A 66-year-old male presented to his primary care physician with the right upper chest pain, progressive malaise, generalized weakness, loss of appetite, and a 10 lb weigh loss for 2 months. Past medical history was significant for rheumatoid arthritis, chronic pulmonary obstructive disease, and 60-pack-year of cigarette smoking. He had been treated for rheumatoid arthritis with weekly subcutaneous injection of etanercept for 10 months, and symptoms of rheumatoid arthritis were well-controlled. He denied cough, dyspnea, fever, chills, night sweat, or known tuberculosis exposure. Physical examination was unremarkable, and routine laboratory tests did not reveal significant abnormalities. A chest radiograph showed a right upper lobe density. Etanercept therapy was subsequently discontinued because of the concern of opportunistic infections secondary to etanercept. The tuberculin skin test (TST) was noted 2 mm prior to initiation of etanercept treatment. The patient underwent chest computed tomography (CT) which was reported a pleura-based consolidated mass (1.5 x 2 x 1 cm) on the lateral aspect of the right upper lobe and a thick-walled cavitary lesion (2.5 x 3 x 3.5 cm) on the superomedial side of the right lung apex, highly suggestive of a Pancoast tumor (Figures 1 and 2). There were background emphysematous pulmonary changes, without bronchiectasis, mediastinal, or hilar lymphadenopathy. It was followed by the 18F-FDG PET study, which demonstrated hypermetabolic uptake foci in these areas located within the right upper lobe (Figures 3 and 4). The standardized uptake values (SUVs) of the lesions were ranging from 7.4 to 12.8, consistent with pulmonary malignancy.
The bronchoscopy with bronchoalveolar lavage (BAL) was performed to establish the diagnosis of lung cancer. The bronchoscopy did not reveal endobronchial tumors. BAL cytology examination failed to demonstrate malignant cells. BAL Gomori methenamine-silver (GMS) stain and fungal culture was negative. The Ziehl-Neelsen acid-fast bacilli (AFB) smears of several BAL samples were positive. BAL Mycobacterium tuberculosis complex DNA probe and Mycobacterium avium intracellulare DNA probe were performed, and they were negative. Mycobacterium kansasii DNA probes on multiple BAL specimens reported positive, and a clinical diagnosis of pulmonary M. kansasii infection was then entertained. His HIV serology was negative. A triple drug regimen:isoniazid 300 mg/day, rifampin 600 mg/day, and ethambutol 1200 mg/day:was initiated while awaiting the final culture result. Chest pain and malaise were resolved in a week, and appetite returned in two weeks from the initiation of antimicrobial therapy. M. kansasii was eventually isolated from the culture after 6 weeks. The isolate was susceptible to rifampin, ethambutol, clarithromycin, rifabutin, ciprofloxacin, moxifloxacin, and amikacin. Serial CT chest imaging studies at the 6-week and the 6-month of antimycobacterial therapy revealed significant radiological improvement of pulmonary lesions (Figures 5 and 6). The patient continued to improve clinically, and a total resolution of pulmonary lesions was achieved (Figure 7) on completion of a 12-month course of triple drug therapy.