An 86-year-old male presented to the hospital with hypotension, chronic left shoulder pain, and an associated effusion in 2014. Remotely, he had undergone left shoulder acromioplasty, followed by hemiarthroplasty in 2010, for severe rotator cuff arthropathy. In 2012, he developed pain at the site of the left shoulder after a fall. Shoulder radiographs showed a stable hemiarthroplasty without evidence of complication. The shoulder pain persisted, and he gradually developed swelling over the left shoulder joint. In 2013, computed tomography (CT) of the shoulder showed a lytic destructive process involving the scapula associated with a large extra-articular proliferative soft tissue process centered on the glenohumeral joint. The mass measured  cm and contained internal calcifications (Fig. 1a). Lysis and fragmentation of adjacent bony structures (especially the acromion) were noted. A neoplastic process such as chondrosarcoma was suspected. A subsequent CT-guided biopsy of the left clavicle lytic lesion was nondiagnostic.
Four months prior to admission, the patient underwent a second, open biopsy of the left shoulder mass and distal clavicle. Bacterial cultures were negative. No fungal or mycobacterial cultures were obtained. Pathology from the clavicle demonstrated multiple non-necrotizing granulomata. Special stains on the formalin-fixed tissues were negative for fungal and mycobacteria organisms.
The past medical history included diabetes complicated by retinopathy, atrial fibrillation, diastolic heart failure, stage III chronic kidney disease, chronic obstructive pulmonary disease, penicillin allergy, and previously treated bladder cancer.
On examination, a draining sinus tract over the left deltoid was noted. The tract had appeared after the open biopsy 4 months previously. A radiograph of the left shoulder demonstrated erosive changes and extensive demineralization of the left proximal humerus with left shoulder arthroplasty hardware in place (Fig. 1b), erosion and separation of the acromioclavicular joint, ossific debris in the subacromial-subdeltoid bursa, and destruction of the glenoid. The findings were felt to be consistent with hardware-associated osteomyelitis. Inflammatory markers were elevated (C-reactive protein 19.5 mg/dL; erythrocyte sedimentation rate 46 mm/h). Bacterial culture of sinus tract fluid yielded Proteus mirabilis.
The patient was taken to the OR for hemiarthroplasty removal, biopsy of the distal clavicle, and placement of an antibiotic-impregnated cement spacer. Four days later, he underwent a second irrigation and drainage, at which time the spacer was removed. Pathology on the resected bone revealed granulomas. Operative samples grew Peptostreptococcus. Fungal cultures were negative. No mycobacterial cultures were obtained. He received intravenous clindamycin and aztreonam for approximately 6 weeks, with minimal change in symptoms or inflammatory markers. Subsequently, he was treated with vacuum-assisted wound closure and required several additional washouts for bleeding into the shoulder joint space, along with intermittent courses of oral and IV antibiotic therapy.
Eighteen months after arthroplasty removal, the patient was readmitted to the hospital with persistent left shoulder pain and effusion, 38 kg weight loss, and malaise. A radiograph of the left shoulder revealed erosion of the left proximal humerus at the site of explanted arthroplasty hardware, along with other findings highly suspicious for osteomyelitis and septic arthritis of the proximal humerus and acromioclavicular joint (Fig. 2a). Magnetic resonance imaging (MRI) demonstrated a peripherally enhancing glenohumeral joint effusion and intra-humeral abscess (Fig. 2b). An aspirate of synovial fluid containing 7000 white cells/mm (76 % neutrophils) was pan-cultured. Cutibacterium acnes and a Kocuria species were recovered from bacterial culture. After 18 d, growth from the mycobacterial cultures of the shoulder joint aspirate was observed; the organism was identified as the Mycobacterium tuberculosis (MTb) complex by a commercial DNA probe assay. The patient's QuantiFERON -TB Gold blood test was negative. Chest imaging showed no evidence of tuberculosis in the lungs, pleura, or lymph nodes. Sputum samples were submitted for acid fast stain and culture, both of which were negative. Abdominal CT imaging revealed cirrhosis and ascites, previously undiagnosed.
Resistance testing to all first-line anti-mycobacterial drugs was requested, and preliminary results were reported 27 d after cultures became positive (final results were available 42 d after culture positivity). The isolate was susceptible to isoniazid, rifampin, and ethambutol but resistant to pyrazinamide. These results raised suspicion for infection due to M. bovis, a member of the MTb complex, which is intrinsically resistant to pyrazinamide. Using spacer oligonucleotide typing (spoligotyping) and analysis of mycobacterial interspersed repetitive units (MIRU), the isolate was subsequently confirmed to be the BCG strain of M. bovis.
Detailed review of the patient's medical history revealed that he had been treated for urothelial carcinoma with transurethral bladder resection and BCG therapy in 1996. In 2012, the bladder cancer had recurred and was treated with a second course of BCG, which was complicated by persistent cystitis and bladder ulcerations.
A liver-sparing anti-tuberculosis regimen (rifampin, ethambutol, and levofloxacin) was initiated, which the patient tolerated well. However, because of his symptoms of cachexia and weakness, he elected to enter hospice care. All anti-mycobacterial drugs were discontinued, and he expired 13 d after hospital discharge.