Infective arthritis - eMedWiki

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Infective arthritis
From eMedWiki
Infective arthritis describes joint infections caused by microorganisms [1]. Joint
infection is serious as it can cause rapid destruction of articular cartilage, loss
of joint function, and diagnostic and management problems in existing
rheumatoid arthritis [3] [4].

Contents
1 Classification & Aetiology
2 Pathophysiology
3 Risk Factors
4 Clinical Manifestations
4.1 Bacterial Infections
4.2 Mycobacterial/Fungal Arthritis
4.3 Viral Arthritis
5 Diagnosis
6 Treatment
7 Infective Arthritis & Ageing
8 References

Figure 1: The knee joint is a

synovial joint and a common
site of infective arthritis [2]

Classification & Aetiology

Infective arthritis can be caused either by direct infection of a joint space (suppurative arthritis) or immune
responses to systemic infections (non-suppurative arthritis) by various microorganisms shown in Figure 2 [2].
Although Neisseria gonorrhoeae remains the most common pathogen (75% of
cases) among younger sexually active individuals, Staph. aureus infection is
the main cause of bacterial arthritis in adults and in children older than 2 years
(65%) [5]. Staph. aureus is also the primary pathogen in hip infections and in
polyarticular septic arthritis [2].
Haemophilus influenzae, a gram negative bacilli predominates in children
under 2 years and other gram negative organisms are more common in older or
immunocompromised patients than in young adults

[6].

Figure 2: Common causative

agents of infective arthritis.
Adapted from [2]

While viral and fungal joint infections are rare, there have been increasing cases of Candida infections causing
arthritis in both native and prosthetic joints [7].
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The rate of infection ranges from 05% to 2% for hip and knee replacements [8]. While early-onset infections are
usually the result of perioperative wound contamination, joint infections that begin later than three months after
the joint implant are haematogenously acquired. Staph. aureus and Streptococci are the most common causative
agents in late-onset prosthetic joint infections [2].

Pathophysiology
Bacterial arthritis is usually spread haematogenously but may also be introduced by direct inoculation during
joint surgery or, rarely, during joint aspiration. Also, in children, osteomyelitis may spread to adjacent joints [9].
The bacteria enter the closed joint space and within hours, trigger an influx of inflammatory cells. Release of
cytokines and proteases leads to cartilage degradation and irreversible subchondral bone loss within days [2].
Similarly, fungal arthritis can be caused by:
direct intra-articular inoculation of fungi that inhabit the skin, causing infection in a single joint
a complication of haematogenously disseminated fungi of the Candida family that also results in
monoarthritis or pauciarthritis [7]
Viral arthritis is a result of the body's immune responses to systemic infection and the resultant presence of
proinflammatory and anti-inflammatory cytokines is what causes inflammation and joint deformity even after
the virus is cleared [10].

Risk Factors
Host factors that predispose to infective arthritis include age, decreased immunocompetence seen in such
conditions as HIV AIDS, preexisting joint disease including osteoarthritis and rheumatoid arthritis, diabetes
mellitus and intravenous drug use [2][6]. The most important risk factor for prosthetic joint infection is revision
arthroplasty in which the joint is surgically refashioned. This carries a 510% risk of infection [2].

Clinical Manifestations
The knee is the site of infection in most cases of infective arthritis and hip infections are more common in
young children [11]. Furthermore, 1020% of infections are polyarticular, usually involving two or three joints.
In 50% of cases, the source of infection can be found to stem from the skin, lungs or bladder.

Bacterial Infections
Non-gonococcal infective arthritis usually presents with the acute onset of a single hot, swollen, and very
painful joint. Most patients are febrile, and young children in particular may present with chills and spiking
fevers. Both passive and active range of motion are limited and cause discomfort.

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A minority of patients (28%) with gonococcal infection will present with a single purulent joint effusion, and
inflammation or tenderness of multiple tendons of the wrist, ankles, and small joints [12]. Accompanying skin
lesions are typically painless and pustular, and found predominantly on fingers, hands, wrists and feet [13].

Mycobacterial/Fungal Arthritis
Two distinct clinical presentations can be observed with fungal arthritis:
acute onset of synovial symptoms (about two thirds of patients) with an established diagnosis
within the first week, and
indolent presentation, with mild systemic and arthritic symptoms, and delay in diagnosis for
months or years [7]

Viral Arthritis
Viral arthritis is associated with systemic symptoms such as fever, and rash. Parvovirus B19 is the most
common viral agent and presents as a symmetric polyarticular arthritis [14].

Diagnosis
Diagnosis of infective arthritis requires the identification of
the microorganism present in the synovial fluid. If synovial
fluid cannot be obtained with closed needle aspiration, a
second attempt with imaging guidance is used for less
accessible joints such as the shoulders and sacroiliac joints
[6].

In a blood sample, elevated erythrocyte sedimentation rates,

C-reactive protein concentrations or white cell counts
(>500000 per mm3) reflect an acute-phase response, and are
suggestive of infective arthritis. Although these values alone
do not definitively diagnose for infective arthritis, the
measurements are useful in monitoring response to
treatment [16]. Bacterial infections are determined by Gram
Figure 3: MRI of staphylococcal infective arthritis
stain or by synovial fluid culture, which is positive in 90%
of left hip, with arrows indicating fluid collection
of cases of non-gonococcal bacterial arthritis. Gram stains
[15]
are positive in only 50% as clumps of stain or cellular debris
may be mistaken for bacteria. Blood cultures are positive in
5070% of patients with non-gonococcal bacterial arthritis. In contrast, the synovial fluid Gram stain is positive
in less than 25% of patients with gonococcal arthritis, and culture is positive in only 50%. A diagnosis of
gonococcal infection is often made based on the patient history and examination, and a identification of
Neisseria gonorrhoeae from a genitourinary source [2].
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Identification of microbial DNA by PCR will be most useful in patients with partly treated or culture-negative
bacterial arthritis and in non-suppurative arthritis.
In acute infective arthritis, radiographs are only used to detect joint effusion and to demonstrate concurrent
osteomyelitis or arthritis. Computed tomography is used to detect effusions and as a guide in joint aspiration
while scintigraphy and magnetic resonance imaging (MRI) allow for differentiation between infective arthritis
and osteoarthritis [15].

Treatment
The treatment of acute infective arthritis requires antibiotics
and joint drainage. The initial choice of antibiotics should
be based on the synovial fluid Gram stain as well as the age
and risk factors of the patient. Empirical therapy usually
includes broad-spectrum parenteral antibiotics against
Staph. aureus and Streptococci due to their high causative
rates and therapy is then modified based on the culture and
sensitivity of the synovial fluid or blood culture [18].

Figure 4: Needle aspiration of knee joint.

Arthrocentesis, the draining of synovial fluid, is a
similar looking procedure [17].

Daily draining of infected joints may be necessary in

beginning stages of treatment, with arthroscopy being the
preferred method in knee or shoulder infections because of
better irrigation and visualisation. If joint drainage cannot
be maintained by needle aspiration or arthroscopy, open
surgical drainage is recommended [19].

In prosthetic joint infections, bacteria attach to the prosthetic material and form a biofilm of exopolysaccharide
that protects against host phagocytes and thus contributes to antibiotic resistance. Therefore, treatment of
infection in prosthetic joints usually requires the surgical removal of all bioprosthetic components. High-risk
patients or those refusing replacement arthroplasty have been successfully treated with longterm suppressive
antimicrobial therapy [2].

Infective Arthritis & Ageing

Osteoarthritis and rheumatoid arthritis are the focus in Ageing & Endings A, being more common in ageing
populations, affecting an estimated 1.6 million and 428,000 Australians respectively [20]. However,
osteoarthritis and rheumatoid arthritis are risk factors for the development of infective arthritis, but can also be
differential diagnoses for the presenting symptoms of infective arthritis. Therefore, infective arthritis remains a
concern because of its rapid progression and fatal consequences if left undetected or untreated [2].

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References
1. L. Eder, D. Zisman, M. Rozenbaum, and I. Rosner. (2005). "Clinical features and aetiology of septic
arthritis in northern Israel", Rheumatology 44(12):1559-1563
2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 Goldenburg DL. (1998). "Septic Arthritis". The Lancet,
351:197-202.
3. Russell AS & Ansell BM. (1972). "Septic Arthritis". Annals of the Rheumatic Diseases 31:40-44.
4. Kumar, V., Abbas, A., Fausto, N., & Mitchell, R. (2007). Robbins Basic Pathology (8th ed.).
Philadelphia: Saunders Elsevier.
5. Ross JJ, Saltzman CL, Carling P, and Shapiro DS. (2003). "Pneumococcal septic arthritis: review of
190 cases". Clinical Infectious Diseases 36:319-327
6. 6.0 6.1 6.2 Mathews CJ, Kingsley G, Field M, Jones A, Weston VC, Phillips M, Walker D, and Coakley
G. (2007). "Management of Septic Arthritis: A Systematic Review". Annals of the Rheumatic Diseases,
66: 440-445.
7. 7.0 7.1 7.2 Cuella ML, Silveira LH, and Espinoza LR. (1992). "Fungal Arthritis". Annals of the
Rheumatic Diseases, 51: 690-697.
8. Brause B. (2005). "Infections with prostheses in bones and joints". Principles and Practices of
Infectious Diseases, 1332-1337
9. Kaandorp CJ, Dinant HJ, van de Laar MA, Moens HJ, Prins AP, and Dijkmans BA.(1997). "Incidence
and sources of native and prosthetic joint infection: a community based prospective survey". Annals of
the Rheumatic Diseases, 56:470-475
10. Reimold, A. (2010). "Viruses and Arthritis: New Challenges in Diagnosis, Therapy, and
Immunization". American Journal of Medical Science, 339(6):549556.
11. Goldenburg DL. (1998). "Infectious Arthritis Complicating Rheumatoid Arthritis and Other Chronic
Rheumatic Disorders". Arthritis and Rheumatism, 32(4):496-502.
12. Sharp JT, Lidsky MD, Duffy J, and Duncan MW. (1979). "Infectious Arthritis". Archives of Internal
Medicine 139:1125-1130
13. Bardin T. (2003). "Gonococcal arthritis". Best Practice and Research Clinical Rheumatology 17:201208
14. Woolf AD, Campion GV, and Chishick A. (1989). "Clinical manifestations of human parvovirus B19
in adults". Archives of Internal Medicine, 149:1153-6.
15. 15.0 15.1 Mathews CJ, Weston VC, Jones A, Field M, and Coakley G. (2010). "Bacterial Septic Arthritis
in Adults". The Lancet, 375:846-855
16. Li SF, Henderson J, Dickman E, and Darzynkiewicz R. (2004). "Laboratory tests in adults with
monoarticular arthritis: can they rule out a septic joint?". Academic Emergency Medicine, 11: 276280
17. McNeill P. (2011). "Arthritis 1 - Rheumatoid Arthritis [Lecture Notes]. Sydney, Australia: University
of New South Wales.
18. Siva C, Velazquez C, Mody A, and Brasington R. (2003). "Diagnosing acute monoarthritis in adults: a
practical approach for the family physician". American Family Physician, 68:83-90
19. Ohl C. (2005). "Infectious arthritis of native joints". Principles and Practice of Infectious Diseases,
1311-1322
20. Australian Institute of Health and Welfare (AIHW). (2010). "A snapshot of Arthritis in Australia 2010".
Arthritis series no. 13. Cat. no. PHE 126. Canberra: AIHW.

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