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Tubercular monoarthritis of the glenohumeral joint in a non-endemic region: Vancouver, Canada
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  1. Tyler Murray
  1. Department of Internal Medicine, The University of British Columbia Faculty of Medicine, Vancouver, British Columbia, Canada
  1. Correspondence to Dr Tyler Murray; t.murray{at}mail.utoronto.ca

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Description

A previously healthy 24-year-old man presented to an emergency department in Vancouver, Canada with a 4-month history of atraumatic, chronic progressive, monoarticular right shoulder pain. Physical examination revealed restricted abduction, external rotation at the shoulder with moderate deltoid and bicep muscle wasting. On review of systems, the only associated symptom was 5 kg of unintentional weight loss despite a preserved appetite. He had no recurrent fevers, night sweats, lymphadenopathy or respiratory symptoms. He was not started empirically on antimicrobial therapy on admission due to a lack of septic clinical features.

The initial musculoskeletal ultrasound showed severe tenosynovitis, glenohumeral joint erosions with a small effusion not amenable to bedside arthrocentesis. Laboratory investigations showed a modest neutrophilic leukocytosis and mildly elevated C-reactive protein (CRP) of 26, a negative rheumatoid factor, anti-citrullinated protein antibody (anti-CCP) and anti-nuclear antibody (ANA) panel. A chest X-ray was normal with no evidence of granulomatous disease. The infectious disease and rheumatology services were consulted. The provisional diagnosis at this stage, given local epidemiology and joint erosions on ultrasound was monoarticular rheumatoid arthritis.

An interventional radiology-guided arthrocentesis and biopsy of the glenoid articular cartilage were completed; the initial bacterial cultures, acid-fast bacilli smear, cytology and crystal microscopy were negative. The polymorphonuclear cell count was minimal. The subsequent musculoskeletal MRI showed an interosseous abscess with infarct of the humeral head, suspicious of chronic infection without malignant features (figures 1 and 2). The articular cartilage biopsy was then sent for tuberculosis (TB)-PCR that resulted positive for Mycobacterium tuberculosis after several days, to confirm the diagnosis of this unusual monarthritis case.1 Orthopaedics surgery was consulted; the preference was medical treatment with antimicrobial therapy prior to surgical intervention. The patient was started initially on rifampin, isoniazid, pyrazidamide and ethambutol due to antimicrobial resistance rates and planned 9 months of treatment. He was discharged from the hospital with infectious disease follow-up.

Figure 1

Right shoulder MRI T1 signal sagittal view illustrating interosseous abscess and cortical infarct of the humeral head.

Figure 2

Right shoulder MRI T2 signal sagittal view illustrating interosseous abscess and cortical infarct of the humeral head.

Early diagnosis in septic arthritis is crucial for the preservation of joint function, sepsis treatment and mortality.2 Coexistence of gout and septic arthritis is common, therefore prompt treatment with empiric antibiotics is often warranted until the definitive diagnosis is made. Physical examination and history alone are often not sufficient to make the diagnosis.3 Useful differentiating diagnostic tests include radiographs of the affected and contralateral joint, synovial fluid analysis for culture, gram stain, crystals, gross appearance and cell count. An initial positive response to empiric treatment in gout or bacterial septic arthritis cases can be diagnostic. Serum inflammatory markers such as erythrocyte sedimentation rate (ESR) and CRP are not helpful.4 Synovial fluid smear sensitivity for acid-fast bacilli in cases of tubercular arthritis is low (20%–40%).5 A synovial biopsy was required for the diagnosis of single TB in the literature case studies identified as was required in our case.

The early diagnosis and treatment in the emergency department of acute septic arthritis is crucial to prevent sepsis, joint destruction, the need for surgical intervention and death. Coexistence of acute gout and septic arthritis is common, which often warrants empiric antibiotic coverage until the definitive diagnosis is made. Physical examination and history are often not enough to make the diagnosis.3 Useful diagnostic tests include radiographs of affected and contralateral joint, synovial fluid analysis for culture, gram stain, crystals and cell count.2–7 Gout and bacterial septic arthritis response to initial treatment can be diagnostic.2 3 Serum inflammatory markers such as ESR and CRP are non-specific and not helpful differentiators.4 Synovial fluid smear sensitivity for acid-fast bacilli in true cases of tubercular arthritis is low (20%–40%),5 requiring a high index of suspicion and usually a synovial tissue biopsy for diagnosis. The synovial biopsy should be cultured and in capable laboratories, sent for TB-PCR as was required in our case to confirm the diagnosis.

The prevalence of monarthritis diagnoses in a sample of studies conducted in Canada and USA are listed here in descending order from the most common: undetermined (16%–36%), gout (15%–27%), septic arthritis (8%–27%), osteoarthritis (5%–17%), rheumatoid arthritis (11%–16%), trauma (11%), lupus (7%), psoriatic arthritis (5%), reactive arthritis (5%), pseudogout (3%), spontaneous haemarthrosis (3%), aseptic necrosis (2%) and TB (2%, one case in one study).3–8 Approximately 10% of extrapulmonary TB (1%–3% of total TB cases) affect the joints and bones, with the most common manifestation site being the spine; if peripheral joints are involved, it is typically a monarthritis of the knee or hip (85%), load-bearing joints.5 9 10 It is rare to see the upper extremity joints involved. Very occasionally, the TB arthritis is oligoarticular causing diagnostic confusion with other inflammatory arthritis.5 10

The differential diagnosis of acute monarthritis in a TB endemic region, such as India for example, is similar to North America with septic arthritis and gout being the most common diagnoses.5 8 11 However, in subacute or chronic monarthritis, the most common causes are TB, fungal infections, followed then by autoimmune conditions rheumatoid arthritis, spondyloarthropathies and reactive arthritis.5 11

Learning points

  • Mycobacterium tuberculosis should be included in any differential diagnosis of monarthritis even in non-endemic regions when your patient has epidemiologic risk factors until a definitive diagnosis is made. Delays in diagnosis are common and associated with increased morbidity and mortality.

  • If there is any clinical suspicion for tuberculosis infection, persistent workup will be necessary to confirm or refute the diagnosis including a synovial biopsy with smear, culture and PCR for M. tuberculosis.

  • When tuberculosis infects the peripheral joints, the clinical presentation is more typically monoarticular in load-bearing joints as opposed to disseminated infection or polyarticular involvement.

Acknowledgments

(1) University of British Columbia, Internal Medicine Residency Program. (2) Vancouver General Hospital. (3) St Paul’s Hospital. (4) Vancouver Coastal Health Authority.

References

Footnotes

  • Contributors TM is the sole contributor, currently employed as an Internal Medicine Resident Physician through Vancouver Coastal Health Authority affiliated with the University of British Columbia, Vancouver Program.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent for publication Obtained.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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