A previously healthy 28-year-old man with a history of extensive plaque psoriasis on treatment with subcutaneous adalimumab for over two years presented to the infectious diseases clinic with a two month history of low-grade fevers, myalgias, and a severe nonproductive cough. The patient had been treated with a course of doxycycline followed by azithromycin approximately one month earlier, causing temporary improvement in his symptoms. 
The patient had emigrated from Vietnam 11 years previously. The patient's grandfather had been treated for pulmonary mycobacterium tuberculosis (MTB) in Vietnam 15 years previously, and the patient had been treated for latent tuberculosis with nine months of isoniazid in 2004. The patient lived in Washington, DC, worked in a healthcare setting, was a nonsmoker, had no pets, and had never received a pneumococcal vaccine. 
Outpatient evaluation by a pulmonologist three weeks previously included unremarkable laboratory studies and clear chest X-ray. On evaluation in our clinic, the patient was noted to be nontoxic appearing and able to speak in full sentences. His temperature on initial evaluation was 37.2 C, blood pressure 109/73 mmHg, heart rate 85 beats per minute, and respiratory rate 14 breathes per minute. His lung examination was unremarkable with clear breath sounds bilaterally without rhonchi or wheezes. 
A computed tomography (CT) scan of the chest performed the same day showed a 1.1 cm lobular opacity in the right lower lobe, a moderate right pleural effusion (Figure 1), hilar lymphadenopathy, and a small amount of perihepatic and perisplenic ascites. Due to the concern for tuberculosis, the patient was admitted to the hospital for further evaluation. 
On hospital admission, his temperature was 39 C, blood pressure 121/87 mmHg, heart rate 95 beats per minute, and respiratory rate 22 breathes per minute, with an oxygen saturation of 97% on ambient air. Physical exam was notable for bilateral crackles in his lungs and a diffuse psoriatic rash. A CT scan of the abdomen and pelvis performed with intravenous contrast revealed diffuse nodularity of the omentum and peritoneal lining (Figure 2), raising the concern for tuberculous peritonitis (TBP). 
 On the second hospital day, the patient underwent an unremarkable bronchoscopy and a thoracentesis which revealed serosanguinous pleural fluid. The pleural fluid was exudative with an 80% lymphocytic predominance. No acid fast bacilli (AFB) were seen. The pleural fluid adenosine deaminase (ADA) was elevated at 110.3 u/L. A subsequent percutaneous peritoneal biopsy was performed revealing bloody peritoneal fluid. Grocott's methenamine silver stain, AFB stain, Fite's stain, and mucin stains on the fluid were negative. Surgical pathology revealed necrotizing granulomatous inflammation with no AFB seen on Auramine-rhodamine stain. The patient was empirically started on isoniazid, rifampin, pyrazinamide, and ethambutol based on the imaging and pathology results. 
The patient underwent an abdominal laparoscopy one week after admission in an attempt to make a definitive diagnosis. This revealed extensive peritoneal and omental studding measuring 2 to 3 mm in size. A modest amount of bloody ascites was present. Pathology revealed granulomatous inflammation and one AFB on Fite's stain but no AFB on Auramine-rhodamine stain. Growth of MTB complex was noted from the percutaneous peritoneal biopsy after 16 days, and subsequently all other culture specimens showed growth by day 30. Sensitivities revealed no antimicrobial resistance. 
The patient was continued on his four drug MTB therapy, but the rifampin was discontinued after 2 weeks due to drug-induced hepatitis. Once his hepatitis had resolved, the rifampin was restarted without further transaminitis. He completed 2 months of directly observed therapy with isoniazid, rifampin, pyrazinamide, and ethambutol and a further 7 months of isoniazid and rifampin. He has made a full recovery.