A 47-year-old male born in the Philippines who immigrated to the US approximately 2 years ago presents to a gastroenterologist with symptoms of abdominal pain, unintentional 60 lb weight loss over the past 6 months, fatigue, and diarrhea without hematochezia. A CT scan of the abdomen showed only nonspecific colitis of the ascending colon and descending colon. He had a colonoscopy which showed segmental areas of inflammation and deep ulcerations at the hepatic flexure and in the ascending colon with edema, granularity, and loss of vascularity (Figure 1). The terminal ileum was not intubated during this procedure. Pathology showed severe lymphoplasmacytic infiltration, marked architectural distortion, and chronic inflammation without granulomas. The patient was diagnosed with Crohn's disease and was treated with prednisone and mesalamine. However, his symptoms progressively worsened over the next three months, so his treatment was escalated. He was tested for latent tuberculosis infection (LTBI) with the Quantiferon gold assay, which returned indeterminate and a subsequent tuberculin skin test (TST) was negative. Chest X-ray did not show any evidence of active or prior TB infection, so the patient was thus presumed to be TB negative and started on the TNF-alpha inhibitor infliximab. One month later, the patient presented with worsening abdominal pain, diarrhea, fatigue, and new fevers, claiming that his symptoms had significantly worsened since starting the infliximab. He was in shock with a blood pressure of 73/51 mmHg and laboratory results were notable for white blood cell count of 8.7 x 109/L (normal 3.4-9.6 x 109/L) with bandemia, albumin 1.5 g/dL (normal 3.5-5.0 g/dL), lactic acid 5.3 mmol/L (normal 0.5-1 mmol/L), and a cholestatic liver function pattern. He was treated for septic shock with broad-spectrum IV antibiotics and vasopressors, but required intubation due to clinical deterioration. CT imaging revealed ascites, large bilateral pleural effusions, and multiple hypodense lesions within the liver with an obstructing mass at the confluence of the bile ducts. Diffuse full-thickness small and large bowel wall thickening along with increased attenuation involving the terminal ileum and cecum was present. A workup for infection was pursued with liver lesion biopsy, thoracentesis, and paracentesis. These studies were negative for malignant cells, but were positive for numerous acid-fast bacilli (AFB). A repeat CT was performed where it was seen that the patient developed intraperitoneal free air and fistulas requiring exploratory laparotomy (Figure 2). Surgery revealed extensive adhesions associated with dense granulomatous disease and perforation of the small bowel and right colon. A hemicolectomy and small bowel excision was performed with pathology of the terminal ileum and right colon showed extensive caseating and noncaseating granulomatous inflammation that stained positive for AFBs in a skip lesion pattern consistent with intestinal tuberculosis (ITB). The patient was diagnosed with disseminated TB and started on anti-mycobacterial therapy with significant improvement in his clinical condition. After discharge, he no longer complained of diarrhea, weight loss, or abdominal pain on two month follow-up. The diagnosis of Crohn's Disease was no longer considered and removed from his medical history.