Mycobacterium mageritense pulmonary disease in patient with compromised immune system.
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.
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 [greater than or equal to] 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.
We thank Steven McNulty, Linda Bridge, and Ravikiran Vasireddy for laboratory assistance and Joanne Woodring for typing the manuscript.
R. Gordon Huth, Barbara A. Brown-Elliott, and Richard J. Wallace, Jr.
Author affiliations: University of Texas Southwestern Residency Programs, Austin, Texas, USA (R.G. Huth); and University of Texas Health Science Center, Tyler, Texas, USA (B.A. Brown-Elliott, R.J. Wallace, Jr.)
(1.) Domenech P, Jimenez MS, Menendez MC, Bull TJ, Samper S, Manrique A, et al. Mycobacterium mageritense sp. nov. Int J Syst Bacteriol. 1997;47:535-40. DOI: 10.1099/00207713-47-2-535
(2.) Wallace RJ, Brown-Elliott BA, Hall L, Roberts G, Wilson RW, Mann LB,
et al. Clinical and laboratory features of Mycobacterium mageritense. J Clin Microbiol. 2002;40:2930-5. DOI: 10.1128/JCM.40.8.2930-2935.2002
(3.) Appelgren P, Farnebo F, Dotevall L, Studahl M, Jonsson B, Petrini B. Late-onset posttraumatic skin and soft tissue infections caused by rapid-growing mycobacteria in tsunami survivors. Clin Infect Dis. 2008;47:e11-6. DOI: 10.1086/589300
(4.) Gira AK, Reisenauer AH, Hammock L, Nadiminti U, Macy JT, Reeves A, et al. Furunculosis due to Mycobacterium mageritense associated with footbaths at a nail salon. J Clin Microbiol. 2004;42:1813-7. DOI: 10.1128/JCM.42.4. 1813-1817.2004
(5.) Miki M, Shimizukawa M, Okayama H, Kazumi Y. Case of pulmonary Mycobacterium mageritense infection: the difficulty of differential diagnosis of granulomatous lung disease. Kekkaku. 2007;82:189-94.
(6.) Steingrube VA, Gibson JL, Brown BA, Zhang Y, Wilson RW, Rajagopalan M, et al. PCR amplification and restriction endonuclease analysis of a 65-kiloDalton heat shock protein gene sequence for taxonomic separation of rapidly growing mycobacteria [ERRATUM 1995;33:1686]. J Clin Microbiol. 1995;33:149-53.
(7.) Woods GL, Brown-Elliott BA, Desmond EP, Hall GS, Heifets L, Pfyffer GE, et al. Susceptibility testing of mycobacteria, nocardia, and other aerobic actinomycetes; approved standard. NCCLS Document M24-A. Wayne (PA): Clinical and Laboratory Standards Institute; 2003.
(8.) Adekambi T, Colson P, Drancourt M. rpoB-based identification of nonpigmented and late pigmented rapidly growing mycobacteria. J Clin Microbiol. 2003;41:5699-708. DOI: 10.1128/JCM. 41.12.5699-5708.2003
(9.) Griffith DE, Aksamit T, Brown-Elliott BA, Catanzaro A, Daley C, Gordin F, et al. An official ATS/IDSA statement: diagnosis, treatment and prevention of nontuberculous mycobacterial diseases. Am J Respir Crit Care Med. 2007;175:367-416. DOI: 10.1164/ rccm.200604-571ST
(10.) Nash KA, Andini N, Zhang Y, Brown-Elliott BA, Wallace RJ Jr. Intrinsic macrolide resistance in rapidly growing mycobacteria. Antimicrob Agents Chemother. 2006;50:3476-8. DOI: 10.1128/AAC.00402-06
Address for correspondence: R. Gordon Huth, 601 E 15th St, Austin, TX 78701, USA; email: email@example.com
Table. In vitro activity of 23 isolates of Mycobacterium mageritense, United States, 2009 * MICs of No. current Intermediate isolates isolate, breakpoint, Antimicrobial agent tested [micro]g/mL [micro]g/mL Amikacin 23 8 32 Cefoxitin 23 16 32-64 Ciprofloxacin 23 0.25 2 Clarithromycin ([dagger]) 23 8 4 Doxycycline 22 1 2-8 Imipenem 22 4 8 Linezolid 22 4 16 Sulfamethoxazole 21 4 32 Trimethoprim/ sulfamethoxazole 6 1/19 2/38 ([double dagger]) Tobramycin 23 [less than or 8 equal to] 2 Tigecycline 5 0.12 -- ([section]) MIC range, Antimicrobial agent [micro]g/mL Amikacin [less than or equal to] 1-32 Cefoxitin [less than or equal to] 8-256 Ciprofloxacin [less than or equal to] 0.25-0.5 Clarithromycin ([dagger]) 1->64 Doxycycline 0.25->64 Imipenem [less than or equal to] 0.5-8 Linezolid [less than or equal to] 2-16 Sulfamethoxazole [less than or equal to] 2-32 Trimethoprim/ sulfamethoxazole [less than or equal to] 0.25/4.8-2/38 Tobramycin 2-64 Tigecycline [less than or equal to] 0.03-0.12 [MIC.sub.50], [MIC.sub.90], Antimicrobial agent [micro]g/mL [micro]g/mL % S/I Amikacin 16 32 100 Cefoxitin 32 64 91 Ciprofloxacin 0.25 0.5 100 Clarithromycin ([dagger]) >32 >64 4 Doxycycline 8 >32 50 Imipenem 2 4 100 Linezolid 4 8 100 Sulfamethoxazole 8 32 100 Trimethoprim/ sulfamethoxazole 0.5/9.5 2/38 100 Tobramycin >16 >32 30 Tigecycline 0.06 0.12 NA * Includes 6 isolates previously reported (2). S, susceptible; I, intermediate; NA, not available. ([dagger]) Three days' incubation. ([double dagger]) Proposed breakpoint (7). ([section]) No Clinical and Laboratory Standards Institute breakpoints established for tigecycline.
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|Author:||Huth, R. Gordon; Brown-Elliott, Barbara A.; Wallace, Richard J., Jr.|
|Publication:||Emerging Infectious Diseases|
|Article Type:||Letter to the editor|
|Date:||Mar 1, 2011|
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