Beyond the Lungs: A Case Report of Disseminated Tuberculosis With Multisystem Involvement

Tuberculosis (TB) is an infectious disease caused by acid-fast bacillus pertaining to the <i>Mycobacterium tuberculosis</i> complex. Pulmonary TB is the most common presentation, resulting either from primary infection or reactivation of latent disease. In rare cases, wide dissemination of <i>M. tuberculosis</i> can occur, usually by hematogenous or lymphatic route, leading to multiorgan involvement and potentially life-threatening conditions known as disseminated TB. We present the case of a 55-year-old man who presented to the emergency department (ED) with complaints of inflammatory polyarthralgia and myalgia, gradually worsening in the last four months. Other symptoms included fatigue, cough with purulent sputum, and weight loss within the last month. The patient's past medical history included pulmonary silicosis and tobacco use. On physical examination, he had an emaciated appearance, fever (38.4 ºC), normal thoracic examination, and no evidence of arthritis. Blood tests displayed anemia, leucopenia, mild hepatic cytolysis, and elevated acute phase reactants. Urine sediment revealed mild hematuria with red blood cell casts. A thoraco-abdominal-pelvic computerized tomography scan revealed diffuse ground-glass peribronchovascular densification, left pleural effusion, homogenous hepatosplenomegaly, and multiple mediastinal, retroperitoneal, periportal, iliac, and inguinal lymphadenopathy. After admission, polymerase chain reaction (PCR) of <i>M. tuberculosis</i> DNA was positive in sputum and urine. Disseminated TB, with pulmonary and renal involvement, was diagnosed, and antituberculous therapy was initiated with isoniazid, rifampicin, pyrazinamide, and ethambutol. Additionally, 24-hour urine was collected, and proteinuria of 1,566 mg/24 hour was evident. An ultrasound-guided percutaneous kidney biopsy was performed, revealing mesangioproliferative glomerulonephritis due to immune complexes deposition. Polyarthralgia persisted with new-onset arthritis, so arthrocentesis was performed. Both mycobacteriology and PCR detection of <i>M. tuberculosis</i> DNA were negative. While in the ward, sudden onset dyspnea with lower limb edema developed, and jugular vein distention with hypotension was detected. Point-of-care cardiac ultrasound revealed a large volume of pericardiac effusion without cardiac tamponade. Ultrasound-guided pericardiocentesis was performed. Pericardial fluid's mycobacteriology and PCR detection of <i>M. tuberculosis</i> DNA were negative. Six weeks after admission, <i>M. tuberculosis</i> was identified in Lowenstein-Jensen cultures of sputum. The patient was discharged after 145 days of hospital stay, with an indication to maintain antituberculous treatment for a minimum of 12 months, with prolonged treatment decisions dependent on clinical evolution. Twelve months after discharge, the patient was asymptomatic, with analytical and imagiological improvement; therefore, antituberculous therapy was discontinued. Disseminated or miliary TB is a rare condition that poses a diagnostic challenge for every clinician, as clinical presentation is non-specific. Multiorgan involvement may impair diagnostic workup if TB is not initially suspected. Clinicians should be aware of heterogeneous disease progression, as initial detection of organ involvement does not exclude possible further disseminated disease. Diagnosis should be swift to allow early antituberculous therapy initiation and prevent potentially life-threatening situations.