may occur months after the gastrointestinal or

genitourinary process has resolved.

Local infection

Prosthetic joint infections (PJIs) may be a consequence of local infection, such as

intraoperative contamination (60-80% of cases), or of bacteremias (20-40% of cases). [2]
The bacteremias may be spontaneous (ie, gingival disease) or secondary to various
manipulations. Delayed wound healing is a major factor behind early prosthetic joint
infection. Until the fascia has healed, the usual tissue barriers to infection of the implant
are not present. Eventually, the implanted hardware becomes less susceptible to infection
by hematogenous spread, because the pseudocapsule develops around it.

The biofilm of coagulase-negative S aureus (CoNS) protects the pathogen from the host's
defenses, as well as from various antibiotics. Polymethylmethacrylate cement inhibits
WBC and complement function.

Overall, the most common organisms of prosthetic joint infections are CoNS (22% of
cases) and S aureus (22% of cases). Enteric gram-negative organisms account for 25%

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 of isolates. [17] Streptococci, including S viridans, enterococci, and the beta-hemolytic
streptococci, cause 21% of cases. Anaerobes are isolated from 10% of patients.

Other distinctive host and/or situation-pathogen associations have been described,

including Pasteurella multocida, Capnocytophaga species (dog and cat bites), Eikenella
corrodens, anaerobes (especially Fusobacterium nucleatum and streptococcal species
[human bites]), Aeromonas hydrophila (myelogenous leukemia), P aeruginosa, Serratia
species, Candida species (particularly common in persons who abuse intravenous drugs),
Mycobacterium marinum (water exposure), S schenckii (gardening), and S pneumoniae
(sickle cell anemia).

Unlike osteomyelitis, Salmonella species are not associated with the septic arthritis of
sickle cell anemia. Ten to 30% of patients with brucellosis have lumbosacral spine
involvement.

Prognosis
The primary morbidity of septic arthritis is significant dysfunction of the joint, even if
treated properly. Fifty percent of adults with septic arthritis have significant sequelae of
decreased range of motion or chronic pain after infection. [1] Thirty percent of cases of
reactive arthritis may become chronic. Complications include dysfunctional joints,
osteomyelitis, and sepsis.

Predictors of poor outcome in suppurative arthritis include the following:

Age older than 60 years

Infection of the hip or shoulder joints

Underlying rheumatoid arthritis

Positive findings on synovial fluid cultures after 7 days of appropriate therapy

Delay of 7 days or longer in instituting therapy

The mortality rate depends primarily on the causative organism. N gonorrhoeae septic
arthritis carries an extremely low mortality rate, whereas that of S aureus can approach
50%. [18] S aureus is the most common cause of septic arthritis in all age groups. Among
those aged 15-50 years, N gonorrhea runs a close second, especially among those who
are sexually active.

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 Clinical Presentation

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