A 25-year-old woman arrived at our hospital citing fever and chills for 2 days. She also complained of a productive cough, night sweats, and general weakness for several weeks. She had been treated as if she had pulmonary tuberculosis (TB) three times previously, 17, 12, and 5 years earlier. Although the results from the mycobacterial studies of the first two episodes of TB were not available, the anti-TB treatments for the first and second episodes of TB had each continued for 6 months, and she reported that she took every medication as scheduled. Five years ago, she was diagnosed as having recurrent pulmonary TB based on an acid-fast staining of sputum. A mycobacterial culture was not performed. Treatment with isoniazid, rifampicin, ethambutol, and pyrazinamide was again started. However, the regimen was transiently changed to non-hepatotoxic drugs, including ethambutol, streptomycin, and cycloserine. She experienced several adverse drug effects: pancytopenia of rifampicin, ototoxicity of streptomycin, and neurotoxicity of cycloserine.
On admission to our hospital, her vitals were as follows: blood pressure, 110/50 mmHg; body temperature, 38.4C; pulse rate, 126 bpm; and respiration rate, 20 breaths per minute. A physical examination revealed crackles in both lower lobes and inspiratory wheezing in the right middle lobe and the left upper lobe, and there was no scarring indicating a BCG vaccination on either arm. A chest roentgenogram showed air space consolidation in both lower lung zones with nodules and a right middle lobe collapse. A computerized tomography (CT) scan of the chest revealed bronchiectasis with a collapse of the right middle lobe and air space consolidation with cavity formation in the left lower lobe. In addition, in the right upper lobe and both lower lobes, there was branching linear opacity, revealing bronchogenic spread (Fig. 1). Laboratory findings included a white blood cell count of 20,500 cells/mm3 (segment form, 83.7%), hemoglobin of 11.6 g/dL, and platelet cell count of 241,000 cells/mm3. Arterial blood gas analysis performed while breathing without oxygen supplements revealed a pH of 7.39, partial pressure of oxygen of 82.2 mmHg, partial pressure of carbon dioxide of 37.8 mmHg, and oxygen saturation of 95.9%. Hepatic function was normal, except for a mildly elevated aspartate aminotransferase (AST) level of 62 U/L. Renal function was normal, and an human immunodeficiency virus (HIV) test was negative. Acid-fast staining of her sputa revealed numerous bacilli (1-9/10 HPF).
Assuming that she had drug-resistant pulmonary TB, we started a regimen that included isoniazid, ethambutol, levofloxacin, prothionamide, pyrazinamide, and p-aminosalicylic acid. We did not use rifampicin or aminoglycoside because of previous adverse effects. P-aminosalicylic acid was also discontinued within 2 weeks due to abdominal pain. Colonies of mycobacteria were identified in her sputa after 40 days of culture in the Lowenstein-Jensen medium. These bacilli were proved to be NTM, instead of M. tuberculosis complex, by a Gen-Probe test (Gen-Probe Inc., San Diego, CA, USA). These mycobacteria were identified as M. intracellulare by a previously reported polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method using cultured mycobacterial colonies at the Korean Institute of Tuberculosis. Under the diagnosis of M. intracellulare lung disease, the regimen was changed to clarithromycin, ethambutol, and moxifloxacin. Despite the regular intake of medication, her symptoms did not improve, and the results of smears for acid-fast bacilli were repeatedly positive (1-9/100 HPF). After 8 months of medication, M. abscessus was isolated instead of M. intracellulare (Table 1). A chest CT performed 1 year after the treatment began revealed minimal improvement (Fig. 1). Amikacin was added to the regimen after careful evaluation of her hearing function. However, she refused to try cefoxitin and imipenem because of possible leukopenia and high cost. We performed a bronchoscopic lavage to identify causative mycobacteria, and M. abscessus was isolated from the cultures of lavaged fluid from the right middle and left lower lobes.
Considering the poor symptomatic response to anti-mycobacterial medications and the persistence of a cavitary lesion, we decided to conduct a surgical resection. She underwent a video-assisted thoracoscopic right middle lobe lobectomy, right lower lobe wedge resection, and right upper lobe wedge resection. She was discharged 6 days after the operation without postoperative complication. On the second operation, which was conducted 1 month later, a video-assisted thoracoscopic left lower lobe basal segmentectomy and left upper lobe wedge resection were performed. She was discharged 11 days after the operation without postoperative complication. After the second operation, negative sputum conversion was achieved. At 11 months after the operation, the results of the smears for acid-fast bacilli were negative, and the amount of sputum had decreased. She was being kept on chemotherapy regimens with clarithromycin, ethambutol, and moxifloxacin without complaining of any respiratory symptoms (Table 1). Amikacin was discontinued after 12 months because of increasing tinnitus. A CT of the chest performed 9 months after the second operation revealed no new lesions (Fig. 1).