Vertebral Aspergillus Osteomyelitis Mimicking Tuberculosis in an Adolescent With Chronic Granulomatous Disease

To the Editors: In tuberculosis-endemic settings, vertebral osteomyelitis is often presumed to be caused by Mycobacterium tuberculosis, which may delay recognition of alternative pathogens and underlying immunodeficiency.1 We report an adolescent in whom presumed Pott disease ultimately proved to be invasive aspergillosis and led to the diagnosis of chronic granulomatous disease (CGD). A previously healthy 15-year-old girl presented with nearly 3 months of progressive back pain accompanied by intermittent fever, night sweats and weight loss. On admission, inflammatory markers were elevated, including a markedly increased erythrocyte sedimentation rate. Chest radiography demonstrated bilateral patchy opacities, initially interpreted as pneumonia. Empiric antibiotic therapy was initiated, but no clinical improvement was observed. Tuberculosis investigations using gastric aspirate samples were negative for M. tuberculosis by acid-fast bacilli staining, polymerase chain reaction and culture. Spinal magnetic resonance imaging revealed destructive lesions involving the T3–T7 vertebrae, including collapse of T4, extensive paravertebral and epidural abscesses, and severe spinal cord compression (Fig. 1A), strongly suggestive of Pott disease. Subsequently, biopsy of a superficial paraspinal lesion revealed granulomatous inflammation, and standard antituberculosis therapy was initiated.FIGURE 1.: A: Thoracic magnetic resonance imaging demonstrates destructive lesions between T3–T7 vertebrae with collapse of T4, extensive paravertebral and epidural abscesses, and severe spinal cord compression, radiologically suggestive of Pott’s disease. B: Intraoperative image of abscess drainage and debridement, demonstrating a large fungal mass. Surgical intervention again confirmed the presence of Aspergillus fumigatus.Due to the patient’s clinical and radiologic deterioration, a repeat biopsy was performed. Direct microscopy demonstrated hypha-like elements, and histopathology revealed necrosis with suppurative inflammation. Therefore, empiric liposomal amphotericin B was initiated for suspected invasive fungal infection. With continued radiologic progression and development of new abdominal soft-tissue lesions, surgical drainage and debridement were performed. Aspergillus fumigatus was isolated from operative specimens (Fig. 1B), confirming invasive aspergillosis. Antifungal therapy was escalated to voriconazole plus an echinocandin, a combination that may be considered in selected severe or refractory cases of invasive aspergillosis.2,3 Because of persistent severe infection, neutrophil oxidative burst testing was performed and demonstrated near-absent activity, establishing a diagnosis of CGD. Adjunctive interferon-γ therapy was initiated, resulting in gradual clinical improvement. This case highlights 2 practical lessons. First, fungal vertebral osteomyelitis should be considered in patients with presumed spinal tuberculosis who fail to respond to therapy, particularly in the absence of microbiologic confirmation.1,2 Second, invasive aspergillosis in a child should prompt evaluation for underlying immunodeficiency, including CGD.4,5