A 25-year-old Indian male without any significant past medical history presented to a hospital in the United States with progressively worsening systemic symptoms over the course of three months. Symptoms included fatigue, night sweats, and fever, as well as a non-productive cough. He reported unintentional weight loss of 30 pounds over three months, as well as ten days of worsening low back pain that radiated to his thighs. Notably, the patient had immigrated to the United States from India two-and-a-half years prior to this admission and had briefly visited India one year prior. He had no history of tuberculosis, and he denied any known exposures to tuberculosis.
In the emergency department, he was febrile to 103.1 F and tachycardic to 160 beats per minute. However, he was normotensive and breathing comfortably on room air with an oxygen saturation of 97%. On general examination, he appeared thin but was awake and alert in no acute distress. On pulmonary examination, he was found to have decreased breath sounds and dullness to percussion over the right middle and lower lung fields, as well as mild clubbing of the digits. The remainder of the physical examination was unremarkable.
He received a chest x-ray and subsequent CT angiogram of the chest, which demonstrated a large right loculated pleural effusion, right upper lobe density, right-sided compressive atelectasis, multiple bilateral subcentimeter nodules, and a 1.5 cm right hepatic lesion (Fig. 1).
To evaluate his reported back pain, an MRI of the lumbar spine was ordered, and the results showed multiple poorly defined bony lesions consistent with metastatic disease in the vertebral bodies (Fig. 2A).
In an attempt to identify the primary source of the metastases, an ultrasound of the testes was then performed, which demonstrated bilateral masses suspicious for additional metastases, though primary testicular malignancy could not be excluded by imaging alone. Follow-up serum alpha fetoprotein (AFP) and beta-hCG levels were within normal limits.
Initial hematologic studies revealed a mild normocytic anemia, leukocytosis, and mild thrombocytosis. A metabolic panel revealed hyponatremia (127 mmol/dL) and elevated alkaline phosphatase (201 IU/L), and hypoalbuminemia.
Thoracentesis was performed upon admission, which showed a lymphocyte-predominant exudative effusion. No acid fast bacteria were isolated from the pleural fluid, and an adenosine deaminase (ADA) level was normal.
The patient subsequently underwent bronchoscopy, and the culture was negative for acid fast bacilli after six weeks. However, transbronchial biopsy demonstrated necrotizing granulomas in the lung and fibrous tissue. Stains for mycobacteria and fungi were negative. This was followed by pleural biopsy, which was also negative for mycobacterial culture but demonstrated focal granulomatous inflammation.
Interferon gamma release assay (QuantiFERON Gold) and tuberculin skin test were both positive.
The patient was started on antibiotic therapy of rifampin, isoniazid, pyrazinamide, and ethambutol. After a week of treatment, the patient continued spiking fevers, we proceeded to ruling out central nervous system involvement. An MRI of the brain was done and demonstrated calcanerium abscesses, infiltration of the bone marrow, and thickening of the dura (Fig. 2B). Given these findings, a bone marrow biopsy and lumbar puncture were performed, which were both normal with once again negative acid fast bacilli staining and culture.
The patient continued with standard antituberculous therapy and gradually improved. After his fevers resolved and mental status normalized, the patient was discharged.