Open access peer-reviewed chapter

Nontuberculous Mycobacterial Infections: Negligent and Emerging Pathogens

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Thet Tun Aung and Roger W. Beuerman

Submitted: November 23rd, 2017 Reviewed: July 23rd, 2018 Published: November 5th, 2018

DOI: 10.5772/intechopen.80444

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Nontuberculous mycobacteria (NTM) are a heterogeneous group of microorganisms other than Mycobacterium tuberculosis (M. tuberculosis) complex and Mycobacterium leprae. NTM infections have increased globally and are now considered an emerging infection as they are often encountered in developed countries. NTMs require extended treatment adding considerably to the economic burden. The increasing number of patients with immunocompromised disorders, increasing usage of immunosuppressive agents, general awareness of the NTM diseases due to the advancement in molecular diagnostic techniques and aging of the population increase the prevalence rate of NTM infections. However, several barriers such as the requirement of better diagnostic techniques, settled treatment guidelines, clinician awareness and knowledge of pathogenesis are limiting and NTM infections are often not treated promptly. Etiology and epidemiology of NTM infections [Mmycobacterium avium complex (slowly growing mycobacteria, SGM) and rapidly growing mycobacteria (RGM)] are discussed in this chapter. Clinical features, diagnosis and currently available treatment guidelines for these infections in skin, eye and lung are summarized. Suggestions for future research directions are suggested particularly for the better understanding of host-pathogen crosstalk and new therapeutic strategies.


  • nontuberculous mycobacteria
  • rapidly growing mycobacteria
  • slowly growing mycobacteria
  • biofilms
  • eye
  • lung
  • skin

1. Introduction

1.1. Etiology, epidemiology and possible sources of NTM infections

The NTM group of mycobacteria is nonmotile aerobic bacilli, acid-fast (AF) staining organisms [1]. The lipid-enriched hydrophobic cell well is usually thicker than other bacteria characterized by tolerance to many disinfectants, heavy metals and antibiotics [1, 2]. They are frequently found in the environment such as soil and water. They readily form biofilms, which contributes to their resistance against a variety of antibiotics [3] as well as high temperatures and a wide range of pH [4]. Environmental recovery of these NTM is the same when they do in similar culture techniques in different geographical regions [5]. However, western countries are reporting a greater prevalence of NTM infections compared to Tuberculosis (TB) than most Asian countries due to very stringent prevention and treatment of tuberculosis [6]. Not all the culture-positive samples represent infection and only half of the culture-positive patients have active respiratory infections, highlighting that NTM can be silent in presence of a normal immune response [7]. Reports suggest that older patients and women have higher chances of NTM infections [8]. As an outcome of the Human Immunodeficiency Virus (HIV) epidemic, NTM infections are frequently isolated from the blood of HIV patients [9]. In the United States, NTM cultures (more than 90%) are from pulmonary disease [10]. According to the Infectious Diseases Society of American Emerging Infections Network and Information from referral centers report, NTM infections are emerging pathogens, particularly rapidly growing mycobacteria (RGM) such as Mycobacterium abscessus (M. abscessus), Mycobacterium chelonae (M. chelonae) and Mycobacterium fortuitum (M. fortuitum) [11]. The prevalence and trend of NTM pulmonary infections are increasing, particularly in Florida and New York, calculated from United States census data from 1998 through 2005 [12]. NTM are the most common pathogens after cosmetic surgeries such as tattooing and Laser in situ keratomileusis (LASIK) [13, 14]. Increasing reports of NTM infections are expected in eye, skin, and lung due to the popularity of LASIK, increasing population of immunocompromised patients and older population. NTM pulmonary infections are found in the areas with heavy population, indicating that urban water supply increases individual’s exposures to NTM [15]. NTM infections are frequently associated with farmers in Japan, suggesting that soil is the main source of infection there [16]. For NTM lung infections, aerosolization of droplets by bathroom showers may be another route of infection [17]. Water is considered to be a normal habitat for NTM and households with low water heater temperature are found to correlate with NTM infections [18]. Hospital water supply is considered to be vital in controlling NTM infections and dialysis solutions contaminations have led to the NTM outbreaks [19, 20, 21]. Contaminated tap water and increased demand of cosmetic surgeries in freestanding health centers that cannot be reviewed frequently by the infectious diseases control center are other concerns for NTM outbreaks [22].

1.2. Runyon’s classification

Runyon classified NTM into four groups, I–IV [23, 24, 25]. Group I, photochromogens, which usually grow slowly about 2–4 weeks and change to yellow with light exposure. Group II, scotochromogens, consist mainly of M. gordonae and appear as yellow colonies at 2–4 weeks in agar plates when cultured in the dark. Group III are nonphotochromogens, slowly growing mycobacteria, which grow slowly over 2–4 weeks. The rapid growers, group IV NTMs are the most pathogenic and important for human disease. They are divided into three subgroups: M. fortuitum, M. chelonae/abscessus, and M. smegmatis. According to the literature, they are susceptible to various antibiotics such as sulfonamide, polymyxin B, and the third- and fourth-generation fluoroquinolones [25]. Group III organisms are lung pathogens and Group IV organisms are the most important and prevalent strains for the eye, lung cutaneous and subcutaneous infections [25].

1.3. Laboratory diagnosis and barriers

Culture technique is the typical standard method for the identification of suspicious NTM. The organisms must be cultured on specific media such as AF smear, Lowenstein-Jensen (LJ) media, Middlebrook media and MacConkey agar since it cannot be differentiated by Gram-stain [26]. The organisms must be cultured in both liquid medium for growing a large amount of organism for other tests and solid medium to observe colony morphology and characteristic [27]. Moreover, the organisms should be further identified into subspecies level for different appropriate antimicrobial therapy. Subspecies level can be achieved by using gene sequencing, high-performance liquid chromatography (HPLC), and molecular-based methods [28]. HPLC is a fast, reliable method for identifying NTM. However, HPLC has limitations: it cannot separate between M. abscessus and M. fortuitum/M. chelonae [29]. Molecular probes, acridinium ester-labeled DNA probes have been made commercially and approved by the U.S. Food and Drug Administration (FDA) for the rapid identification of NTM [30]. MicroSeq 500 16S rDNA Bacterial Sequencing Kit (PE Applied Biosystems, Foster City, CA) has been developed to identify the NTM strain [31]. However, misdiagnoses frequently occur due to the low frequency of these infections, coupled with a lack of diagnostic experience for NTM infections, as well as confusing morphological features in stained smears [28]. Misdiagnosis can be complicated by incorrectly correlating laboratory results by physicians [32]. Misdiagnosis of NTM infections can lead to fatal incidents and NTM often exhibit the microbiological features of Corynebacterium species with long filamentous beaded appearances [33, 34]. NTM microscopic features are also similar to Nocardia species [35]. Therefore, clinicians are taking note of these emerging infections for prompt and focused diagnosis to initiate effective treatment.

1.4. NTM incidence in Singapore (2007–2017)

The incidences of NTM cases in Singapore are rising in the recent years, about 3000 cases per year [36] (Figure 1). Among NTM, M. abscessus is responsible for most of the identified NTM cases in Singapore, followed by M. fortuitum, M. avium complex and M. chelonae (Figure 1).

Figure 1.

Bar graph showing the incidences of NTM in Singapore (2007–2017). Other NTM consists of M. szulgai, M. terrae complex, M. haemophilum, M. intracellulare, M. marinum, M. mucogenicum, M. neoaurum, M. scrofulaceum, M. simiae, M. mageritense, M. wolinskyi, M. asiaticum, M. celatum, M. chimaera, M. duvalli, M. cookii, M. cosmeticum, M. chlorophenolicum, M. genavense, M. kubicae, M. lentiflavum, M. mantenii, M. obuense, M. stomatepiae, M. triplex and M. xenopi.


2. NTM cutaneous and subcutaneous infections

2.1. Mycobacterium abscessus

M. abscessus, a fast-growing NTM, is commonly found in water drainage systems and sewage. It is a subset of the M. chelonae complex and it is vital to segregate from the M. chelonae complex due to the dissimilar antibacterial treatment option. It is well known that the clinical success of M. abscessus depends on the host’s immune defense [37]. It was reported that M. abscessus caused posttransplant infection in cystic fibrosis (CF) patients in spite of having antimicrobial treatment [38]. They are responsible for the major causes of skin and soft tissue infections in the literatures [39] and they are the most common cause of identified NTM infections in Singapore (Figure 1). The path of entries for this organism is direct inoculation such as skin piercing or injury [40] or secondary involvement from disseminated infection [41]. The most likely source of infection is from tap water. Water and soil are the natural habitats for M. abscessus [4, 42]. M. abscessus outbreaks have been reported in clinic and hospitals worldwide and the contaminated instruments or disinfectants are the major sources of the outbreaks [41].

2.1.1. Clinical features and causes of M. abscessus cutaneous and subcutaneous infections

M. abscessus infected skin usually presents with painful, swollen and tender to the touch, accompanying with pus-filled vesicles. Nonspecific symptoms of infections may be present such as fever with chills, muscle aches, and malaise. Causes of M. abscessus infections include posttraumatic wound infections [20], postinjection wound infections [20] and surgical wound infections (mammoplasties, plastic surgeries, and heart surgeries) [20].

2.2. Mycobacterium fortuitum

M. fortuitum is a principal cause of cutaneous and subcutaneous infections associated with catheters [43, 44] as well as post surgical wound infections [45]. The route of entry for M. fortuitum is direct inoculation from contaminated water through the lesions.

2.2.1. Clinical features and causes of M. fortuitum cutaneous and subcutaneous infections

Small, erythematous papules are frequent signs of the early stages of infection and large, fluctuant, painful violaceous boils and ulcerations are signs for late stage infections [45, 46]. They can be caused by mesotherapy and present with indurated, erythematous and violaceous papules with 3–20 numbers, the diameter ranging from 0.5 to 6 cm, accompanied by inguinal or axillary lymphadenopathy [47]. M. fortuitum can also be recovered from blood and purulent discharge from patients with venous catheters [43, 44] and is the cause of post surgical wound infections such as liver transplant patients, electromyography and punch biopsy procedures [44, 48, 49].

2.3. Mycobacterium chelonae

M. chelonae infections are usually associated with immunocompromised hosts such as HIV patients [50]. It can be seen in postsurgical wounds and can disseminate hematogenoulsy to cause sepsis. Contaminated water is the most common source of infection and the route of entry is direct inoculation.

2.3.1. Clinical features and causes of M. chelonae cutaneous and subcutaneous infections

Circumscribed, red, infiltrative plaques, umbilicated papules, and pustules on the upper part of the body and face are features of M. chelonae skin lesions and frequently accompanied by cervical lymphadenopathy [51]. Immunocompromised patients, HIV/AIDS patients often contract M. chelonae infections [50]. Kidney transplant patients, liver transplant patients, tattooing, kidney dialysis patients and peritoneal dialysis patients are also frequently associated with M. chelonae infections [13, 52, 53]. Reports suggest that immunosuppressive drugs such as prednisolone, methotrexate, and adalimumab [54, 55], and autoimmune diseases such as Cushing’s syndrome and rheumatoid arthritis are often associated with M. chelonae skin infections [55, 56].

2.4. NTM cutaneous and subcutaneous infections

The correct choice of antimicrobial agent, anatomic locations of the lesions, intracellular uptake and target binding are essential for the management of NTM cutaneous and subcutaneous infections. Moreover, an appropriate route of drug administration (oral, intravenous or intramuscular), acceptable and effective drug concentration is required for the treatment plan. Drug resistance mechanisms for rapidly growing mycobacteria (RGM) involving erm gene must be considered due to the prolonged treatment period. Therefore, it is critical to differentiate and identify rapidly growing mycobacterial at the subspecies level [25, 57]. The decision of choosing either surgical debridement in combination with mono or multidrug therapy, or only mono or multidrug therapy depends on the anatomical location and severity of the lesion, patient’s immune status with presence of underlying pathology (Table 1) and the Minimum Inhibitory Concentration (MIC) breakpoints from the microbiology lab (Tables 2 and 3).

RGMDisease patternAntimicrobial agents
M. fortuitum2–8 week duration with significant signs and symptomsCombination of amikacin, quinolones or tobramycin (imipenem)
After IV treatment or disease with reduced signs and symptomsLinezolid
M. abscessus2–8 week duration with significant signs and symptomsCombination of clarithromycin, amikacin, cefoxitin (imipenem) or tigecycline
After IV treatment or disease with reduced signs and symptomsLinezolid
M. chelonae2–8 week duration with significant signs and symptomsCombination of clarithromycin, linezolid (tobramycin, imipenem, tigecycline or oral drug)
After IV treatment or disease with reduced signs and symptomsGatifloxacin

Table 1.

Clinicians’ choice of antibiotic regimes for different RGM infections [112].


Table 2.

MIC breakpoints for RGM [112, 113].

M. fortuitumClarithromycinTrailing endpoints, report as resistant
ImipenemNew breakpoint (8–16 μg/ml) for reproducible MIC
M. abscessusAmikacinIf MIC is more than 64 μg/ml, need to repeat/confirm
M. chelonaeTobramycinIf MIC is more than 4 μg/ml, need to repeat/ confirm

Table 3.

Reporting MICs of RGM [112].

2.4.1. M. abscessus cutaneous and subcutaneous infections

Macrolides are the gold standard treatment for M. abscessus infections. They exhibit bactericidal actions against M. abscessus when the lesion has a small population of bacteria. Reports suggest that azithromycin and clarithromycin are the gold standard for treating M. abscessus infections in disseminated cases; however, there are reports suggesting the evolution of resistance against these drugs in prolonged monotherapy [11, 58]. Tigecycline, a new antibiotic, may be another choice for M. abscessus infections [59]. Amikacin is known to be the treatment of choice since it is active against all the subspecies of RGM and imipenem or cefoxitin can be added to overcome treatment failures [11, 58]. Surgical debridement plays a role in the better treatment outcomes for M. abscessus infections [60].

2.4.2. M. fortuitum cutaneous and subcutaneous infections

M. fortuitum infections are chronic in nature and in vitro drug susceptibility tests are required for a guidance of choosing the correct antibiotics. Usually, M. fortuitum are sensitive to several oral antimicrobials such as quinolones, sulfonamides, and macrolides [61, 62]. Amikacin is the treatment of choice for M. fortuitum with 100% efficacy, while sulfonamide and imipenem/cilastatin also account for 100%, clarithromycin stands for 80% and linezolid and doxycycline accounts for 50% [63]. Due to rising chances of bacterial resistance to macrolide due to the inducible erm gene, clarithromycin uses should be carefully assessed and monitored [526364]. Linezolid is another good candidate for M. fortuitum in in vitro; however, more human clinical studies would be warranted for the future use [65]. The minimum 4 months duration of the combination of two drugs is required for severe or critical M. fortuitum cutaneous and subcutaneous infections. Reports are suggested that surgical debridement or surgical drainage is indicated for the better antimicrobial treatment therapy or helping to cure the M. fortuitum infections particularly in extensive disease and abscesses [66]. M. fortuitum usually possess the erm gene, which is inducible to promote resistance to clarithromycin. There was a report showing that sensitivity testing of M. fortuitum isolates showed trailing MICs against macrolides [67]. However, the relevance of the erm gene in M. fortuitum and clarithromycin treatment remains to be determined in clinical management.

2.4.3. M. chelonae cutaneous and subcutaneous infections

Clofazimine is shown to be effective and the addition of sub MIC concentration of amikacin synergies with clofazimine against RGM including M. chelonae [68]. Tobramycin has been suggested to be a better treatment option than amikacin [69]. However, M. chelonae isolates showed resistant to cefoxitin and imipenem is the alternative option. There is MIC susceptibility of clarithromycin (100%), tobramycin (100%), linezolid (90%), imipenem (60%), amikacin (50%), doxycycline (25%), clofazimine (25%) and ciprofloxacin (20%) [63]. However, M. chelonae is susceptible only to clarithromycin, tobramycin, and tigecycline [70]. Monotherapy is not advisable for M. chelonae infections due to its facility to acquire drug resistance and combination treatment is advised [71]. Excision and treatment is still the optimal treatment step in combination with antibiotics in treating M. chelonae cutaneous and subcutaneous infections [66]. Treatment guidelines are not yet reported; however, current guidelines recommend using antimicrobial susceptibility tests to predict therapeutic efficacy.


3. NTM eye infections

3.1. Clinical features and causes of NTM eye infections

The most prevalent NTM strains causing eye infections are M. fortuitum and M. chelonae [7273]. Keratitis is standing as the most common real situation accounting for 69% of ocular NTM infections (Table 4).

Different types of ocular NTM infectionPercentage
1. Ocular surface infections
 a. Keratitis69
 b. Scleritis4.3
 c. Conjunctivitis0.7
2. Periocular and adnexal infections13.3
3. Intraocular infections and uveitis12.6

Table 4.

Different types of ocular infection caused by NTM [14].

Late presentation of symptoms and diagnosis was reported in NTM keratitis [74]. Pain, decreased vision, and photophobia were present in gradual increasing patterns in the course of NTM keratitis [75]. The multifocal or single lesion surrounded by radiating corneal infiltrates, ‘cracked windshield’ appearance, was reported [74, 76, 77]. Infiltrates had irregular margins, mimicking fungal keratitis [78]. Hypopyon is present in untreated or poorly treated cases [74]. There have been reports of infectious crystalline keratopathy, intrastromal opacity and minimal inflammation in some cases of NTM keratitis leading to a misleading diagnosis of herpetic keratitis [79, 80] (Table 5).

Varying degree of painMultiple lesions or single lesion surrounded by the radiating projections
PhotophobiaCracked windshield appearance
Tearing and foreign body sensationHypopyon
Decreased visual acuityMild or Silent anterior chamber

Table 5.

Signs and symptoms of NTM keratitis.

The most common association of NTM keratitis is LASIK (47.6%), followed by trauma (14.8%), foreign body (17.6%), implants (17.3%) and contact lens (6.4%) [14]. LASIK is the most popular refractive corrective surgery implemented worldwide since it offers less stromal scarring and rapid recovery of visual acuity. The symptoms for post-LASIK mycobacterial keratitis are less severe than other causes [26]. The time frame of 3 to 14 weeks duration is reported to present post-LASIK NTM keratitis. Some cases of post-LASIK mycobacterial keratitis present within 10 days post surgery [26, 81]. The most probable route of entry for post-LASIK NTM keratitis is during the surgery. Corneal infiltrates are within the lamellar flap or interface presenting with either single white lesion or multiple white granular appearances. Anterior extension of corneal infiltrates is common to form a corneal ulceration. Late diagnosis or treatment can result in the posterior extension into the corneal stroma. The anterior chamber is usually silent or has the mild inflammatory reaction [26, 82].

3.2. Treatment of NTM eye infections

Management of NTM keratitis is challenging due to its rarity, potential to acquire antibiotic resistance, natural resistance to a variety of commercially available antibiotics and delayed response to antibiotics. Identification of NTM keratitis can be delayed and one report revealed that the time to identification was delayed for 4 months due to slow growth of the organism [83]. Drug sensitivity tests need to be carried out using a prolonged incubation time, resulting in the delayed treatment of NTM eye infections. Moreover, there are several reports showing that a wide range of antibiotic sensitivities exists in different isolates [84]. Consequently, a combination of two or three drugs helps to prevent acquired antibiotic resistance in long-term management and clarithromycin, amikacin, and fourth generation fluoroquinolones are mentioned [85]. Topical delivery is the most used method followed by the combination of topical and systemic administration [14]. Amikacin is known to be the treatment of choice for NTM keratitis, however, there have been reports showing corneal toxicity toward the long-term usage of amikacin in high concentration [86]. According to the systemic review, amikacin was given alone in the majority of NTM keratitis cases, followed by amikacin and macrolide (Table 6) [14]. Fluoroquinolones, particularly fourth-generation fluoroquinolones, have been accepted as effective for eye infections [3, 86]. Fourth generation fluoroquinolones offer noteworthy benefits over the older generations because of their superior bactericidal activity, decreased risk for resistance and higher corneal concentrations. In contrast, one report suggested that the majority of nontuberculous mycobacteria are resistant to second-generation fluoroquinolones, highlighting the better efficacy properties of fourth generation fluoroq-uinolones [87].

Different antibiotic regimenPercentage
Amikacin only29.2
Combination of amikacin and macrolide14.1
Combination of amikacin and fluoroquinolone12.5
Combination of amikacin, fluoroquinolone and macrolide9.4
Combination of fluoroquinolone and macrolide8.3
Other antibiotics7.3
Fluoroquinolone only6.8

Table 6.

Different antibiotic regimens for NTM keratitis [14].

Recent reports suggest a strong synergism between amikacin and fourth generation fluoroquinolone, gatifloxacin, in treating nontuberculous mycobacteria in in vitro and in vivo mouse keratitis model [88]. Moreover, it was reported that the NTM habitat in a keratitis infection is in the biofilm mode (Figure 2) hindering antibiotic penetration and adding DNase to the antibiotic may make a more effective treatment [88]. Surgical debridement can help to facilitate penetration and lower the bacterial load. Topical steroids are controversial for NTM keratitis and one study suggested that a steroid accelerates the infection [89]. Careful follow up of NTM keratitis patients is suggested; if the lesion is in progression, or stromal thinning and symptoms persistence continues after 2 days of antibiotics, drug sensitivity should be rechecked for an alternative sensitive antimicrobial. However, there is no agreed-upon treatment plan for NTM keratitis and more research including evaluation of new treatment plans and an in-depth knowledge of NTM keratitis pathogenesis is warranted to treat NTM keratitis effectively.

Figure 2.

Slit lamp photograph showing central haziness in NTM keratitis mouse model. Confocal microscopy images showing presence of atypical mycobacterial microcolonies biofilm formation (green color) with abundance of extracellular DNA (a major constituent of mycobacterial biofilm matrix in red color) [88].


4. NTM lung infections

4.1. Clinical features and causes of NTM lung infections

NTM lung infections are often due to Mycobacterium avium complex (MAC) and RGM. NTM lung disease may be misdiagnosed as Tuberculosis and require weeks or months [90]. The clinical diagnosis and treatment remain challenging due to its nonspecific symptoms such as low-grade fever, wet chronic cough, weight loss and malaise similar to M. tuberculosis [91]. Radiological imaging is a vital test to screen for NTM lung disease. A broad range of radiological patterns such as bronchiectasis, cavitary lesions, nodular lesions and parenchymal lesions, have been observed in NTM lung disease [92]. However, two major radiological findings have been listed, fibrocavitary and nodular bronchiectatic forms [93]. The first form is similar to pulmonary TB and it usually affects elderly male with underlying pathology of the lung. Cavities with increased opacity are usually seen in the upper parts of the lung in the fibrocavitary form [94]. Thin-walled cavities without lymph node involvement and atelectasis are the common findings in this form [95]. The nodular bronchiectatic form often presents with bilateral, small nodules and multilobar bronchiectasis in the lower and middle parts of the lung [96]. This disease pattern is associated with elderly nonsmoking women without underlying lung diseases [97]. There is a connection between bronchiectasis and NTM lung diseases [98]. Because of NTM’s nonspecific symptoms and similar radiological findings as M. tuberculosis and other lung pathologies, it is extremely hard to diagnose NTM lung disease. Risk factors causing NTM lung disease are still poorly understood but immune status is vital for NTM lung disease. A study showed that disseminated NTM infection is often associated in patients with profound immunosuppression [99]. NTM are important pathogens for patients who have undergone or are awaiting lung transplant and cystic fibrosis patients [100]. Defects in the crucial elements of the host defense such as interleukin-12 (IL-12) and interferon-gamma (IF-γ) increase susceptibility to NTM lung infections [101]. Increasing usage of tumor necrosis factor (TNF-α) receptor antagonists usage enhances NTM infections [102]. The rate of NTM prevalence in TNF-α receptor antagonists usage is 74/100,000 persons per year [103].

4.2. Treatment of NTM lung infections

4.2.1. MAC lung infections

Macrolides are the treatment of choices for MAC lung infections [104]. Rifampin or ethambutol can be added to macrolide administration for 18–24 months [63]. Rifampin 600 mg/kg, ethambutol 25 mg/kg with either azithromycin 500 mg/kg or clarithromycin 1000 mg/kg is frequently given as three-times-weekly intermittent therapy for NTM noncavitary lung disease [63]. It has been suggested that intermittent therapy is more efficient and reduced toxicity than daily therapy [105]. A cocktail of rifampin 10 mg/kg/day, ethambutol 15 mg/kg/day with either azithromycin 250 mg/kg/day or 1000 mg/kg is given daily for cavitary nodular bronchiectatic NTM lung disease, with a possibility of adding either streptomycin or amikacin in the first 2 or 3 months of therapy in severe disease [63].

The addition of moxifloxacin to the standard treatment showed a better response if a standard treatment plan fails [106]. Clofazimine has shown that it can be an alternative option to the rifampin or in refractory MAC lung infections [107]. The successful treatment of NTM lung infections totally relies on the prevention of macrolide-resistant MAC infections with the optimal treatment strategies.

4.2.2. RGM lung infections

The management for RGM lung infections typically depends on drug’s toxicity and drug sensitivity tests. Treatment for M. abscessus lung infection is challenging as shown in previous studies [108]. The recommended guideline for treating RGM lung infection includes a combination of treatment which involves two parenteral antibiotics and an oral macrolide for a relatively long duration (several months) [63]. The most active and useful parenteral agents consist of amikacin 10–15 mg/kg/day, imipenem 500–1000 mg2, cefoxitin 200 mg/kg/day, and tigecycline 50 mg/day [108]. Moxifloxacin has been shown as an alternative option for treating RGM lung infections [109]. Aggressive parenteral therapy is suggested for initial 4 months of treatment accompanied later by a treatment combination of macrolide and linezolid or clofazimine or fluoroquinolone for coping with toxicity [108]. Treatment with macrolides for RGM infection should be carefully accessed on the patient’s tolerance and treatment compliance due to the possibility of drug resistance evolved [110]. Surgical resection should be considered to combine with chemotherapy in treating RGM lung infections [111].


5. Conclusion

Etiology and epidemiology of NTM infections highlight that NTMs are emerging pathogens, warranting more research. Clinical features, barriers in the diagnosis of NTM and a lack of more effective treatment strategies were discussed for NTM infections in lung, skin and eye system. This overview prompts comments that can be made for NTM infections for future research. (1) NTM infections are considered emerging pathogens around the world including Singapore. (2) Better understanding of microbial life in real human clinical scenarios is important in dealing with the easy biofilm forming NTMs. (3) More research is critically needed to fill a huge gap of host-pathogen interactions in NTM infections. (4) A Multidisciplinary approach, better diagnostic tools, increase public awareness and standard treatment guidelines and new therapeutic research is urgently required.


Conflict of interest

TTA, RWB- Nil.


Notes/thanks/other declarations

The authors would like to acknowledge the Central Tuberculosis Laboratory, Department of Microbiology, Singapore General Hospital, for the contribution of Singapore NTM registry. The authors would like to thank the advices and help from A/Prof. Koh Tse Hsien (Department of Microbiology, Singapore General Hospital), A/Prof. Sng Li-Hwei (Central Tuberculosis Laboratory, Singapore General Hospital), A/Prof. Tan Thuan Tong (Department of Infectious Diseases, Singapore General Hospital), A/Prof. Timothy Mark Sebsatian Barkham (Laboratory Medicine, Tan Tock Seng Hospital) and the support of funding from NMRC/TCR/002-SERI/2012/R1018.


  1. 1. Ray C, Ryan K, Enteroviruses. In: Ryan KJ, Ray CG, editors. Sherris Medical Microbiology. 4th ed. New York, USA: The McGraw-Hill Companies; 2004. pp. 531-541
  2. 2. Jarlier V, Nikaido H. Mycobacterial cell wall: Structure and role in natural resistance to antibiotics. FEMS Microbiology Letters. 1994;123(1-2):11-18
  3. 3. Aung TT et al. Biofilms of pathogenic nontuberculous mycobacteria targeted by new therapeutic approaches. Antimicrobial Agents and Chemotherapy. 2016;60(1):24-35
  4. 4. Falkinham Iii J. Surrounded by mycobacteria: Nontuberculous mycobacteria in the human environment. Journal of Applied Microbiology. 2009;107(2):356-367
  5. 5. Von Reyn CF et al. Isolation of Mycobacterium avium complex from water in the United States, Finland, Zaire, and Kenya. Journal of Clinical Microbiology. 1993;31(12):3227-3230
  6. 6. Cassidy PM et al. Nontuberculous mycobacterial disease prevalence and risk factors: A changing epidemiology. Clinical Infectious Diseases. 2009;49(12):e124-e129
  7. 7. Winthrop KL et al. Pulmonary nontuberculous mycobacterial disease prevalence and clinical features: An emerging public health disease. American Journal of Respiratory and Critical Care Medicine. 2010;182(7):977-982
  8. 8. Adjemian J et al. Prevalence of nontuberculous mycobacterial lung disease in US Medicare beneficiaries. American Journal of Respiratory and Critical Care Medicine. 2012;185(8):881-886
  9. 9. Horsburgh CR Jr, RM Selik. The epidemiology of disseminated nontuberculous mycobacterial infection in the acquired immunodeficiency syndrome (AIDS). The American Review of Respiratory Disease. 1989;139(1):4-7
  10. 10. O'Brien RJ, Geiter LJ, Snider DE Jr. The epidemiology of nontuberculous mycobacterial diseases in the United States: Results from a national survey. American Review of Respiratory Disease. 1987;135(5):1007-1014
  11. 11. De Groote MA, Huitt G. Infections due to rapidly growing mycobacteria. Clinical Infectious Diseases. 2006;42(12):1756-1763
  12. 12. Billinger ME et al. Nontuberculous mycobacteria-associated lung disease in hospitalized persons, United States, 1998-2005. Emerging Infectious Diseases. 2009;15(10):1562
  13. 13. Drage LA et al. An outbreak of Mycobacterium chelonae infections in tattoos. Journal of the American Academy of Dermatology. 2010;62(3):501-506
  14. 14. Kheir WJ et al. Nontuberculous mycobacterial ocular infections: A systematic review of the literature. BioMed Research International. 2015;2015:17
  15. 15. Winthrop KL et al. Pulmonary disease associated with nontuberculous mycobacteria, Oregon, USA. Emerging Infectious Diseases. 2011;17(9):1760
  16. 16. Maekawa K et al. Environmental risk factors for pulmonary Mycobacterium avium-intracellulare complex disease. Chest. 2011;140(3):723-729
  17. 17. Falkinham JO et al. Mycobacterium avium in a shower linked to pulmonary disease. Journal of Water and Health. 2008;6(2):209-213
  18. 18. Falkinham JO. Factors influencing the chlorine susceptibility of Mycobacterium avium, Mycobacterium intracellulare, and Mycobacterium scrofulaceum. Applied and Environmental Microbiology. 2003;69(9):5685-5689
  19. 19. Mandel AS et al. State regulation of hospital water temperature. Infection Control & Hospital Epidemiology. 1993;14(11):642-645
  20. 20. Uslan DZ et al. Skin and soft tissue infections due to rapidly growing mycobacteria: Comparison of clinical features, treatment, and susceptibility. Archives of Dermatology. 2006;142(10):1287-1292
  21. 21. Carson LA et al. Prevalence of nontuberculous mycobacteria in water supplies of hemodialysis centers. Applied and Environmental Microbiology. 1988;54(12):3122-3125
  22. 22. Le Dantec C et al. Occurrence of mycobacteria in water treatment lines and in water distribution systems. Applied and Environmental Microbiology. 2002;68(11):5318-5325
  23. 23. Runyon EH. Identification of mycobacterial pathogens utilizing colony characteristics. American Journal of Clinical Pathology. 1970;54(4):578-586
  24. 24. Murray P, Barron E, Pfaller M. Mycobacterium: General characteristics, islation, and staining procedures. In: Manual of Clinical Microbiology. Washington DC: American Society for Microbiology; 2003
  25. 25. Brown-Elliott BA, Wallace RJ. Clinical and taxonomic status of pathogenic nonpigmented or late-pigmenting rapidly growing mycobacteria. Clinical Microbiology Reviews. 2002;15(4):716-746
  26. 26. Moorthy RS, Valluri S, Rao NA. Nontuberculous mycobacterial ocular and adnexal infections. Survey of Ophthalmology. 2012;57(3):202-235
  27. 27. Pfyffer GE, Palicova F. Mycobacterium: General characteristics, laboratory detection, and staining procedures. In: Manual of Clinical Microbiology. 10th ed. Washington DC, USA: American Society of Microbiology; 2011. pp. 472-502
  28. 28. Somoskovi A, Salfinger M. Nontuberculous mycobacteria in respiratory infections: Advances in diagnosis and identification. Clinics in Laboratory Medicine. 2014;34(2):271-295
  29. 29. Butler WR, Guthertz LS. Mycolic acid analysis by high-performance liquid chromatography for identification of Mycobacterium species. Clinical Microbiology Reviews. 2001;14(4):704-726
  30. 30. Somoskövi Á et al. False-positive results for Mycobacterium celatum with the AccuProbe Mycobacterium tuberculosis complex assay. Journal of Clinical Microbiology. 2000;38(7):2743-2745
  31. 31. Hall L et al. Evaluation of the micro Seq system for identification of mycobacteria by 16S ribosomal DNA sequencing and its integration into a routine clinical mycobacteriology laboratory. Journal of Clinical Microbiology. 2003;41(4):1447-1453
  32. 32. Somoskovi A et al. Laboratory diagnosis of nontuberculous mycobacteria. Clinics in Chest Medicine. 2002;23(3):585-597
  33. 33. Boltin D et al. Corynebacterium striatum—A classic pathogen eluding diagnosis. European Journal of Internal Medicine. 2009;20(3):e49-e52
  34. 34. Williamson JC et al. Fatal Mycobacterium abscessus endocarditis misidentified as Corynebacterium spp. Scandinavian Journal of Infectious Diseases. 2010;42(3):222-224
  35. 35. Paul J, Baigrie C, Parums D. Fatal case of disseminated infection with the turtle bacillus Mycobacterium chelonae. Journal of Clinical Pathology. 1992;45(6):528-530
  36. 36. Tang SS et al. Rapidly growing mycobacteria in Singapore, 2006-2011. Clinical Microbiology and Infection. 2015;21(3):236-241
  37. 37. Wang H, Jin P, Wu Q. Disseminated cutaneous infection with Mycobacterium abscessus in a patient with a low CD4+ T cell count. European Journal of Dermatology. 2008;18(3):337-340
  38. 38. Taylor JL, Palmer SM. Mycobacterium abscessus chest wall and pulmonary infection in a cystic fibrosis lung transplant recipient. The Journal of Heart and Lung Transplantation. 2006;25(8):985-988
  39. 39. Lee M-R et al. Mycobacterium abscessus complex infections in humans. Emerging Infectious Diseases. 2015;21(9):1638
  40. 40. Ferringer T, Pride H, Tyler W. Body piercing complicated by atypical mycobacterial infections. Pediatric Dermatology. 2008;25(2):219-222
  41. 41. Kothavade R et al. Clinical and laboratory aspects of the diagnosis and management of cutaneous and subcutaneous infections caused by rapidly growing mycobacteria. European Journal of Clinical Microbiology & Infectious Diseases. 2013;32(2):161-188
  42. 42. Appelgren P et al. Late-onset posttraumatic skin and soft-tissue infections caused by rapid-growing mycobacteria in tsunami survivors. Clinical Infectious Diseases. 2008;47(2):e11-e16
  43. 43. TAZAWA S et al. Mycobacterium fortuitum infection caused by the organism in subcutaneous abscess mediated by central venous catheter. Kekkaku (Tuberculosis). 2006;81(10):609-612
  44. 44. Zainal MA, Tan A. Mycobacterium fortuitum catheter-related sepsis in acute leukaemia. Singapore Medical Journal. 2006;47(6):543
  45. 45. Winthrop KL et al. The clinical management and outcome of nail salon—Acquired Mycobacterium fortuitum skin infection. Clinical Infectious Diseases. 2004;38(1):38-44
  46. 46. Winthrop KL et al. An outbreak of mycobacterial furunculosis associated with footbaths at a nail salon. New England Journal of Medicine. 2002;346(18):1366-1371
  47. 47. Quiñones C et al. An outbreak of Mycobacterium fortuitum cutaneous infection associated with mesotherapy. Journal of the European Academy of Dermatology and Venereology. 2010;24(5):604-606
  48. 48. Ronald Buckley L et al. Mycobacterium fortuitum infection occurring after a punch biopsy procedure. Pediatric Dermatology. 1997;14(4):290-292
  49. 49. Nolan CM, Hashisaki PA, Dundas DF. An outbreak of soft-tissue infections due to Mycobacterium fortuitum associated with electromyography. Journal of Infectious Diseases. 1991;163(5):1150-1153
  50. 50. Ferreira O et al. A cutaneous infection by Mycobacterium chelonae in a patient with rheumatoid arthritis. Dermatology Online Journal. 2010;16(4):3-3
  51. 51. Kullavanijaya P et al. Disseminated Mycobacterium chelonae cutaneous infection: Recalcitrant to combined antibiotic therapy. The Journal of Dermatology. 2003;30(6):485-491
  52. 52. Patel JB et al. Sequence-based identification of Mycobacterium species using the Microseq 500 16S rDNA bacterial identification system. Journal of Clinical Microbiology. 2000;38(1):246-251
  53. 53. Drouineau O et al. Infection cutanée à Mycobacterium chelonae en hémodialyse. Néphrologie & Thérapeutique. 2006;2(3):136-139
  54. 54. Adenis-Lamarre E et al. Cutaneous infection due to Mycobacterium chelonae during anti-TNF therapy. 2009;136(11):811-814
  55. 55. Jankovic M et al. A fatal Mycobacterium chelonae infection in an immunosuppressed patient with systemic lupus erythematosus and concomitant Fahr’s syndrome. Journal of Infection and Chemotherapy. 2011;17(2):264-267
  56. 56. Haas SR, Hodge MB, Duncan RA. Cushing's syndrome presenting as disseminated cutaneous Mycobacterium chelonae infection. Clinical Infectious Diseases. 2001;33(6):e51-e53
  57. 57. Nash KA, Brown-Elliott BA, Wallace RJ. A novel gene, erm (41), confers inducible macrolide resistance to clinical isolates of Mycobacterium abscessus but is absent from Mycobacterium chelonae. Antimicrobial Agents and Chemotherapy. 2009;53(4):1367-1376
  58. 58. Colombo RE, Olivier KN. Diagnosis and treatment of infections caused by rapidly growing mycobacteria. In: Seminars in Respiratory and Critical Care Medicine. New York, USA: Thieme Medical Publishers; 2008
  59. 59. Wallace RJ et al. Comparison of the in vitro activity of the glycylcycline tigecycline (formerly GAR-936) with those of tetracycline, minocycline, and doxycycline against isolates of nontuberculous mycobacteria. Antimicrobial Agents and Chemotherapy. 2002;46(10):3164-3167
  60. 60. Petrini B. Mycobacterium abscessus: An emerging rapid-growing potential pathogen. APMIS. 2006;114(5):319-328
  61. 61. Brown B et al. Activities of four macrolides, including clarithromycin, against Mycobacterium fortuitum, Mycobacterium chelonae, and M. chelonae-like organisms. Antimicrobial Agents and Chemotherapy. 1992;36(1):180-184
  62. 62. Swenson JM et al. Antimicrobial susceptibility of five subgroups of Mycobacterium fortuitum and Mycobacterium chelonae. Antimicrobial Agents and Chemotherapy. 1985;28(6):807-811
  63. 63. Griffith DE et al. An official ATS/IDSA statement: Diagnosis, treatment, and prevention of nontuberculous mycobacterial diseases. American Journal of Respiratory and Critical Care Medicine. 2007;175(4):367-416
  64. 64. Chang C-Y et al. Venous catheter-associated bacteremia caused by rapidly growing mycobacteria at a medical center in Central Taiwan. Journal of Microbiology, Immunology, and Infection = Wei mian yu gan ran za zhi. 2009;42(4):343-350
  65. 65. Srivastava BK et al. Oxazolidinone antibacterials and our experience. Anti-Infective Agents in Medicinal Chemistry (Formerly Current Medicinal Chemistry-Anti-Infective Agents). 2008;7(4):258-280
  66. 66. Girard D et al. Comparison of azithromycin, roxithromycin, and cephalexin penetration kinetics in early and mature abscesses. Journal of Antimicrobial Chemotherapy. 1993;31(suppl_E):17-28
  67. 67. da Costa ARF et al. Molecular identification of rapidly growing mycobacteria isolates from pulmonary specimens of patients in the State of Pará, Amazon region, Brazil. Diagnostic Microbiology and Infectious Disease. 2009;65(4):358-364
  68. 68. Shen G-H et al. High efficacy of clofazimine and its synergistic effect with amikacin against rapidly growing mycobacteria. International Journal of Antimicrobial Agents. 2010;35(4):400-404
  69. 69. Chopra S et al. Identification of antimicrobial activity among FDA-approved drugs for combating Mycobacterium abscessus and Mycobacterium chelonae. Journal of Antimicrobial Chemotherapy. 2011;66(7):1533-1536
  70. 70. Regnier S et al. Clinical management of rapidly growing mycobacterial cutaneous infections in patients after mesotherapy. Clinical Infectious Diseases. 2009;49(9):1358-1364
  71. 71. Tebas P et al. Rapid development of resistance to clarithromycin following monotherapy for disseminated Mycobacterium chelonae infection in a heart transplant patient. Clinical Infectious Diseases. 1995;20(2):443-444
  72. 72. Girgis DO, Karp CL, Miller D. Ocular infections caused by non-tuberculous mycobacteria: Update on epidemiology and management. Clinical & Experimental Ophthalmology. 2012;40(5):467-475
  73. 73. Turner L, Stinson I. Mycobacterium fortuitum: As a cause of corneal ulcer. American Journal of Ophthalmology. 1965;60(2):329-331
  74. 74. Huang S et al. Non-tuberculous mycobacterial keratitis: A study of 22 cases. British Journal of Ophthalmology. 1996;80(11):962-968
  75. 75. Lalitha P, Rathinam S, Srinivasan M. Ocular infections due to non-tuberculous mycobacteria. Indian Journal of Medical Microbiology. 2004;22(4):231
  76. 76. Hu F-R, Huang W-J, Huang S-F. Clinicopathologic study of satellite lesions in nontuberculous mycobacterial keratitis. Japanese Journal of Ophthalmology. 1998;42(2):115-118
  77. 77. Lazar M et al. Mycobacterium fortuitum keratitis. American Journal of Ophthalmology. 1974;78(3):530-532
  78. 78. Brancato R et al. Mycobacterium chelonae keratitis after excimer laser photorefractive keratectomy. Archives of Ophthalmology. 1997;115(10):1316-1318
  79. 79. Hu F-R. Infectious crystalline keratopathy caused by Mycobacterium fortuitum and Pseudomonas aeruginosa. American Journal of Ophthalmology. 1990;109(6):738-739
  80. 80. Dugel PU et al. Mycobacterium fortuitum keratitis. American Journal of Ophthalmology. 1988;105(6):661-669
  81. 81. Alvarenga L et al. Infectious post-LASIK crystalline keratopathy caused by nontuberculous mycobacteria. Cornea. 2002;21(4):426-429
  82. 82. Chang MA, Jain S, Azar DT. Infections following laser in situ keratomileusis: An integration of the published literature. Survey of Ophthalmology. 2004;49(3):269-280
  83. 83. Wunsh SE et al. Mycobacterium fortuitum infection of corneal graft. Archives of Ophthalmology. 1969;82(5):602-607
  84. 84. Abshire R et al. Topical antibacterial therapy for mycobacterial keratitis: Potential for surgical prophylaxis and treatment. Clinical Therapeutics. 2004;26(2):191-196
  85. 85. de la Cruz J, Behlau I, Pineda R. Atypical mycobacteria keratitis after laser in situ keratomileusis unresponsive to fourth-generation fluoroquinolone therapy. Journal of Cataract & Refractive Surgery. 2007;33(7):1318-1321
  86. 86. Ford JG et al. Nontuberculous mycobacterial keratitis in South Florida. Ophthalmology. 1998;105(9):1652-1658
  87. 87. Alexandrakis G, Alfonso EC, Miller D. Shifting trends in bacterial keratitis in South Florida and emerging resistance to fluoroquinolones. Ophthalmology. 2000;107(8):1497-1502
  88. 88. Aung TT et al. Discovery of novel antimycobacterial drug therapy in biofilm of pathogenic nontuberculous mycobacterial keratitis. The Ocular Surface. 2017;15:770-783
  89. 89. Aylward G, Stacey A, Marsh R. Mycobacterium chelonei infection of a corneal graft. British Journal of Ophthalmology. 1987;71(9):690-693
  90. 90. Kwon YS, Koh W-J. Diagnosis of pulmonary tuberculosis and nontuberculous mycobacterial lung disease in Korea. Tuberculosis and Respiratory Diseases. 2014;77(1):1-5
  91. 91. Koh W et al. Pulmonary TB and NTM lung disease: Comparison of characteristics in patients with AFB smear-positive sputum. The International Journal of Tuberculosis and Lung Disease. 2006;10(9):1001-1007
  92. 92. Jeong YJ et al. Nontuberculous mycobacterial pulmonary infection in immunocompetent patients: Comparison of thin-section CT and histopathologic findings. Radiology. 2004;231(3):880-886
  93. 93. Marras TK et al. Opinions differ by expertise in Mycobacterium avium complex disease. Annals of the American Thoracic Society. 2014;11(1):17-22
  94. 94. Yuan M-K et al. Comparative chest computed tomography findings of non-tuberculous mycobacterial lung diseases and pulmonary tuberculosis in patients with acid fast bacilli smear-positive sputum. BMC Pulmonary Medicine. 2014;14(1):65
  95. 95. Chu H et al. Chest imaging comparison between non-tuberculous and tuberculosis mycobacteria in sputum acid fast bacilli smear-positive patients. European Review for Medical and Pharmacological Sciences. 2015;19(13):2429-2439
  96. 96. Koh W-J et al. Bilateral bronchiectasis and bronchiolitis at thin-section CT: Diagnostic implications in nontuberculous mycobacterial pulmonary infection. Radiology. 2005;235(1):282-288
  97. 97. Kim RD et al. Pulmonary nontuberculous mycobacterial disease: Prospective study of a distinct preexisting syndrome. American Journal of Respiratory and Critical Care Medicine. 2008;178(10):1066-1074
  98. 98. Park IK, Olivier KN. Nontuberculous mycobacteria in cystic fibrosis and non–cystic fibrosis bronchiectasis. In: Seminars in Respiratory and Critical Care Medicine. New York, USA: Thieme Medical Publishers; 2015
  99. 99. Horsburgh CR Jr. Epidemiology of disease caused by nontuberculous mycobacteria. 1996;11(4):244-251
  100. 100. Olivier KN et al. Nontuberculous mycobacteria: I: Multicenter prevalence study in cystic fibrosis. American Journal of Respiratory and Critical Care Medicine. 2003;167(6):828-834
  101. 101. Dorman SE, Holland SM. Interferon-γ and interleukin-12 pathway defects and human disease. Cytokine & Growth Factor Reviews. 2000;11(4):321-333
  102. 102. Winthrop KL et al. Nontuberculous mycobacteria infections and anti–tumor necrosis factor-α therapy. Emerging Infectious Diseases. 2009;15(10):1556
  103. 103. Winthrop K et al. Mycobacterial diseases and antitumour necrosis factor therapy in USA. Annals of the Rheumatic Diseases. 2013;72(1):37-42
  104. 104. Egelund EF, Fennelly KP, Peloquin CA. Medications and monitoring in nontuberculous mycobacteria infections. Clinics in Chest Medicine. 2015;36(1):55-66
  105. 105. Wallace RJ et al. Macrolide/azalide therapy for nodular/bronchiectatic Mycobacterium avium complex lung disease. Chest. 2014;146(2):276-282
  106. 106. Koh W-J et al. Treatment of refractory Mycobacterium avium complex lung disease with a moxifloxacin-containing regimen. Antimicrobial Agents and Chemotherapy. 2013;57(5):2281-2285
  107. 107. Jarand J et al. Long-term follow-up of Mycobacterium avium complex lung disease in patients treated with regimens including clofazimine and/or rifampin. Chest. 2016;149(5):1285-1293
  108. 108. Kasperbauer SH, De Groote MA. The treatment of rapidly growing mycobacterial infections. Clinics in Chest Medicine. 2015;36(1):67-78
  109. 109. Kim SY et al. The drug susceptibility profile and inducible resistance to macrolides of Mycobacterium abscessus and Mycobacterium massiliense in Korea. Diagnostic Microbiology and Infectious Disease. 2015;81(2):107-111
  110. 110. Choi G-E et al. Macrolide treatment for Mycobacterium abscessus and Mycobacterium massiliense infection and inducible resistance. American Journal of Respiratory and Critical Care Medicine. 2012;186(9):917-925
  111. 111. Jarand J et al. Clinical and microbiologic outcomes in patients receiving treatment for Mycobacterium abscessus pulmonary disease. Clinical Infectious Diseases. 2011;52(5):565-571
  112. 112. Woods G et al. Susceptibility Testing of Mycobacteria, Nocardiae, and Other Aerobic Actinomycetes; Approved Standard M24-A. Vol. 23, No. 18. Wayne, PA: NCCLS; 2003. pp. 1-56238
  113. 113. Cavusoglu C, Gurpinar T, Ecemis T. Evaluation of antimicrobial susceptibilities of rapidly growing mycobacteria by Sensititre RAPMYCO panel. New Microbiologica. 2012;35(1):73-76

Written By

Thet Tun Aung and Roger W. Beuerman

Submitted: November 23rd, 2017 Reviewed: July 23rd, 2018 Published: November 5th, 2018