Case Presentation: An 84-year-old female with a history of obesity, diabetes, and hypertension presented with 18 months of left knee pain and swelling resulting in progressive functional decline such that she was unable to ambulate. She reported no history of trauma. She had been admitted to another hospital 3 weeks prior and discharged with oral analgesics for presumed Charcot arthropathy. On admission to this hospital she was afebrile with exam notable for edematous left knee with significant effusion and dull erythematous nodule overlying the patella; no significant warmth or erythema otherwise. Initial arthrocentesis showed 626,000 nucleated cells (94% neutrophils), no crystals and gram stain was negative. A complete blood count was normal, C-reactive protein was 16.3. She was started on vancomycin for presumed septic arthritis however gram stain and culture remained negative on serial aspirates. Given the negative microbiologic workup and atypical presentation (i.e. chronic, progressive pain without warmth) acid-fast bacilli stain was done on day 4 of admission and revealed few AFBs; a nucleic acid amplification test (NAAT) confirmed this to be tuberculosis (TB). On day 6 she was started on rifampin, isoniazid, pryazinamide and ethambutol (RIPE). There was progressive decline in the synovial cell count with serial aspirates. Dermatology evaluated the patellar nodule and felt it to be most consistent with scrofuloderma (i.e. extension of an underlying TB infection to the skin). There was no evidence of pulmonary TB on chest x-ray however the patient was unable to produce sputum to rule this out and so remained hospitalized on airborne precautions until she had completed two weeks of RIPE. She was then discharged to a subacute rehab facility and tolerated therapy well. After 2 months she was narrowed to a regimen of isoniazid/rifampin alone for an additional 4 months.

Discussion: Bone/joint TB represents 1-2% of TB cases in the US with about half of these cases involving the spine. The hip and knee are the next most common sites and typically present as a chronic, slowly progressive monoarthritis without significant systemic symptoms. This indolent course contrasts with the acute presentation of bacterial septic arthritis. Direct spread of infection to the skin may result in cold abscesses or draining sinus tracts. The most common symptoms are pain and periarticular edema. Inflammatory markers are typically mildly elevated. Radiographically, Phemister described the triad of juxta-articular osteopenia, osseous erosions and gradual joint space narrowing though these are typically seen late in the disease course. Diagnosis is made by identification of AFB on clinical specimens (e.g. synovial fluid or biopsy, tissue biopsy). Newer molecular diagnostics such as NAATs can confirm the presence of M. tuberculosis, as they did in this case. The treatment follows that of pulmonary TB and resistance testing is essential.

Conclusions: TB monoarthritis represents an uncommon manifestation of EPTB characterized by a chronic, insidious course often complicated by delays in diagnosis and treatment, particularly in lower incidence, developed countries. These delays result in progressive destructive arthropathy and thus it is important for the clinician to consider this diagnosis early, particularly in atypical presentations. Awareness of supportive clinical features, such as scrofuloderma in this patient, may lead to more timely therapy.