A 46-year-old Caucasian female was referred to our institution in December 2012 following a CT-pulmonary angiogram performed to investigate left sided pleuritic chest pain, which revealed a large apical cavity with surrounding consolidation (Fig. 1). The patient reported daily cough productive of brown sputum. There was no associated dyspnoea, malaise or fatigue and no anorexia or weight loss. The patient was Australian born and worked as a computer programmer. Her only overseas travel was to Malta and United Kingdom 30 years prior. She smokes cigarettes and had a past history significant for bilateral pleurodesis for recurrent pneumothoraces as well as an anxiety disorder, for which she took paroxetine. She did not report recurrent infections through childhood or exposure to M. tuberculosis. A chest radiograph 6 years prior to presentation showed 'fibrocalcific lesions in both lung apices'.
Physical examination revealed a thin woman (BMI 19.6 kg/m2) with normal vital signs. There was no clubbing or palpable lymphadenopathy. Respiratory examination revealed coarse breath sounds in the left upper zone upon auscultation. Examination was otherwise unremarkable.
Blood work revealed normal electrolytes, renal function and liver function tests. Complete blood picture showed mild thrombocytosis only. C-reactive protein and ESR were normal. Quantiferon-gold, serum Aspergillus precipitins and HIV antibody were negative. Serum immune-globulins revealed a mild increase in IgA (5.73 g/dL, range 0.85-3.50), but were otherwise normal and alpha-1-antitrypsin was normal. Pulmonary function testing revealed a mild obstructive ventilatory defect and moderately reduced diffusion capacity. The patient underwent a bronchoscopy, which revealed inflammed left lingular segment airways with no endobronchial lesions seen. Cytological analysis of the bronchial specimens did not show any evidence of malignancy. A non-tuberculous mycobacterium was isolated on culture of bronchial washings, which subsequently identified as M. kyorinense.
Between 20 December 2012 and 7 November 2013, seven pulmonary specimens were collected for analysis (two bronchoscopy and five sputum). Small numbers of acid fast bacilli not resembling M. tuberculosis were seen on direct smear from the first bronchial wash specimen. All specimens grew in Bactec MGIT 960 at an average of 13 days (range 7-30 days). MPT 64 TB antigen (BD MGIT  TBc Identification Test) testing was negative on the first isolate and all positive broth culture isolates were submitted to Mycobacterial Reference Laboratory, Victorian Infectious Diseases and Reference Laboratories for further testing (MRL, VIDRL). The MRL identified the non-tuberculous mycobacterium as M. kyorinense by 16S ribosomal RNA gene sequencing. The MRL was unable to perform sensitivity testing of the isolate.
Smoking cessation was encouraged however no anti-mycobacterial treatment was instituted initially due to uncertainty about the significance of the M. kyorinense isolate, and the patient's symptoms deteriorated over the following 3 months. Repeat CT chest showed an increase in the size of the cavity as well as the development of widespread tree-in bud opacities in the left and right upper lobes (Fig. 2). A second bronchoscopy was performed which once again yielded M. kyorinense. Clarithromycin, ethambutol and moxifloxacin were commenced empirically and consideration was given to initiating an injectable aminoglycoside given the extensive cavitation present.
Follow up after 7 months of therapy was completed although the patient had continued to smoke and her adherence with medication was uncertain. The patient continued to cough and M. kyorinense was repeatedly isolated from the expectorated sputum. Repeat CT imaging performed at 7 months showed partial improvement of the lung infiltrates but persistence of the cavity.
CT chest at presentation showing a left upper lobe cavity with areas of consolidation and background changes of centrilobular emphysema.