Acute Infectious Arthritis

1. 1. Mathews CJ, Weston VC, Jones A, Field M, Coakley G. Bacterial septic arthritis in adults. Lancet. 2010;375(9717):846-855. doi:10.1016/S0140-6736(09)61595-6

2. 2. Maneiro JR, Souto A, Cervantes EC, Mera A, Carmona L, Gomez-Reino JJ. Predictors of treatment failure and mortality in native septic arthritis. Clin Rheumatol. 2015;34(11):1961-1967. doi:10.1007/s10067-014-2844-3

3. 3. Ross JJ: Septic arthritis of native joints. Infect Dis Clin North Am. 31(2): 203−218, 2017. Epub 2017 Mar 30. doi: 10.1016/j.idc.2017.01.001

4. 4. Kim HW, Han M, Jung I, Ahn SS. Incidence of septic arthritis in patients with ankylosing spondylitis and seropositive rheumatoid arthritis following TNF inhibitor therapy. Rheumatology (Oxford). 2023;62(8):2740-2747. doi:10.1093/rheumatology/keac721

5. 5. Galloway JB, Hyrich KL, Mercer LK, et al. Risk of septic arthritis in patients with rheumatoid arthritis and the effect of anti-TNF therapy: results from the British Society for Rheumatology Biologics Register. Ann Rheum Dis. 2011;70(10):1810-1814. doi:10.1136/ard.2011.152769

6. 6. Gouveia C, Duarte M, Norte S, et al. Kingella kingae Displaced S. aureus as the Most Common Cause of Acute Septic Arthritis in Children of All Ages. Pediatr Infect Dis J. 2021;40(7):623-627. doi:10.1097/INF.0000000000003105

7. 7. Yagupsky P. Use of blood culture vials and nucleic acid amplification for the diagnosis of pediatric septic arthritis. Clin Infect Dis. 2008;46(10):1631-1632. doi:10.1086/587754

Gonococcal arthritis can cause a distinctive dermatitis-polyarthritis-tenosynovitis syndrome.

Classic manifestations are (5)

• Fever (for 5 to 7 days)

• Multiple skin lesions (petechiae, papules, pustules, hemorrhagic vesicles or bullae, necrotic lesions) on mucosal surfaces and on the skin of the trunk, hands, or lower extremities; however, genital lesions are often absent

• Absence of genital symptoms

• Migratory arthralgias, arthritis, and tenosynovitis (often involves multiple tendons), most often in the small joints of the hands, wrists, elbows, knees, and ankles, and rarely the axial skeletal joints

• Monarthritis or oligoarthritis affecting a knee, ankles, wrists, or elbows (5)

Disseminated Gonococcal Infection (Skin Lesions)

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Image courtesy of Dr. S. E. Thompson and J. Pledger via the Public Health Image Library of the Centers for Disease Control and Prevention.

Symptoms of the original mucosal infection (eg, urethritis, cervicitis) may not be present.

Nongonococcal bacterial arthritis causes progressive moderate to severe joint pain that is markedly worsened by movement or palpation (1). Most infected joints are swollen, erythematous, and warm. Fever is present in most, but not all, cases. Virulent organisms (eg, S. aureus, Pseudomonas aeruginosa) generally cause a more fulminant arthritis, whereas less virulent organisms (eg, coagulase-negative staphylococci, Propionibacterium acnes) cause a less fulminant arthritis.

In 80% of adults, nongonococcal bacterial arthritis is monoarticular and usually occurs in a peripheral joint: knee, hip, shoulder, wrist, ankle, or elbow. In children, ≥ 90% of cases are monoarticular, mostly involving the knee, hip, and ankle (6).

Polyarticular involvement is somewhat more common among patients who are immunosuppressed, who have an underlying chronic arthritis (eg, rheumatoid arthritis, osteoarthritis), or who have a streptococcal or staphylococcal infection (especially beta-hemolytic streptococcus or S. aureus). In people who use injection drugs and patients with indwelling vascular catheters, axial joints (eg, sternoclavicular, costochondral, hip, shoulder, vertebral, symphysis pubis, sacroiliac) are often involved (7). H. influenza may cause a dermatitis-arthritis syndrome similar to gonococcal infection.

Infection due to human, dog, or cat bites (see Human and Mammal Bites) usually develops within 48 hours. Interpretation of the physical examination is often complicated by the presence of traumatic injury as well as infection.

Rat bites cause systemic symptoms such as fever, rash, and joint pain or true arthritis with regional adenopathy within approximately 2 to 10 days (8).

Viral infectious arthritis sometimes causes symptoms similar to acute nongonococcal bacterial arthritis and is more likely to be polyarticular than bacterial arthritis (9).

Patients with B. burgdorferi arthritis may have other symptoms of Lyme disease or present only with acute monarthritis or oligoarthritis, which, if untreated, may resolve spontaneously after a few weeks to months but then recur (10). Lyme arthritis most often involves the knee and large joints and typically presents without fever. Chronic pain that remains after appropriate antibiotic therapy is likely to be of noninfectious etiology.

A polyarticular rheumatoid arthritis–like syndrome is distinctly unusual and more likely to be from another diagnosis.

Synovial fluid examination is the cornerstone of diagnosis of acute joint infection (1). Fluid is examined grossly and sent for cell count and differential, Gram stain, aerobic and anaerobic culture, and crystal analysis. Foul-smelling synovial fluid suggests anaerobic infection. Fluid from an acutely infected joint usually reveals a white blood cell (WBC) count > 50,000 cells/mcL (50 × 10⁹/L) (sometimes > 100,000 cells/mcL [100 × 10⁹/L ]) consisting of > 95% polymorphonuclear leukocytes (2). WBC counts tend to be higher in nongonococcal bacterial than in gonococcal infectious arthritis. WBC counts may also be lower in early or partially treated infections; therefore, a white cell count < 50,000 cells/mcL does not exclude infectious arthritis (3,4).

Gram stain reveals organisms in only 50 to 75% of joints with acute bacterial arthritis, most often staphylococci. A positive Gram stain is suggestive (5), but false positive results occur. Cultures are definitive, but are limited in the presence of prior antibiotic use (6).

Inoculation of synovial fluid into aerobic blood culture bottles can improve detection of Kingella kingae (7).

The presence of crystals does not exclude coexisting infectious arthritis. Initial synovial fluid analysis cannot differentiate between infectious and other inflammatory synovial fluid (8). There is significant overlap between the synovial cell counts in fluids from patients with gout, calcium pyrophosphate crystal–associated arthritis, and infection. If differentiation is impossible by clinical means or synovial fluid examination, infectious arthritis should be assumed and treated, pending culture results.

Blood tests, such as blood cultures, complete blood count, and erythrocyte sedimentation rate (or C-reactive protein), are usually obtained. However, normal results do not exclude infection. WBC count, erythrocyte sedimentation rate, or C-reactive protein may be increased in noninfectious joint inflammation (including gout) as well as infectious joint inflammation (4). The serum urate level should not be used to diagnose or exclude gout as the cause of the arthritis, because the level can be normal or even low in gout, and may be high, although unrelated to gout, in patients with an acute bacterial infection (8).

Molecular testing (eg, polymerase chain reaction) may be used to directly detect organisms in clinical specimens. Gonococci may be detected outside of the infected joint with nucleic acid amplification testing (NAAT) of specimens from the cervix, urethra, oropharynx, or rectum (9). The approach to diagnosing gonococcal arthritis is discussed in more detail below. Some difficult-to-cultivate organisms, such as Mycobacterium tuberculosis and Tropheryma whipplei, may be directly detected in synovial fluid using polymerase chain reaction (PCR). Metagenomic next-generation sequencing (mNGS) may also be used as a tool for pathogen identification in difficult cases. mNGS has higher sensitivity compared with microbial culture and may be a useful diagnostic tool to test for pathogens in patients treated with antibiotics (10).

Radiographs of the involved joint are not diagnostic of acute infection but can exclude other conditions sometimes under consideration (eg, fractures). Abnormalities in early acute bacterial arthritis are limited to soft-tissue swelling and signs of synovial effusions (11). After 10 to 14 days of untreated bacterial infection, destructive changes of joint space narrowing (reflecting cartilage destruction) and erosions or foci of subchondral osteomyelitis may appear. Gas visible within the joints suggests infection with Escherichia coli or anaerobes.

MRI of Gonococcal Arthritis in the Wrist

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© Springer Science+Business Media

MRI is considered if the joint is not easily accessible for examination and aspiration (eg, an axial joint). MRI or ultrasound can identify sites of effusion or abscess that can be aspirated or drained for both diagnosis and therapy (12). MRI can provide early suggestion of associated osteomyelitis (13). Bone scans using technetium-99m can be falsely negative in infectious arthritis. Also, because they show increased uptake with increased blood flow in inflamed synovial membranes and in metabolically active bone, they can be falsely positive in noninfectious inflammatory arthritis such as gout. Nuclear imaging and MRI do not distinguish infection from crystal-induced arthritis (11).

If gonococcal arthritis is suspected, blood and synovial fluid samples should be immediately plated on nonselective chocolate agar. Specimens should also be collected from the urethra, endocervix, rectum, and pharynx and be plated on selective Thayer-Martin medium. Genital, rectal, and oral cultures or NAAT testing is also recommended. Blood cultures may be positive during the first week and may assist in microbiologic diagnosis.

Synovial fluid cultures from joints with frank purulent arthritis may be positive, and fluid from skin lesions may also be positive. PCR testing from the synovial fluid should be completed because PCR may be positive in patients whose synovial fluid cultures are negative (9). If disseminated gonococcal infection is suspected based on clinical criteria, it is assumed to be present even if all gonococcal cultures are negative. Clinical response to antibiotics (anticipated within 5 to 7 days) can strongly support the diagnosis of gonorrhea.

Initial antibiotic selection is directed at the most likely pathogens (1). The regimen is adjusted based on the results of culture and susceptibility testing.

Gonococcal arthritis is treated with

Chlamydia trachomatis2).

If nongonococcal gram-positive infection is suspected by Gram stain in an adult, or if no organisms are seen, initial treatment is with

Because methicillin resistance is common in community-acquired S. aureus, for patients with gram-positive cocci in clusters on Gram stain or a negative Gram stain when S. aureusS. aureus3).

If gram-negative infection3).

NeonatesS. aureusK. kingae infection) (1).

Children > 48 months of age should be treated with empiric therapy to cover S. aureus. The need for coverage against community-acquired methicillin-resistant Staphylococcus aureus (MRSA) is based on local susceptibility data (1).

Parenteral antibiotics are continued until clinical improvement is clear, and oral antibiotics should be given at high doses for another 2 to 4 weeks according to the clinical response. Children with rapid clinical improvement with no evidence of osteomyelitis may be treated with a course of therapy as short as 10-14 days. For those with a slower clinical response, inadequate source control, or ongoing signs of infection (eg, elevated C-reactive protein) a 21-28 day course of therapy is preferred (1).

Infections caused by streptococci and Haemophilus are usually eradicated after 2 weeks of oral antibiotics after IV treatment.

Staphylococcal infections and other routine bacterial pathogens are treated with antibiotics for at least 3 weeks and often 4 weeks or longer, especially in patients with prior arthritis in the affected joint, with immunosuppression, or whose diagnosis was delayed.

In addition to antibiotics, acute nongonococcal bacterial arthritis requires large-bore needle aspiration of intra-articular fluid at least once a day, or tidal irrigation lavage, arthroscopic lavage, or arthrotomy for debridement. Patients with rheumatoid arthritis receiving immunosuppressive therapy or those with a delayed diagnosis should generally undergo early and aggressive surgical debridement and drainage. Arthroscopic wash out and open arthrotomy are commonly used as surgical interventions with similar efficacy. Arthroscopy seems to be preferable because it has a lower all-cause complication rate (4, 5).

For gonococcal arthritis with persistent effusion, infected fluid is aspirated and drainage may need to be repeated as necessary.

Acute bacterial arthritis requires joint splinting for the first few days to reduce pain, followed by passive and active range-of-motion exercises to limit contractures, with muscle strengthening as soon as it can be tolerated. nonsteroidal anti-inflammatory drugs (NSAIDs) can help decrease pain and inflammation once a diagnosis is confirmed (5). Intra-articular corticosteroids should be avoided during the acute infection. Because bacteriologic tests may be falsely negative, potent anti-inflammatory therapy should generally be avoided until a bacterial source has been definitively excluded. Opioids can be used for pain control.

1. 1. Woods CR, Bradley JS, Chatterjee A, et al. Clinical Practice Guideline by the Pediatric Infectious Diseases Society (PIDS) and the Infectious Diseases Society of America (IDSA): 2023 Guideline on Diagnosis and Management of Acute Bacterial Arthritis in Pediatrics [published correction appears in J Pediatric Infect Dis Soc. 2024 Aug 24;13(8):443. doi: 10.1093/jpids/piae065]. J Pediatric Infect Dis Soc. 2024;13(1):1-59. doi:10.1093/jpids/piad089

2. 2. Workowski KA, Bachmann LH, Chan PA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep. 2021;70(4):1-187. Published 2021 Jul 23. doi:10.15585/mmwr.rr7004a1

3. 3. Ohl, CA. Infectious Arthritis of Native Joints. In: Bennett JE, Dolin R, Blaser, MJ. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. Elsevier; 2019:103.

4. 4. McKenna DP, Miller P, McAleese T, Cleary M. Arthroscopy or arthrotomy for native knee septic arthritis: A systematic review. J Exp Orthop. 2024;11(3):e12041. Published 2024 Jun 6. doi:10.1002/jeo2.12041

5. 5. Donatto KC. Orthopedic management of septic arthritis. Rheum Dis Clin North Am. 1998;24(2):275-286. doi:10.1016/s0889-857x(05)70009-0

1. 1. Gardner GC, Weisman MH. Pyarthrosis in patients with rheumatoid arthritis: a report of 13 cases and a review of the literature from the past 40 years. Am J Med. 1990;88(5):503-511. doi:10.1016/0002-9343(90)90430-l