An 80-year-old woman presented to an outside hospital with fever and a dry cough. The patient's vital signs were as follows: respiratory rate, 20 breaths/min; blood pressure, 123/57 mmHg; heart rate, 85 beats/min; blood oxygen saturation, 96 %; and body temperature, 38.5 C. Based on her medical history, the patient was diagnosed with hypertension, without diabetes mellitus, and connective tissue disease. She had not taken any medications, except those for hypertension. She was a nonsmoker with no family history of interest. An outside posteroanterior chest radiograph performed 3 weeks before showed multiple consolidations and ground-glass opacities in both the mid and lower lung zones (Fig. 1). A subsequent chest CT scan showed multiple pulmonary nodules and masses with internal cavitation in both lungs (Fig. 2). There was no evidence of pulmonary thromboembolism, mediastinal or hilar lymphadenopathy, or pleural or pericardial effusion. Based on the impression of septic pneumonia or necrotizing pneumonia, empiric antibiotic treatment with vancomycin, tazolactam, and ertapenem was administered. However, she did not respond to antibiotics, and fever persisted. Therefore, the patient was referred to our hospital for further investigation.
At our hospital, the patient complained of fever and a cough without any clinically significant comorbidities. Laboratory data showed leukocytosis, (13,360/uL [normal, 4800-10,800 /uL]: 82.6 % neutrophils, 10.4 % lymphocytes, 3.9 % monocytes, and 2.0 % eosinophils), increased C-reactive protein levels (10 mg/dL [normal, <0.5 mg/dL]), an increased erythrocyte sedimentation rate (86 mm/h [normal, 0-20 mm/h]), and an increased procalcitonin levels (0.346 ng/mL [normal, 0-0.100 ng/mL]). Her renal and liver function tests were within the normal range. Considering the ineffectiveness of antibiotics at the outside hospital, our first impressions were of vasculitis, such as granulomatosis with polyangiitis (GPA), fungal pneumonia, pulmonary tuberculosis, or an NTM pulmonary infection. The tests for antinuclear antibodies, myeloperoxidase antibodies, and proteinase-3 antibodies were all negative. Moreover, blood cultures for fungi and bacteria were also negative. Blood, sputum, and bronchoalveolar lavage samples tested negatively for Mycobacterium tuberculosis and acid-fast bacilli on an interferon-gamma release assay and polymerase chain reaction. An ultrasound-guided percutaneous needle biopsy of the mass in the right lower revealed a chronic granulomatous inflammation, inflammatory cell infiltration, and distortion of the lung architecture (Fig. 3). One month later, a sputum culture showed growth of Mycobacterium intracellulare, confirming an NTM pulmonary infection.
Following treatment with anti-mycobacterial medications (ethambutol, rifampicin, and azithromycin), her symptoms and radiological findings greatly improved (Fig. 4). However, the previously hidden reticular densities in both lower lung zones were detected on a posteroanterior chest radiograph. Two years after the anti-mycobacterial treatment, a follow-up chest CT showed an improvement of the previously observed multiple masses and ground-glass opacities. Furthermore, it showed a predominant lower lobe pulmonary fibrosis with mild ground-glass opacity, reticulation, and traction bronchiectasis that was not identified on the initial chest CT (Fig. 5). She is now on outpatient follow-up with no clinical symptoms.