Background Tuberculosis (TB) remains a leading opportunistic infection in immunocompromised hosts. Disruption of host–pathogen interactions under cumulative immunosuppression may result in atypical extrapulmonary disease with indolent clinical manifestations and tumor-mimicking radiologic features, leading to substantial diagnostic delay. Case presentation A 67-year-old man with Crohn’s disease on cumulative immunosuppressive therapy, including biologics and a Janus kinase inhibitor, developed progressive mediastinal lymphadenopathy and a paravertebral mass with associated vertebral destruction on chest computed tomography, despite prior completion of isoniazid prophylaxis for latent TB infection. The aggressive, tumor-like imaging appearance raised a strong suspicion of metastatic malignancy. Conventional endobronchial ultrasound–guided transbronchial needle aspiration was nondiagnostic. As a salvage diagnostic approach, endobronchial ultrasound–guided tunneling biopsy obtained histological core tissue from a subcarinal lymph node. Although histopathology showed nonspecific fibrous changes without identifiable acid-fast bacilli, Xpert MTB/RIF testing detected Mycobacterium TB complex DNA at trace levels. A diagnosis of mediastinal tuberculous lymphadenitis complicated by a paravertebral cold abscess and secondary vertebral osteomyelitis was ultimately established. The patient subsequently showed marked radiological improvement with standard anti-TB therapy. Conclusion This case illustrates how cumulative immunosuppression can profoundly alter host immune responses to Mycobacterium TB, resulting in tumor-like extrapulmonary disease and diagnostic ambiguity. Integration of advanced tissue acquisition with molecular testing may be essential for diagnosing TB when disrupted host–pathogen interactions limit conventional diagnostic yield.
Zhou et al. (Fri,) studied this question.