Case report: Tumor-like mediastinal tuberculous lymphadenitis with paravertebral cold abscess under cumulative immunosuppression: a case highlighting altered host–pathogen interactions

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.