Mycobacterium mageritense Pulmonary Disease in Patient with Compromised Immune System

To the Editor: Mycobacterium mageritense is one of the rapidly growing mycobacteria (RGM). It was first isolated in Spain in 1987, described as a new species in 1997 by Domenech et al. (1), and first described and associated with disease in the United States in 2002 (2). In the 2002 report, 6 isolates were recovered from sputum, a bronchoscopy sample, a wound infection after liposuction, the blood of an immunosuppressed patient with a central catheter and sepsis, a patient with severe sinusitis, and from a wound infection in a patient who had probable osteomyelitis after fixation of an open fracture. It has since been reported as a cause of water-related skin and soft tissue infections (3,4). A study from Japan in 2007 reported recovery of M. mageritense from the sputum of a woman with noncaseating granulomas by transbronchial biopsy who improved without therapy (5). We describe a case of M. mageritense pneumonia in an immunocompromised patient. 
 
In 2009, a 54-year-old woman was admitted to the hospital in Austin, Texas, with a 5-day history of upper back pain and occasional hemoptysis and yellow sputum production. She had a long history of systemic lupus erythematosus and associated nephritis and vasculitis, rheumatoid arthritis, hypothyroidism, sleep apnea, and hepatitis C infection. She was taking prednisone 15 mg/day at the time of admission. 
 
Five months earlier, organizing pneumonia was diagnosed in the patient by computed tomography–guided lung biopsy of a pleura-based mass; special stains and cultures on tissue for acid-fast bacilli (AFB), other bacteria, and fungi were negative. She was readmitted several times over subsequent months and treated with various antimicrobial agents and corticosteroids but did not show clinical or radiographic improvement. Chest computed tomographic scan performed at admission again demonstrated bilateral lung masses and infiltrates, with new areas of necrosis. A second needle biopsy sample showed chronic inflammation with a histiocytic reaction and negative stains for AFB and fungi, but it was deemed nondiagnostic. Subsequent open lung biopsy sample showed necrotizing granulomatous inflammation with possible vascular involvement suggestive of Wegener granulomatosis. 
 
Fite staining showed rare clusters of AFB within the granulomas. The postoperative course was complicated by a multiloculated left pleural effusion. AFB smear of pleural fluid obtained from video-assisted thoracoscopy showed 1–5 bacilli per high power field. Cultures of lung tissue and pleural fluid grew mycobacteria initially identified as M. fortuitum group but subsequently identified as M. mageritense by PCR followed by restriction enzyme analysis of the 65-kDa heat-shock protein (hsp65) (6). Results of susceptibility testing by broth microdilution are shown in the Table. 
 
 
 
Table 
 
In vitro activity of 23 isolates of Mycobacterium mageritense, United States, 2009* 
 
 
 
Testing for Wegener granulomatosis by antineutrophilic cytoplasmic and myeloperoxidase antibody testing yielded negative results. Imipenem and amikacin were prescribed, and gradual resolution of clinical signs and symptoms was observed. Oral linezolid and trimethoprim/sulfamethoxazole were prescribed at discharge. Chest radiographs taken 4 months after the open lung biopsy showed resolution of the masses. 
 
The isolate was a nonpigmented RGM that matched the American Type Culture Collection (Manassas, VA, USA) type strain and 10 published clinical isolates of M. mageritense by PCR restriction enzyme analysis of the 65-kDa hsp gene (6). By gene sequencing of region V of the RNA polymerase (rpoB) gene, it exhibited 99.7% identity to the GenBank type strain sequence of M. mageritense (acceptable interspecies relatedness for this sequence is >98.5% identity) (8). The most closely related species determined by using this sequence and previously submitted sequences were other M. fortuitum species: M. porcinum (94% sequence identity), M. wolinskyi (94%), and M. peregrinum (93%). 
 
Susceptibility testing of 23 clinical isolates of M. mageritense from the United States previously submitted to the Mycobacteria/Nocardia Research Laboratory (University of Texas Health Science Center, Tyler, TX, USA) and identified by hsp65 PCR restriction analysis (6,7) was performed (Table). These results confirmed the potential utility of the drugs used in this case for future cases. 
 
M. mageritense has not been reported as a cause of pulmonary disease in an immunocompromised patient. However, most cases of M. fortuitum pneumonia were reported before the use of molecular technology for species identification. Newer species such as M. mageritense resemble M. fortuitum and would not have been differentiated without this method. 
 
Our patient met the criteria for diagnosing nontuberculous mycobacterial lung disease as established by the American Thoracic Society and the Infectious Diseases Society of America (9). Her therapeutic response also supports a cause-and-effect relationship. 
 
The identity of an RGM isolate as M. mageritense may be suspected by its unusual antimicrobial drug susceptibility pattern, which showed an intermediate MIC to amikacin and resistance to clarithromycin at 3 days (Table). However, definitive identification requires molecular methods. Previous studies have shown that M. mageritense contains an inducible erythromycin methylase gene (erm 40) that confers macrolide resistance (10). The use of molecular studies and greater attention to susceptibility patterns should enable increased recognition of M. mageritense as a human pathogen.

been reported as a cause of waterrelated skin and soft tissue infections (3,4). A study from Japan in 2007 reported recovery of M. mageritense from the sputum of a woman with noncaseating granulomas by transbronchial biopsy who improved without therapy (5). We describe a case of M. mageritense pneumonia in an immunocompromised patient.
In 2009, a 54-year-old woman was admitted to the hospital in Austin, Texas, with a 5-day history of upper back pain and occasional hemoptysis and yellow sputum production. She had a long history of systemic lupus erythematosus and associated nephritis and vasculitis, rheumatoid arthritis, hypothyroidism, sleep apnea, and hepatitis C infection. She was taking prednisone 15 mg/day at the time of admission.
Five months earlier, organizing pneumonia was diagnosed in the patient by computed tomographyguided lung biopsy of a pleura-based mass; special stains and cultures on tissue for acid-fast bacilli (AFB), other bacteria, and fungi were negative. She was readmitted several times over subsequent months and treated with various antimicrobial agents and corticosteroids but did not show clinical or radiographic improvement. Chest computed tomographic scan performed at admission again demonstrated bilateral lung masses and infi ltrates, with new areas of necrosis. A second needle biopsy sample showed chronic infl ammation with a histiocytic reaction and negative stains for AFB and fungi, but it was deemed nondiagnostic. Subsequent open lung biopsy sample showed necrotizing granulomatous infl ammation with possible vascular involvement suggestive of Wegener granulomatosis.
Fite staining showed rare clusters of AFB within the granulomas. The postoperative course was complicated by a multiloculated left pleural effusion. AFB smear of pleural fl uid obtained from video-assisted thoracoscopy showed 1-5 bacilli per high power fi eld. Cultures of lung tissue and pleural fl uid grew mycobacteria initially identifi ed as M. fortuitum group but subsequently identifi ed as M. mageritense by PCR followed by restriction enzyme analysis of the 65-kDa heat-shock protein (hsp65) (6). Results of susceptibility testing by broth microdilution are shown in the Table. Testing for Wegener granulomatosis by antineutrophilic cytoplasmic and myeloperoxidase antibody yielded negative results. Imipenem and amikacin were prescribed, and gradual resolution of clinical signs and symptoms was observed. Oral linezolid and trimethoprim/sulfamethoxazole were prescribed at discharge. Chest radiographs taken 4 months after the open lung biopsy showed resolution of the masses.
The isolate was a nonpigmented RGM that matched the American Type Culture Collection (Manassas, VA, USA) type strain and 10 published clinical isolates of M. mageritense by PCR restriction enzyme analysis of the 65-kDa hsp gene (6). By gene sequencing of region V of the RNA polymerase (rpoB) gene, it exhibited 99.7% identity to the GenBank type strain sequence of M. mageritense (acceptable interspecies relatedness for this sequence is >98.5% identity) (8). The most closely related species determined by using this sequence and previously submitted sequences were other M. fortuitum species: M. porcinum (94% sequence identity), M. wolinskyi (94%), and M. peregrinum (93%).
Susceptibility testing of 23 clinical isolates of M. mageritense from the United States previously submitted to the Mycobacteria/Nocardia Research Laboratory (University of Texas Health Science Center, Tyler, TX, USA) and identifi ed by hsp65 PCR restriction analysis (6,7) was performed (Table). These results confi rmed the potential utility of the drugs used in this case for future cases.
M. mageritense has not been reported as a cause of pulmonary   (9). Her therapeutic response also supports a cause-and-effect relationship.
The identity of an RGM isolate as M. mageritense may be suspected by its unusual antimicrobial drug susceptibility pattern, which showed an intermediate MIC to amikacin and resistance to clarithromycin at 3 days (Table). However, defi nitive identifi cation requires molecular methods. Previous studies have shown that M. mageritense contains an inducible erythromycin methylase gene (erm 40) that confers macrolide resistance (10). The use of molecular studies and greater attention to susceptibility patterns should enable increased recognition of M. mageritense as a human pathogen.