A 51-year-old kidney transplanted patient was admitted to the department of nephrology with abdominal pain and significant weight loss for several weeks. CT scan showed multiple contrast-enhancing peritoneal nodules and large intraperitoneal soft-tissue masses radiologically impressing as severe peritoneal carcinomatosis (Figure 1), a hypodense lesion within the right adrenal gland radiologically appearing as a metastasis as well as enlarged retroperitoneal lymph nodes, while the lung was unremarkable on CT scan. The patient was then referred to our endoscopy unit for tumor screening. Colonoscopy with virtual chromoendoscopy (i-scan) revealed a polypoid lesion at the hepatic flexure with irregular mucosa, hemorrhages, contact bleeding, and a central ulceration (Figure 2). On histopathology, no dysplasia or cancer was found. Importantly, histopathology was also negative for the presence of granulomas. A second colonoscopy for targeted biopsies was initiated and histopathology was again negative for cancer; however, subsequently performed Ziehl-Neelsen stain revealed acid-fast bacteria. In a third colonoscopy, biopsies for microbiological analysis and resistance testing were obtained and DNA of rifampicin-sensitive M. tuberculosis complex was detected using the Xpert MTB/RIF assay on the GeneXpert Dx System (Cepheid, Sunnyvale, CA) on the same day. Immediately thereafter, first-line antituberculostatic treatment was initiated. Liquid culture (BACTEC  MGIT , Becton Dickinson, Franklin Lakes, NJ) was positive after 4 days. The strain was identified as M. tuberculosis based on gyrB sequence analysis and phenotypically susceptible to all first-line tuberculostatic drugs. The subsequent course of disease was complicated by episodes of epileptic seizures with aphasia and hemiparesis. Cranial CT and MRI showed bilateral ischemic lesions and contrast-enhancing lesions directly adjacent to the dura, radiologically consistent with multiple septic emboli and tuberculosis manifestation within the CNS (Figure 3). Under tuberculostatic therapy, neurological symptoms slowly ameliorated; however, organic brain syndrome persisted.