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Figure 1: The knee joint is asynovial joint and a common

site of infective arthritis [2]

Figure 2: Common causative

agents of infective arthritis.

Adapted from [2]

Infective arthritis

From eMedWiki

nfective arthritis describes joint infections caused by microorganisms [1]. Jointnfection is serious as it can cause rapid destruction of articular cartilage, loss

of joint function, and diagnostic and management problems in existing

heumatoid arthritis [3][4].

Contents

1 Classification & Aetiology2 Pathophysiology3 Risk Factors4 Clinical Manifestations

4.1 Bacterial Infections4.2 Mycobacterial/Fungal Arthritis4.3 Viral Arthritis

5Diagnosis6Treatment7Infective Arthritis & Ageing8References

Classification& Aetiologynfective arthritis can be caused either by direct infection of a joint space (suppurative arthritis) or immune

esponses to systemic infections (non-suppurative arthritis) by various microorganisms shown in Figure 2 [2]

AlthoughNeisseria gonorrhoeaeremains the most common pathogen(75% of

ases) among younger sexually active individuals, Staph. aureusinfection is

he main cause of bacterial arthritis in adults and in children older than 2 years

65%) [5]. Staph. aureusis 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

mmunocompromised patients than in young adults [6].

While viral and fungal joint infections are rare, there have been increasing cases of Candidainfections causi

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

usually the result of perioperative wound contamination, joint infections that begin later than three months af

he joint implant are haematogenously acquired. Staph. aureusand Streptococciare the most common causat

agents in late-onset prosthetic joint infections [2].

Pathophysiology

Bacterial arthritis is usually spread haematogenously but may also be introduced by direct inoculation during

oint surgery or, rarely, during joint aspiration. Also, in children, osteomyelitis may spread to adjacent joints

The bacteria enter the closed joint space and within hours, trigger an influx of inflammatory cells. Release of

ytokines 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 jointa complication of haematogenously disseminated fungi of the Candidafamily 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 afte

he virus is cleared [10].

Risk Factors

Host factors that predispose to infective arthritis include age, decreased immunocompetence seen in such

onditions 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 revisio

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 join

n 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

evers. Both passive and active range of motion are limited and cause discomfort.
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Figure 3: MRI of staphylococcal infective arthriti

of left hip, with arrows indicating fluid collection

[15]

A minority of patients (28%) with gonococcal infection will present with a single purulent joint effusion, and

nflammation or tenderness of multiple tendons of the wrist, ankles, and small joints [12]. Accompanying skin

esions 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 diagnosiswithin the first week, andindolent 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

ommon viral agent and presents as a symmetric polyarticular arthritis [14].

Diagnosis

Diagnosis of infective arthritis requires the identification of

he microorganism present in the synovial fluid. If synovial

luid cannot be obtained with closed needle aspiration, a

econd attempt with imaging guidance is used for less

accessible joints such as the shoulders and sacroiliac joints

6]

.

n 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

uggestive of infective arthritis. Although these values alone

do not definitively diagnose for infective arthritis, the

measurements are useful in monitoring response to

reatment [16]. Bacterial infections are determined by Gram

tain or by synovial fluid culture, which is positive in 90%

of cases of non-gonococcal bacterial arthritis. Gram stainsare 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 posit

n 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 gonorrhoeaefrom a genitourinary source [2].
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Figure 4: Needle aspiration of knee joint.

Arthrocentesis, the draining of synovial fluid, is a

similar looking procedure [17].

dentification of microbial DNA by PCR will be most useful in patients with partly treated or culture-negativ

bacterial arthritis and in non-suppurative arthritis.

n 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 arthrit

and osteoarthritis [15].

Treatment

The treatment of acute infective arthritis requires antibioand joint drainage. The initial choice of antibiotics shouldbe based on the synovial fluid Gram stain as well as the aand risk factors of the patient. Empirical therapy usuallyincludes broad-spectrum parenteral antibiotics againstStaph. aureusand Streptococcidue to their high causativrates and therapy is then modified based on the culture an

sensitivity of the synovial fluid or blood culture [18].

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

better irrigation and visualisation. If joint drainage canno

be maintained by needle aspiration or arthroscopy, open

surgical drainage is recommended [19].

n prosthetic joint infections, bacteria attach to the prosthetic material and form a biofilm of exopolysacchari

hat protects against host phagocytes and thus contributes to antibiotic resistance. Therefore, treatment of

nfection 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 b

differential diagnoses for the presenting symptoms of infective arthritis. Therefore, infective arthritis remains

oncern 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. !2.002.012.022.032.042.052.062.072.082.092.10Goldenburg DL. (1998). "Septic Arthritis". The Lance

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. !6.06.16.2Mathews CJ, Kingsley G, Field M, Jones A, Weston VC, Phillips M, Walker D, and Coakl

G. (2007). "Management of Septic Arthritis: A Systematic Review".Annals of the Rheumatic Disease66: 440-445.

7. !7.07.17.2Cuella 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 ofInfectious Diseases, 1332-1337

9. !Kaandorp CJ, Dinant HJ, van de Laar MA, Moens HJ, Prins AP, and Dijkmans BA.(1997). "Inciden

and sources of native and prosthetic joint infection: a community based prospective survey".Annals ofthe 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 Interna

Medicine 139:1125-113013. !Bardin T. (2003). "Gonococcal arthritis".Best Practice and Research Clinical Rheumatology 17:201

20814. !Woolf AD, Campion GV, and Chishick A. (1989). "Clinical manifestations of human parvovirus B1

in adults".Archives of Internal Medicine, 149:1153-6.

15. !15.015.1Mathews CJ, Weston VC, Jones A, Field M, and Coakley G. (2010). "Bacterial Septic Arthr

in Adults". The Lancet, 375:846-85516. !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: 27628017. !McNeill P. (2011). "Arthritis 1 - Rheumatoid Arthritis [Lecture Notes]. Sydney, Australia: Universit

of New South Wales.18. !Siva C, Velazquez C, Mody A, and Brasington R. (2003). "Diagnosing acute monoarthritis in adults

practical approach for the family physician".American Family Physician, 68:83-9019. !Ohl C. (2005). "Infectious arthritis of native joints". Principles and Practice of Infectious Diseases,

1311-132220. !Australian Institute of Health and Welfare (AIHW). (2010). "A snapshot of Arthritis in Australia 20

Arthritis series no. 13. Cat. no. PHE 126. Canberra: AIHW.
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