Group IV: Rapid Growing Mycobacteria (RGM)

Authors: Michael D. Iseman, M.D.

 Rapid-growing mycobacteria are a distinctive subset of the "atypical" or non-tuberculous mycobacteria. Widely distributed in the environment, they appear to be generally acquired from soil or water, but they are unfortunately common as agents of nosocomial infection.  


M. abscessusM. chelonaeM. fortuitum and M. smegmatis are the RGM species most commonly associated with human disease. Other RGM which have been reported in association with human disease include M. peregrinumM. mucogenicum and some rare exotic species (19). 

Genetically the RGM are relatively remote from the various slow growing mycobacteria (42). The biological separation is reflected in several important clinical distinctions: (a) dosing schedules for RGM antimicrobial agents are more frequent, commensurate with the relatively shorter replication times, (b) therapy of the RGM typically involves agents without activity against other mycobacterial pathogens and (c) the RGMs commonly elicit a weakly granulomatous tissue response or a frankly dimorphic reaction (a combination of granulomatous and/or pyogenic features).  

back to top


These mycobacteria are widely distributed in water and soil and presumably are commonly acquired from these environmental sources (13). The great majority of RGM cases, both pulmonary and extra pulmonary have been reported from the southeast U.S., notably Texas and Florida (10,16,44,47-49); however, recent experience documents disease due to RGM in all the United States including Alaska and Hawaii. There is no evidence of human-to-human transmission. The capacity of the RGM to survive, even proliferate in water may partially explain their association with iatrogenic infections. M. chelonae in particular has been associated with water or other liquid-borne infections in a variety of medical settings including bronchoscopy (17), xenographic heart valves (27), otologic (29); and ophthalmologic (25) surgery, gentian violet used to mark skin lines for plastic surgery (34), cardiac surgery (20,26) augmentation mammaplasty prostheses (48) liposuction instruments (8,31) and DPTP vaccine (2). M. abscessus has also been reported in association with iatrogenic disease related to renal dialysis (1), sternotomy for cardiac surgery (24) unlicensed preparation of adrenal extract (7), contamination of pacemaker wires (11) acupuncture (50), body-piercing (40) and prosthetic valve endocarditis (41). Recent reports have also documented increased numbers of cases of soft tissue and bone infections due to M. fortuitum and M. smegmatis including those associated with cardiac surgery (20,26) mammaplasty (48) and peritoneal dialysis (18). Shower-born colonization of the respiratory tracts of 16 patients by M. fortuitum was seen in an East Coast Veterans Administration Hospital (6). Excellent reviews have recently been published on nosocomial outbreaks and pseudo-outbreaks due to NTM (43) and infections due to NTM (33). Both articles emphasized the predominant role of RGM in these settings. 

Risk factors commonly associated with pulmonary disease due to the RGM include the unusual body habitus among females previously described in association with MAC disease-slender, mild thoracic scoliosis, pectus excavatum and/or narrowed anterior-posterior thoracic dimensions, with or without mitral valve prolapse (23). Another apparent but not well-documented risk factor for RGM pulmonary disease includes esophageal achalasia or other disorders of motility associated with vomiting (5,16). Additional predisposing host conditions include previously damaged or scarred lungs from disorders such as prior tuberculosis, MAC disease, sarcoidosis, rheumatoid arthritis/ankylosing spondylitis, lipoid pneumonia, and previous or co-existent disease due to M. avium complex. Inherited disorders including cystic fibrosis and deficiency of alpha-1 antitrypsin may also play a substantial role (12). 

Common host conditions associated with multifocal or disseminated RGM disease includes renal failure, dialysis, organ transplantation, connective tissue disorders and other conditions treated with steroids and/or cytotoxic agents, leukemia and (1,22,39,44). Disseminated RGM infection with prominent lymphadenopathy was reported in 16 HIV negative patients from Thailand (9); although they were described as "Immunocompetent Hosts", the RGM disease and other opportunistic infections belie that appellation.   

back to top


Extrapulmonary disease due to the RGMs largely takes two forms--localized-direct inoculation, typically in normal hosts, and disseminated-multifocal disease, usually associated with an immunosuppressed state. Notable in the latter group is the relative paucity of disseminated RGM infection in persons with AIDS. Among nearly 2,000 cases of disseminated mycobacterial infections in persons with AIDS reported by the CDC in 1989 there were only 10 instances of RGM disease (21). Given the frequency with which the RGMs can be isolated from the environment, their infrequency in this group suggests possibly that an alternative immune mechanism is primarily responsible for defense against the RGMs. Direct inoculation disease with RGM occurs both with environmental puncture wounds (1530-32) and with iatrogenic procedures including the injection of inflamed joints or bursae with steroids (33). Endocarditis may evolve in the presence of chronic infection with RGMs elsewhere (14). One case of meningitis due to M. fortuitum has been reported in association with a puncture wound and foreign body, while another has been reported with AIDS (35).  


The RGM predictably grow rapidly on culture medium when subcultured in the laboratory. However, on initial isolation from respiratory secretions, abscesses, or other body tissues, recovery may take several weeks. The usual method of diagnosis is mycobacterial blood cultures in patients with AIDS.


Mycobacteria are successful intracellular pathogens that not only penetrate host defense cells, but replicate within them. Organisms engulfed by the macrophages are taken into intracellular vacuoles and the prevention of acidification of the intracellular vacuole may be an important mechanism of mycobacterial evasion of host defenses and a virulence factor. If the mycobacteria persists and multiplies, within the macrophage, then a lymphocyte-mediated immune response including CD4+ T lymphocytes and natural killer (NK) cells is triggered by the infected macrophage. The infected macrophage and stimulated lymphocytes then produce soluble factors, including cytokines and prostaglandins that modulate a complicated immune interaction. The immune mediators include tumor necrosis factor (TNF)-a, interferon (IFN)-g, interleukins (IL) 2,6,10 and 12, and granulocyte-macrophage colony stimulating factor. Because most non tuberculous mycobacteria (NTM) are non pathogenic and those NTM that are pathogens frequently cause disease in limited circumstances, there is interest in identifying virulence factors for NTM. Plasmids may encode for virulence genes, as they are more common in MAC isolates from people who have AIDS than in environmental isolates. Other potential virulence factors are prevention of acidification of phagocytic vesicles, prevention of phagosome-lysosome fusion, delay in TNF secretion by infected host cells and catalase activity.  

back to top


The RGM generally show in vitro resistance to the standard anti-tuberculosis agents. In addition, RGM species show variable patterns of susceptibility to the drugs most likely to be active against that species, e.g., even wild strains (not previously exposed to antimicrobial therapy) do not have consistent patterns of in vitro susceptibility. Furthermore, it is common to find disparate results between different laboratories. The technique which appears most reliable is both microdilution (3,37,38). A recent study compared the reproducibility of Etest strips at various centers with various isolates of M. abscessusM. chelonae, and M. fortuitum (51). Unfortunately, the Etest performed unreliably in this trial. 

The probabilities of in vitro susceptibility to the three major pathogenic species of RGM are delineated in Table 1. Although these data may be assumed to be generally helpful in selecting drug regimens, it is important to emphasize that the validity of in vitro susceptibility testing (correlation with clinical outcomes) for RGM therapy has not been proven in rigorous trials. Important variables include the methodology of the in vitro susceptibility testing technique and the choice of "critical concentrations". No evidence documents in vitro synergistic or antagonistic drug interactions. Multidrug therapy is typically employed to prevent the evolution of acquired drug resistance; however, the utility of this practice has not been clearly demonstrated. No distinctions regarding optimal regimens in the setting of pulmonary, extrapulmonary, or disseminated disease have been made, although the understandable inference is commonly made that disseminated disease and/or immunocompromised hosts merit more aggressive treatment (more drugs, higher doses, and/or longer therapy).  

back to top


In large measure, treatment of RGM disease is empirical and derived from the principles enumerated above rather than randomized trials. For patients with disease due toM. abscessus a regimen of cefoxitin 2 grams IV every 8 hours and amikacin 15 mg/kg IV daily has been widely used. Clarithromycin 500 mg IV orally twice-daily or imipenem 500 mg IV every 8 hours may be substituted for Cefoxitin. The duration of treatment is usually in the range of 8 to 12 weeks depending upon extent and type of disease, response to therapy and tolerance; For those with M. chelonae disease, therapy might entail clarithromycin 500 mg orally twice-daily with amikacin 15 mg/kg IV daily. Although some cases have been rerouted of a curative response to mono-therapy to clarithromycin, it seems prudent to employ two-drug therapy when possible, to prevent or delay acquired drug resistance. 

For cases with serious infection due to M. fortuitum initial therapy might included imipenem 500 mg IV every 8 hours and amikacin 15 mg/kg IV daily. Given the expanded list of agents active versus the usual strain of M. fortuitum, it may be possible to switch to an all-oral regimen after 4 to 8 weeks of intravenous treatment. The decision to modify chemotherapy in RGM cases is usually driven evidence of lack of efficacy (persistent or worsening constitutional symptoms or progressive local disease) or drug toxicity (rash and fever related to cefoxitin or 8th nerve dysfunction related to aminoglycosides).

The RGM have been reported to involve a variety of organs or tissues depending upon the route of infection and host defenses. Obviously, the most ominous forms include mediastinitis, endocarditis, and meningitis. In these situations aggressive therapy including expanded 3 or 4 drug regimens (until reliable susceptibility results from an established laboratory such as The University of Texas in Tyler or National Jewish Medical and Research Center in Denver are reported) and high-dosing are appropriate.  

Alternative Therapy 

In cases of in vitro resistance to or intolerance of the agents enumerated above, we should select agents based on the likelihood of activity (see Table 1) or demonstrated favorable MICs. A promising agent based on in vitro activity and a small clinical experience is linezolid (46). However, caution is warranted based on reports of rerouted hematologic complications (28) and painful peripheral neuritis (MD Iseman, unpublished data).  

back to top


The role of surgery in the management of RGM disease varies according to the form and location of the infection. For cases of pulmonary disease in which there is anatomically localized disease, chemotherapy followed by resection may be useful in minimizing symptoms, slowing the progression, or--in a few cases--actually curing the disease (16) (MD Iseman, unpublished data). For extrapulmonary disease, drainage or debridement of necrotic debris may promote healing of localized abscesses. Aggressive debridement has proven particularly helpful in our care of RGM infections of the hand where tendinous damage may seriously threaten function. Also, we have observed the complimentary role of surgical debridement of lower extremity multinodular abscesses as described above. Topical heat may be useful in some superficial abscesses. 

Immune modulation may be appropriate in some cases. Certainly for patients whose RGM disease appears related to immunosuppressive drug therapy (steroids, cytotoxic agents, anti-rejection medications), reducing these agents to their minimally required dosages is desirable. The role of IFN-g as an immunity-enhancing adjuvant for "normal hosts" with refractory pulmonary RGM disease has not been determined. Bronchial hygiene is an essential and often overlooked element of management of patients with bronchiectatic pulmonary RGM disease. Inhaled beta-agonists may be useful both for bronchodilating (a substantial portion of patients with bronchiectasis develop reversible obstructive airways dysfunction) and accelerating ciliary activity (to help clear secretions). Purulent secretions may be cleared more effectively with the use of the Flutter-Valve® or Pep-Valve® variously combined with postural drainage, clapping, or vibration techniques. In addition, attention should be directed toward the potential for non-mycobacterial bronchitis with organisms such as Pseudomonas aeruginosa or other gram-negative rods, which may require periodic intensive antibiotic therapy.  

back to top


Patients with RGM disease should be monitored with a matrix of clinical, microbiological, radiographic and/or other laboratory techniques. The obvious desired endpoints are clinical and microbiological "cures", but these are difficult to achieve with most RGM disease. In particular, pulmonary disease due to M. abscessus and M. chelonae are extremely difficult to eliminate, with relapses occurring in the great majority of treated cases (16). M. fortuitum pulmonary disease, due in part to the availability of long-term suppressive therapy with oral agents, may be more amenable to medical cures (16). 

Reduction of cough and phlegm are the most immediate markers of clinical response. Semi-quantitative enumeration of sputum smears and cultures also reflect the impact of drug therapy. Routine chest x-rays and computed tomographic radiography studies are useful adjuncts to stage and assess response to treatment. 

Treatment for pulmonary RGM disease varies in duration. For M. fortuitum cases in which there is susceptibility to both oral and parenteral agents, treatment may consist of an initial intensive phase of "mixed" (oral and parenteral) treatment for six to twelve weeks followed by four to nine months of oral suppressive drugs. For M. abscessus or M. chelonae disease we typically treat for six to twelve weeks with a two-drug parenteral regimen directed at suppression of symptoms. Such treatment is initiated when patients find their cough, congestion, or malaise too severe to tolerate, but it is done so with the explicit understanding that treatment palliative, not curative. The patients are also informed that repeated use of these antibiotics entails the risk of acquired resistance to or toxicity from the agents employed. Also it must be emphasized that most patients do not have good insurance coverage for home intravenous therapy and that the arrangements are likely to be both expensive and awkward. Hence, such treatment is not entered into lightly. 

Treatment of extrapulmonary or disseminated disease due to RGM varies according to the site and extent of infection. In some cases, simple drainage may be adequate to promote a cure of a local abscess. In other cases, protracted therapy with multiple antibiotics may be required to eradicate the infection. In most cases, inflammatory collections associated with RGM infection, should be drained surgically. In some cases radical debridement is necessary to affect cure. We have found magnetic resonance imaging to be a useful technique to delineate the boundaries of the inflamed tissue. MRI is generally superior to computed tomography in characterizing soft tissue or peri-osseous abscesses. 

Toxicity monitoring must include periodic audiometric and vestibular testing as well as blood tests for renal dysfunction for persons receiving aminoglycosides. Pharmacokinetic assessment with aminoglycosides will help reduce the likelihood of oto-vestibular toxicity, nerve or renal injury. Symptomatic surveillance for diarrhea, a potential indicator of pseudomembranous colitis--especially for those receiving cefoxitin--and interval tests of hematologic function are required for all of the RGM agents.

back to top


There are no vaccines for RGM.  


There are no preventive measures for RGM. Most data suggest that nosocomial infections with RGM are acquired from the environment rather than primary contamination of devices or products (48).


1. Bolan G, Reingold AL, Carson LA, Silcox VA, Woodley CL, Hayes PS, Hightower AW, McFarland L, Brown JW 3rd, Petersen NJ, et al. Infections with Mycobacterium chelonae in patients receiving dialysis and using processed hemodialyzers. J. Infect. Dis. 1985; 152:1013-1019. [PubMed]

2. Borghans JG, Stanford JL. Mycobacterium chelonei in abscesses after injection of diphtheriea-pertussis-tetanus-polio vaccine. Am Rev Respir Dis 1973; 107:1-8. [PubMed]

3. Brown BA, Swenson JM, Wallace RJ Jr. Broth microdilution MIC test for rapidly growing mycobacteria,. In: Isenberg HD, ed. Clinical Microbiology Procedures Handbook. Washington, D.C.: American Society for Microbiology, 1994:5.11.1. [PubMed]

4. Brown BA, Wallace RJ Jr., Onyi GO, De Rosa V, Wallace RJ 3rd. Activities of four macrolides, including clarithromycin, against Mycobacterium fortuitumMycobacterium chelonae, and m. chelonae-like organisms. Antimicrob. Agents Chemother. 1992; 36:180-184. [PubMed]

5. Burke DS, Ullian RB. Megaesophagus and pneumonia associated with Mycobacterium chelonei. A case report and a literature review. Am. Rev. Respir. Dis. 1977; 116:1101-1107. [PubMed]

6. Burns DN, Wallace RJ Jr, Schultz ME, Zhang YS, Zubairi SQ, Pang YJ, Gibert CL, Brown BA, Noel ES, Gordin FM. Nosocomial outbreak of respiratory tract colonization with Mycobacterium fortuitum: Demonstration of the usefulness of pulsed-field gel electrophoresis in an epidemiologic investigation. Am. Rev. Respir. Dis. 1991; 144:1153-1159.[PubMed]

7. Centers for Disease Control. Infection with Mycobacterium abscessus associated with intramuscular injection of adrenal cortex extract--Colorado and Wyoming, 1995-1996. M.M.W.R. 1996; 45:713-715. [PubMed]

8. Centers for Disease Control and Prevention. Rapidly growing mycobacterial infection following liposuction and liposculpture -- Caracas, Venezuela, 1996-1998. M.M.W.R. 1998; 47:1065-1067. [PubMed]

9. Chetchotisakd P, Mootsikapun P, Anunnatsiri S, Jirarattanapochai K, Choonhakarn C, Chaiprasert A, Ubol PN, Wheat LJ, Davis TE. Disseminated infection due to rapidly growing mycobacteria in immunocompetent hosts presenting with chronic lymphadenopathy: A previously unrecognized clinical entity. Clin. Infect. Dis. 2000; 30:29-34. [PubMed]

10. Cooper JF, Lichtenstein MJ, Graham BS, Schaffner W. Mycobacterium chelonae: A cause of nodular skin lesions with a proclivity for renal transplant recipients. Am. J. Med. 1989; 86:173-177. [PubMed]

11. Cutay AM, Horowitz HW, Pooley RW, Van Horn K, Wormser GP. Infection of epicardial pacemaker wires due to Mycobacterium abscessus. Clin. Infect. Dis. 1998; 26:520-521. [PubMed]

12. DeGroote MA, Huitt GA, Fulton K, Michaelis S, Brown K. Retrospective analysis of aspiration risk and genetic predisposition in bronchiectasis patients with and without non-tuberculous mycobacteria infection. Am. J. Respir. Crit. Care Med. 2001; 163:A763. [PubMed]

13. Falkinham JO. Epidemiology of infection by nontuberculous mycobacteria. Clin. Microbiol. Rev. 1996; 9:177-215.[PubMed]

14. Galil K, Thurer R, Glatter K, Barlam T. Disseminated Mycobacterium chelonae infection resulting in endocarditis. Clin. Infect. Dis. 1996; 23:1322-1323. [PubMed]

15. Gangadharam PR, Hsu KH. Mycobacterium abscessus infection in a puncture wound. Am. Rev. Respir. Dis. 1972; 106:275-277. [PubMed]

16. Griffith DE, Girard WM, Wallace RJ Jr. Clinical features of pulmonary disease caused by rapidly growing mycobacteria. An analysis of 154 patients. Am. Rev. Respir. Dis. 1993; 147:1271-1278. [PubMed]

17. Gubler JG, Salfinger M, von Graevenitz A. Pseudoepidemic of nontuberculous mycobacteria. Chest 1992; 101:245-249. [PubMed]

18. Hakim A, Hisam N, Reuman PD. Environmental mycobacterial peritonitis complicating peritoneal dialysis: Three cases and review. Clin. Infect. Dis. 1993; 16:426-431.[PubMed]

19. Hale YM, Pfyffer GE, Salfinger M. Laboratory diagnosis of mycobacterial infections: New tools and lessons learned. Clin. Infect. Dis. 2001; 33:834-846. [PubMed]

20. Hoffman PC, Fraser DW, Robicsek F, O'Bar PR, Mauney CU. Two outbreaks of sternal wound infections due to organisms of the Mycobacterium fortuitum complex. J. Infect. Dis. 1981; 143:533-542. [PubMed]

21. Horsburgh CR Jr., Selik RM. The epidemiology of disseminated nontuberculous mycobacterial infection in the acquired immunodeficiency syndrome (AIDS). Am. Rev. Respir. Dis. 1989; 139:4-7. [PubMed]

22. Ingram CW, Tanner DC, Durack DT, Kernodle GW Jr., Corey GR. Disseminated infection with rapidly growing mycobacteria. Clin. Infect. Dis. 1993; 16:463-471. [PubMed]

23. Iseman MD, Buschman DL, Ackerson LM. Pectus excavatum and scoliosis: Thoracic anomalies associated with pulmonary disease due to M. avium complex. Am. Rev. Respir. Dis. 1991; 144:914-916. [PubMed]

24. Jauregui L, Arbulu A, Wilson F. Osteomyelitis, pericarditis, mediastinitis, and vasculitis due to Mycobacterium chelonei. Am. Rev. Respir. Dis. 1977; 115:699-703. [PubMed]

25. Khooshabeh R, Grange JM, Yates MD, McCartney ACE, Casey TA. A case report of Mycobacterium chelonae keratitis and a review of mycobacterial infections of the eye and orbit. Tuberc. Lung Dis. 1994; 75:377-382. [PubMed]

26. Kuritsky JN, Bullen MG, Broome CV, Silcox VA, Good RC, Wallace RJ Jr. Sternal wound infections and endocarditis due to organisms of the Mycobacterium fortuitumcomplex. Ann. Intern. Med. 1983; 98:938-939. [PubMed]

27. Laskowski LF, Marr JJ, Spernoga JF, Frank NJ, Barner HB, Kaiser G, Tyras DH. Fastidious mycobacteria grown from porcine prosthetic-heart-valve cultures. N. Engl. J. Med. 1977; 297:101-102. [PubMed]

28. Lawyer MC, Lawyer EZ. Linezolid and reversible myelsuppression. Journal of the American Medical Association 2001; 286:1974. [PubMed]

29. Lowry PW, Jarvis WR, Oberle AD, Bland LA, Silberman R, Bocchini JA Jr, Dean HD, Swenson JM, Wallace RJ Jr. Mycobacterium chelonae causing otitis media in an ear-nose-and-throat practice. N. Engl. J. Med. 1988; 319:978-982. [PubMed]

30. Meredith FT, Sexton DJ. Mycobacterium abscessus osteomyelitis following a plantar puncture wound. Clin. Infect. Dis. 1996; 23:651-653. [PubMed]

31. Newton JA Jr., Weiss PJ, Bowler WA, Oldfield EC 3rd. Soft-tissue infection due to mycobacterium smegmatis: Report of two cases. Clin. Infect. Dis. 1993; 16:531-533.[PubMed]

32. Periyakoil V, Krasner C. Mycobacterium abscessus osteomyelitis following a plantar puncture wound. Clin. Infect. Dis. 1996; 23:651-653. [PubMed]

33. Phillips MS, von Reyn CF. Nosocomial infections due to nontuberculous mycobacteria. Clin. Infect. Dis. 2001; 33:1363-1374. [PubMed]

34. Safranek TJ, Jarvis WR, Carson LA, Cusick LB, Bland LA, Swenson JM, Silcox VA. Mycobacterium chelonae wound infections after plastic surgery employing contaminated gentian violet skin-marking solution. N. Engl. J. Med. 1987; 317:197-201. [PubMed]

35. Santamaría-Jaúregui J, Sanz-Hospital J, Berenguer J, Munoz D, Gómez-Mampaso E, Bouza E. Meningitis caused by Mycobacterium fortuitum. Am. Rev. Respir. Dis. 1984; 130:136-137. [PubMed]

36. Stone MS, Wallace RJ, Swenson JM, Thornsberry C, Christiensen LA. An agar disk elution method for clinical susceptibility testing of Mycobacterium marinum and theMycobacterium fortuitum-complex to sulfonamides and antibiotics. Antimicrob. Agents Chemother. 1983; 34:486. [PubMed]

37. Swenson JM, Thornsberry C, Silcox VA. Rapidly growing mycobacteria: testing of susceptibility to 34 antimicrobial agents by broth microdilution. Antimicrob. Agents Chemother. 1982; 22:186-192. [PubMed]

38. Swenson JM, Wallace RJ, Silcox VA, Thornsberry C. Antimicrobial susceptibility testing of 5 subgroups of Mycobacterium fortuitum and Mycobacterium chelonae. Antimicrob. Agents Chemother. 1985; 28:807. [PubMed]

39. Trulock EP, Bolman RM, Genton R. Pulmonary disease caused by Mycobacterium chelonae in a heart-lung transplant recipient with obliterative bronchiolitis. Am. Rev. Respir. Dis. 1989; 140:802-805. [PubMed]

40. Trupiano JK, Sebek BA, Goldfarb J, Levy LR, Hall GS, Procop GW. Mastitis due to Mycobacterium abscessus after body piercing. Clin. Infect. Dis. 2001; 33:131-134.[PubMed]

41. Vail G, Kohler R, Steiner F, Donepudi R. Successful treatment of Mycobacterium fortuitum prosthetic valve endocarditis: case report. Clin. Infect. Dis. 2000; 30:629-630.[PubMed]

42. Wallace RJ Jr. Treatment of infections caused by rapidly growing mycobacteria in the era of newer macrolides. Res. Microbiol. 1996; 147:30-35. [PubMed]

43. Wallace RJ Jr., Brown BA, Griffith DE. Nosocomial outbreaks/pseudo-outbreaks caused by nontuberculous mycobacteria. Annu. Rev. Microbiol. 1998; 52:453-490.[PubMed]

44. Wallace RJ Jr., Brown BA, Onyi GO. Skin, soft tissue, and bone infections due to Mycobacterium chelonae chelonae: Importance of prior corticosteroid therapy, frequency of disseminated infections, and resistance to oral antimicrobials other than clarithromycin. J. Infect. Dis. 1992; 166:405-412. [PubMed]

45. Wallace RJ Jr., Brown BA, Onyi GO. Susceptibilities of Mycobacterium fortuitum biovar. fortuitum and the two subgroups of Mycobacterium chelonae to Imipenem, Cefmetazole, Cefoxitin, and Amoxicillin-Clavulanic acid. Antimicrob. Agents Chemother. 1991; 35:773-775. [PubMed]

46. Wallace RJ Jr., Brown-Elliott BA, Ward SC, Crist CJ, Mann LB, Wilson RW. Activities of linezolid against rapidly growing mycobacteria. Antimicrob. Agents Chemother. 2001; 45:764-767. [PubMed]

47. Wallace RJ Jr, Musser JM, Hull SI, Silcox VA, Steele LC, Forrester GD, Labidi A, Selander RK. Diversity and sources of rapidly growing mycobacteria associated with infections following cardiac surgery. J. Infect. Dis. 1989; 159:708-716. [PubMed]

48. Wallace RJ Jr., Steele LC, Labidi A, Silcox VA. Heterogeneity among isolates of rapidly growing mycobacteria responsible for infections following augmentation mammaplasty despite case clustering in Texas and other southern coastal states. J. Infect. Dis. 1989; 160:281-288. [PubMed]

49. Wallace RJ Jr., Swenson JM, Silcox VA, Good RC, Tschen JA, Stone MS. Spectrum of disease due to rapidly growing mycobacteria. Rev. Infect. Dis. 1983; 5:657-679.[PubMed]

50. Woo PC, Li JH, Tang W, Yuen KY. Acupuncture mycobacteriosis. N. Engl. J. Med. 2001; 345:842-843. [PubMed]

51. Woods GL, Bergmann JS, Witebsky FG, Fahle GA, Boulet B, Plaunt M, Brown BA, Wallace RJ Jr, Wanger A. Multisite Reproducibility of Etest for Susceptibility Testing ofMycobacterium absessusMycobacterium chelonae, and Mycobacterium fortuitum. J. Clin. Microbiol. 2000; 38:656-661. [PubMed]

back to top


Table 1.  The Probability of in vitro Susceptibility of the Major RGM Pathogens to Various Antimicrobial Agents (4,36,38,45,46).


Agents M. fortuitum M. abscessus M. chelonae

Amikacin (kanamycin)








































  • Wallace's laboratory in Texas describes resistance to cefoxitin as a phenotypic feature of M. chelonae.  By contrast, Heifets’ laboratory at National Jewish reports in vitrosusceptibility in a high proportion of isolates identified as M. chelonae.  In comparing these results it appears as though the discrepancy has to do mainly with species identification rather than variation in susceptibility testing.

Review articles

Cober E, Kaul DR. Non-Tuberculous Mycobacteria in Solid Organ Transplant Recipients.

Mege JL, Meghari S, Honstettre A, Capo C, Raoult D.  The Two faces of interleukin 10 in human infectious diseases.  Lancet Infectious Diseases 2006:7;557-569.]

Griffith DE, Aksamit T, Brown-Elliott BA, Catanzaro A, Daley C, et al.  An Official ATS/IDSA Statement: Diagnosis, Treatment, and Prevention of Nontuberculous Mycobacterial Diseases.  Am J Respir Crit Car Med 2007;175:367-416.

An Official ATS/IDSA Statement: Diagnosis, Treatment, and Prevention of Nontuberculosis Mycobacterial Diseases. Am J Respir Crit Care Med 2007:175;367-416.



Clinical Manifestations





Group IV: Rapid Growing Mycobacteria (RGM)