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Infections with atypical mycobacteria in Australia during 2000 occurred at a rate of 1.8 cases per 100,000 population. The main sites of disease were the respiratory tract, soft tissue, and the lymphatics. The Mycobacterium avium complex was the most common group of mycobacteria isolated from respiratory, lymphatic sites, and blood. The rapidly growing mycobacteria, predominantly the M. fortuitum-M. abscessus-M. chelonae group were the most common soft tissue infections. Atypical mycobacteria were isolated from significant numbers of sputum 'smear positive' patients, requiring further tests to exclude M. tuberculosis. Geographical differences were observed for some Mycobacterium species, notably the isolation of M. haemophilum from Western Australia, and M. ulcerans from Victoria and Queensland. Newer molecular techniques, while improving precision and accuracy of identification, raise additional questions about the ecology of the atypical mycobacteria and their role in disease. Commun Dis Intell 2003;27:180-189.

Introduction

Mycobacteria other than the Mycobacterium tuberculosis complex (commonly referred to as 'atypical', 'nontuberculous', 'environmental' mycobacteria, etc) have been implicated in a variety of clinical conditions including tuberculosis-like pulmonary disease, lymphadenitis, superficial and soft tissue infections, and severe disseminated disease. In addition to humans, a variety of animals, birds, reptiles and fish are susceptible to infection with atypical mycobacteria (AM). Modern taxonomic tools have identified many new species of AM, the majority of which are considered potential pathogens, given appropriate host conditions. Unlike tuberculosis, atypical mycobacteriosis is rarely a disease of public health importance, although nosocomial and iatrogenic outbreaks have been recorded. On the other hand, clinical management of atypical mycobacteriosis can be difficult, depending on the species involved, the site of disease, and co-existing host factors. Many AM infections are refractory to treatment with standard anti-tuberculosis agents.

In Australia, as in Europe and the United States of America, increased reporting of atypical mycobacterial disease can be attributed to a growing pool of immunosuppressed patients (particularly HIV+), and greater awareness on the part of clinical and laboratory personnel. A substantial proportion of laboratory resources in mycobacterial reference laboratories in industrialised countries is expended in the isolation, identification and susceptibility testing of AM. Many of these isolates are not associated with disease, but represent colonisation or environmental contamination of the patient.

Although the AM are environmental organisms, much remains to be elucidated with regard to their ecology and epidemiology. While disease due to M. avium complex (MAC) is apparently common throughout the developed world, species such as M. xenopi and M. malmoense are encountered more commonly in Europe than in the United States of America or Australia. Data for atypical mycobacteriosis in Australia are limited, primarily because cases are not notifiable in every state or territory, cases are not included in the National Mycobacterial Surveillance Scheme, and not all recovered AM are fully identified.

The results of a collaborative study undertaken by the Australian Mycobacterium Reference Laboratory Network (AMRLN) on patients whose specimens were culture-positive for AM in 2000 are reported here.

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Methods

The data in this report are based on clinical specimens that were culture-positive for AM during the calendar year 2000. Almost 80 laboratories performed culture for mycobacteria in 2000 (Royal College of Pathologists of Australasia Quality Assurance Program) and mycobacterial isolates from Australian patients were forwarded to one of the five laboratories that comprise the AMRLN. The reference laboratories identify isolates to species level using standard procedures such as evaluation of phenotypic characteristics, commercial probes, 16S rDNA sequencing, and high performance liquid chromatography.

Reference laboratories provide specific identification of isolates from patients who are likely to have mycobacterial disease, e.g. smear-positive specimens from the respiratory or urinary tract, tissues and biopsies, usually sterile sites, and wound swabs. Single isolates of AM from the respiratory or urinary tract were less likely to be identified to species level as their clinical significance was often doubtful, and the laboratory techniques were expensive and time-consuming. Indeed, these isolates may never be referred to a reference laboratory. For these reasons, the total figure for AM isolations in 2000 (n=1,447) must be regarded as conservative.

For each patient, the nature of the first clinical specimen that yielded an isolate was used to record the nominal site of disease. Patients who had been culture positive for AM in previous years were excluded from the study. For each patient, the following data were collected:

• a unique identifier (usually a laboratory accession number);
• age and sex;
• specimen source of isolate;
• result of acid-fast microscopy; and
• species (or species complex) of isolate.

The reference laboratories liaised with the responsible medical practitioner in an attempt to ascribe clinical significance to each isolate. In cases where HIV-sero-positivity was known, such information was also recorded.

Results were categorised as:

• clinically significant (defined as 'associated with disease');
• not clinically significant (defined as 'colonising' or 'environmental contaminant'); or
• undetermined (including unknown and uncertain).

Data were forwarded to the study coordinators in a standard Excel spreadsheet.

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Results

Isolates from 1,447 patients were included in the study. The AM isolates identified in 2000 by the patient's state or territory of residence and the specimen type are shown in Table 1. The majority of isolates (78.7%) were from pulmonary sources. When all AM isolates were considered, the incidence was 7.5 cases per 100,000 population. There were wide variations between the jurisdictions, from a low of 5.5 cases (New South Wales) to 71.3 cases (Northern Territory) per 100,000 population. The isolate was considered associated with disease, for 341 of 1,447 (23.6%) patients, an incidence of 1.8 cases per 100,000 of population (Table 1). Incidence rates for disease in jurisdictions ranged from 0.78 cases (New South Wales) to 4.1 cases (Northern Territory) cases per 100,000 population.

Table 1. Specimen source of new isolates of atypical mycobacteria by state or territory, Australia, 2000

	Specimen source of isolate				Total	Cases per 100,000 population
	Pulmonary	Lymphatic	Soft tissue	Other
NSW	290 (10)	7 (7)	10 (9)	53 (25)	360 (51)	5.5 (0.78)
NT	135 (4)	1 (1)	3 (2)	1 (1)	140 (8)	71.3 (4.1)
Qld	181 (43)	10 (9)	88 (78)	8 (6)	287 (136)	8.0 (3.8)
SA	73 (12)	3 (3)	4 (4)	4 (2)	84 (21)	5.6 (1.4)
Vic.	259 (20)	20 (20)	21 (20)	22 (4)	322 (64)	6.7 (1.3)
WA	201 (19)	20 (20)	18 (18)	15 (4)	254 (61)	13.4 (3.2)
Total	1,139 (108)	61 (60)	144 (131)	103 (42)	1,447 (341)	7.5 (1.77)
Cases per 100,000 population	5.91 (0.56)	0.32 (0.31)	0.75 (0.68)	0.53 (0.22)	7.5 (1.77)

Numbers in parenthesis refer to cases in which the mycobacterium isolated was judged to be a pathogen.
'Pulmonary' refers to any tissue derived from the lungs (sputum, bronchoscopic collections, biopsies, etc) but not pleurae.
'Lymphatic' refers to any tissue, pus or aspirate clearly associated with a lymph node.
'Soft tissue' refers to skin-associated tissue or pus; bone and joint.
'Other' includes pleural fluid, blood, urine and any isolate from an undefined site.

Since there were few isolates from the Australian Capital Territory, isolations were included with those for New South Wales, and Tasmania was included into that for the testing state (mostly Western Australia).

Although almost all isolates from lymph node (98.4%) and soft tissue (91.0%) were clinically significant, only 108 (9.5%) of 1,139 pulmonary isolates were associated with disease. Incidence rates for each of the four categories of site of disease were less than one isolate per 100,000 population. These data suggest that soft tissue infections are more prevalent in Queensland, and lymph node infections are more common in Western Australia and Victoria (Table 2), but these data need to be interpreted with caution.

Table 2. Predominant species identified among disease-associated isolates of atypical mycobacteria

	Specimen source of isolate
	Pulmonary	Lymphatic	Soft tissue	Other
NSW	n=10	n=7	n=9	n=25
	M.   kansasii (6)	M.   avium complex (6)	M.   fortuitum comp (4)	M.   avium (18)
	M.   avium complex (4)	M.   xenopi (1)	M.   chelonae (2)	M.   intracellulare (6)
			M.   marinum (2)
			M.   abscessus (1)
NT	n=4	n=1	n=2	n=1
	M.   avium complex (4)	M.   avium complex (1)	M.   fortuitum (2)	M.   avium complex (1)
Qld	n=43	n=9	n=78	n=6
	M.   avium complex (24)	M.   avium complex (8)	M.   fortuitum comp (28)	M.   avium (4)
	M.   kansasii (9)	M.  species (1)	M.   marinum (14)	M.   abscessus (2)
	M.   abscessus (7)		M.   chelonae (10)
			M.   abscessus (8)
			M.   ulcerans (7)
Vic.	n=20	n=20	n=20	n=4
	M.   avium complex (17)	M.   avium complex (18)	M.   chelonae (5)	M.   avium (2)
	M.   kansasii (1)	M.   scrofulaceum (2)	M.   haemophilum (3)
			M.   ulcerans (2)
			M.   abscessus (2)
			M.   marinum(2)
SA	n=12	n=3	n=4	n=2
	M.   avium complex (12)	M.   avium complex (3)	M.   marinum (2)	M.   avium complex (2)
			M.   abscessus (1)
			M.   fortuitum (1)
WA	n=19	n=20	n=18	n=4
	M.   avium complex (12)	M.   avium complex (12)	M.   haemophilum (6)	M.   avium (2)
	M.   kansasii (5)	M.   haemophilum (6)	M.   marinum (4)	M.   abscessus (2)
		M.   malmoense (1)	M.   abscessus (2)
		M.  species (1)	M.   fortuitum (2)

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Atypical mycobacteria and site of disease

The M. avium complex was the predominant disease-associated atypical mycobacteriosis in pulmonary (73/108, 67.6%) and lymphatic (48/60, 80%) sites. M. kansasii was found in 21 of 108, (19.4%) pulmonary samples. The M. fortuitum complex, the M. chelonae - M. abscessus group and M. marinum were common isolates from soft tissue (37/131, 28.2%, 31/131, 23.7% and 24/131, 18.3% respectively). M. ulcerans was only recovered from soft tissue in Queensland (n=7) and Victoria (n=2) (Table 2).

Age and site of disease for clinically relevant atypical mycobacteria

The age distribution of mycobacterial disease for the categories of pulmonary, lymphatic and soft tissues are presented in Table 3.

Table 3. Age distribution for new patients from whom a 'pathogenic' atypical mycobacterium was isolated

Age range	Pulmonary	Lymphatic	Soft tissue
	%	%	%
<10 years	0	83	8
10 to 50	23	5	50
>50 years	77	12	42

Lymphatic disease occurred primarily in children, (50/60, 83%), although 7 of 60 (11.7%) cases were diagnosed in adults greater than 50 years of age. In contrast, no pulmonary disease was found in persons less than 10 years of age. Disease of soft tissue occurred less commonly (9%) in the under 10 years age group.

Isolation of atypical mycobacteria from the respiratory tract

There were 1,139 isolates cultured from the respiratory tract representing 78.7 per cent of all isolates (Table 1). Culture-positive specimens collected at bronchoscopy or by gastric lavage were considered to be of pulmonary origin. Only 108 of 1,139 (9.5%) isolates were considered to be disease associated, implying that over 90 per cent of AM cultured from respiratory specimens were not clinically significant. Members of the Mycobacterium avium complex (MAC) were the most common organism isolated accounting for 586 of 1,139 (51.4%) pulmonary isolates (Table 4). Seventy-two of 108 (67.3%) clinically relevant isolates were MAC. There were a small number (n=4) of MAC identified as MAC-X's, a group closely related to, but genetically distinct from M. avium and M. intracellulare¹(Table 5).

Table 4. Species or species complexes identified among atypical mycobacteria from pulmonary sources

	State or territory						Total
	NSW	NT	Qld	SA	Vic.	WA
M. avium complex	164 (4)	47 (4)	106 (24)	37 (12)	119 (16)	113 (12)	586 (72)
M. gordonae	28 (0)		1 (0)	1 (0)	48 (0)	18 (0)	96 (0)
M. fortuitum complex	26 (0)	5 (0)	8 (1)	1 (0)	25 (0)	8 (0)	73 (1)
M. abscessus	13 (0)	1 (0)	20 (7)	1 (0)	5 (0)		40 (7)
M. kansasii	6 (6)	1 (0)	10 (9)		8 (1)	6 (5)	31 (21)
M. chelonae	8 (0)		4 (0)	1 (0)	8 (0)	1 (0)	22 (0)
M. xenopi	5 (0)		1 (0)		3 (0)		9 (0)
M. simiae	6 (0)					1 (0)	7 (0)
M. asiaticum		6 (0)					6 (0)
M. interjectum		1 (0)				3 (0)	4 (0)
M. shimoidei	1 (0)	1 (0)			1 (1)	1 (1)	4 (2)
M. lentiflavum		1 (0)			1 (0)	1 (0)	3 (0)
M. malmoense		1 (0)	1 (0)			1 (1)	3 (1)
M. szulga		1 (0)			1 (1)		2 (1)
M. heckeshornense					1 (0)		1 (0)
Other Mycobacterium sp.	33 (0)	18 (0)	3 (0)		26 (0)	8 (0)	88 (0)
Slow-growers (unidentified)		52 (0)	21 (1)	32 (0)	12 (0)	40 (0)	157 (1)
Rapid-growers (unidentified)			6 (1)		1 (0)		7 (1)
Total	290 (10)	135 (4)	181 (43)	73 (12)	259 (19)	201 (19)	1,139 (107)

Numbers in parenthesis refer to cases in which the mycobacterium isolated was judged to be a pathogen

Table 5. Analysis of disease-associated isolates of MAC

	M.   intracellulare	M.   avium	MAC-x
Pulmonary	19	13	4
Lymphatic	15	7	1

The Queensland, New South Wales and Western Australian reference laboratories use techniques to identify MAC to species level (M. avium, M. intracellulare or MAC-X). The other MRL's use a commercial probe to report the three entities as Mycobacterium avium complex and these identifications are described as 'MAC' in the tables. Mycobacterium intracellulare was recovered almost twice as often as M. avium (ratio of 1.8:1) from pulmonary specimens (data not shown). For clinically relevant isolates identified to species level the ratio was slightly lower (1.5:1) (Table 5). Of the other organisms that were fully identified from pulmonary samples, the 'rapidly growing' mycobacteria and M. gordonae appear to be the next most commonly isolated organisms. Only 2 of 164 (1.2%) mycobacteria described as unidentified slowly (or rapidly) growing mycobacteria were disease associated (Table 4).

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Smear-positivity and association with pulmonary disease

Smear-positivity was not a reliable indicator of disease in pulmonary samples. Approximately 10 per cent of samples in which disease was not established were smear positive for acid fast bacilli. In contrast, some 50 per cent of cases where the recovered AM was deemed to be associated with disease were smear positive (data not shown).

Isolation of atypical mycobacteria from soft tissue and other sites

Soft tissue comprises skin, connective tissue, bone and joint but not blood or lymph node. 'Other sites' include pleural fluid, blood, urine and any isolate from an undefined site.

Of the 144 soft tissue isolates, 131 (91.0%) were considered disease associated. For 'other sites', 42 of 103 (40.8%) isolates were considered clinically relevant (Tables 1 and 2).

Queensland reported 88 of all 144 (61.1%) AM isolates from soft tissue, and of these, 78 of 88 (88.6%) were disease associated. Mycobacterium marinum,M. ulcerans and the rapidly growing mycobacteria were all isolated more frequently compared with the other jurisdictions. The Northern Territory and South Australia reported the fewest cases of soft tissue disease.

In 2000, Mycobacterium haemophilum was isolated only in Western Australia and Victoria, although it has been isolated from the other states and territories previously.

Almost all isolates of rapid growing mycobacteria (e.g. M. fortuitum complex/ M. chelonae-M. abscessus) were considered pathogenic. The significance of MAC isolations from other sites was frequently uncertain. Mycobacterium heckeshornense was recovered from synovial fluid, blood, and sputum from three different patients in Victoria. It was considered a significant finding in the two sterile sites, but of uncertain significance in sputum.

Isolation of atypical mycobacteria from lymphatic tissue

Most lymphatic disease occurred in children. Almost all (98.4%) AM isolated from lymphatic tissue were considered disease associated, representing an incidence rate of 0.31 isolates per 100,000 population (Table 1). Forty-eight of 60 (80.0%) AM were MAC, and of those that were identified to species level, 15 of 23 (65.2%) were M. avium, 7 of 23 (30.4%) were M. intracellulare, and there was a single MAC-X strain isolated (Table 5). In Western Australia, M. haemophilum was recovered from lymphatic tissue on six occasions (Table 2).

Isolation of atypical mycobacteria from blood

Twenty-nine AM were cultured from blood, and of these 25 of 29 (86.2%) isolates were MAC. Almost half the isolations were from New South Wales. Of the MAC identified to species level, 19 of 20 (95%) isolates were M. avium (Table 6). The recently described M. heckeshornense² was recovered from the blood of a Victorian patient. The HIV status of 12 of 29 (41.4%) patients were known and are shown in bold (Table 6).

Table 6. Isolation of atypical mycobacteria from blood, 2000

	State or territory						Total
	NSW	NT	Qld	SA	Vic.	WA
M. avium	13		4			2	19
M. intracellulare	1						1
MAC		1		2	2		5
M. chelonae	1				1		2
M. heckeshornense					1		1
Rapid grower			1				1
Total	15	1	5	2	4	2	29

Known HIV positive cases are in bold.

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Discussion

The present report, based on laboratory data obtained for the year 2000, is an attempt to describe the association of AM with clinical specimens and clinical disease. Conservatively, in the year 2000, there were 1.8 bacteriologically confirmed cases of disease caused by AM per 100,000 population, compared with 4.0 cases of bacteriologically confirmed tuberculosis per 100,000 population.³

In contrast to bacteriological confirmation of tuberculosis, where isolation of the causative agent almost always represents disease, the association between the isolation of AM and clinical disease is less frequent. Australian laboratories undertaking mycobacteriological investigations are increasingly using a broth-based culture system as their primary medium rather than the traditional solid media. The newer systems offer the advantage of reduced time to detection of positive cultures, but they also recover a greater number of AM.^4,5,6,7 Rapid techniques for the preliminary identification of mycobacteria are increasingly available to non-reference laboratories. These tests distinguish between members of the Mycobacterium tuberculosis complex and the AM (AccuProbe; Gen-Probe Inc, San Diego, California). A single, AM isolate from a smear negative sputum or urine specimen is, initially of doubtful clinical relevance and as further identification of the AM isolate is not usually warranted, it may not be forwarded to an AMRLN laboratory for additional testing. For this reason the total numbers of recovered AM in this report do not represent all isolations of AM and the calculated rates of AM disease are likely to be under-estimates.

Most AM are ubiquitous, free-living organisms that may be found in a wide variety of environments including soil, dust, air and water. Water appears to be a particularly attractive environment for AM, and they have been recovered from water distribution systems worldwide.^6,7 It is assumed that most people are infected from environmental sources, but isolation of AM from clinical specimens does not necessarily imply disease. The present report found that less than 10 per cent of AM recovered from the respiratory tract was associated with disease and that sputum smear positivity was not a reliable indicator for disease. The American Thoracic Society have developed diagnostic criteria, based on a combination of clinical, radiological and laboratory findings for pulmonary disease caused by AM.⁸

The last AM Survey conducted by the Special Interest Group in 1988 (David Dawson, unpublished data) produced data similar to the current survey. In 1988, there were 334 significant AM cases, with an incidence rate of two cases per 100,000 population. There were 81 pulmonary cases, 88 lymphatic cases but only 51 soft tissue cases. The figures for MAC were also similar in the 1988 survey (70 cases). However, there was a threefold increase in M. kansasii in 2000 (21 cases compared to only seven cases in 1988), and twice the number of M. fortuitum, M. marinum and M. ulcerans were recovered from soft tissue in 2000. This is probably a reflection of improved technology and skill in recovering AM, rather than an increased infection rate (Table 2).

In an attempt to see if pathogenicity (or lack thereof) could be linked to a particular organism recovered from a pulmonary specimen, data for all slowly growing AM were reviewed (Table 4). M. gordonae, recovered from 96 patients, was never associated with pulmonary disease. M. fortuitum complex organisms (recovered from 73 patients) were rarely associated with disease. M. abscessus (7/40) was more frequently associated with disease than M. chelonae (0/22) although the incidence was still low. M. kansasii, was usually considered pathogenic (21/31). M. asiaticum was isolated only in the Northern Territory and does not appear to be disease associated. Unfortunately the figures are too small to draw conclusions for the other species. As molecular identification methods become more accessible it may be possible to identify species in the many isolates (more than 14% in this survey) that conventional methods cannot identify and to clarify associations between AM species and clinical disease.

Organisms recovered from soft tissue were almost always considered to be clinically significant. There was a higher recovery rate noted from Queensland (61.1% of all isolations) than from other states. M. haemophilum was only isolated in Western Australia (from 6 lymph nodes and from 6 soft tissues) and Victoria (3 soft tissue). This is unlikely to be a reflection of geographical differences but differences in laboratory testing of appropriate tissues for M. haemophilum. While reference laboratories routinely culture lymph nodes, bone/joint and skin samples for this pathogen, which has special growth requirements, this however, may not be the case in routine clinical laboratories. Knowledge of M. haemophilum ecology is still incomplete but it has been isolated from pulmonary sites in immuno-compromised patients. In a detailed analysis of Australian data covering the period 1977-2000 (presented at the Australian Society for Microbiology's Annual Scientific Meeting in Perth, Western Australia in 2001, by this author) it was shown that M. haemophilum was recovered as often from immuno-competent persons as from immuno-compromised (non-HIV) ones, and more often than in HIV+ persons.

Editorial note: The following paragraph was printed incorrectly. The corrected paragraph is reprinted below. 2 September 2003.

The most common isolate from lymphatic tissue was MAC, (48/60 = 80%). Not all MAC are fully identified to species level, so complete data for M. avium and M. intracellulare are unavailable. Where data were available there were twice as many (lymphatic) M. intracellulare isolations as M. avium (Table 5). M. avium accounted for 23 per cent of pulmonary and 57 per cent of lymphatic MAIS disease in 1988, somewhat different (36%, 30% respectively) for MAC disease seen in 2000.

Atypical mycobacteria cause disease in Australia, with an incidence conservatively estimated at 1.8 cases per 100,000 population. The main sites of disease are in soft tissue, pulmonary and in the lymphatics. Pulmonary AM infections may also present as sputum 'smear positive' requiring further tests to exclude Mycobacterium tuberculosis. The Mycobacterium avium complex is the most common encountered mycobacteria, isolated from blood, pulmonary and lymphatic sites in both disease and non-disease. The pathogenic rapid growing mycobacteria (M. fortuitum-M. abscessus-M. chelonae group) were common in the soft tissue infections.

A better understanding of the ecology and etiology of AM in light of the emerging diversity of the genus (as demonstrated by the number of new species described in the past 10 years) will require reference laboratories to continually improve their laboratory practices and identify clinically relevant isolates to species level.

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Acknowledgements

Special thanks to David Dawson for his continued contribution to the work on mycobacterial disease in Australia, despite his recent 'retirement'! Also special thanks to Richard Lumb for invaluable help with this manuscript and to the other members of AMRLN, particularly Peter Howard, Chris Gilpin, and Aina Sievers. Finally, thanks to all the involved members of the Mycobacteria Special Interest Group and the many medical officers and associated health professionals who took the time and effort to supply useful diagnostic information.

The Mycobacterium Reference Laboratory Network comprises:

• Queensland Health Pathology Service, Prince Charles Hospital, Chermside, Queensland.
• Institute of Medical and Veterinary Science, Adelaide, South Australia.
• Victorian Infectious Diseases Reference Laboratory, North Melbourne, Victoria.
• Institute for Clinical Pathology and Medical Research, Westmead, New South Wales.
• Western Australian Centre for Pathology and Medical Research (PathCentre), Nedlands, Western Australia.

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References

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2. Roth A, Reischl U, Schonfeld N, Naumann L, Emler S, Fischer M, et al. Mycobacterium heckeshornense sp. nov. A new pathogenic slowly growing Mycobacterium sp. Causing cavitary lung disease in an immunocompetent patient. J Clin Microbiol 2000 Nov;38:4102-4107.

3. Lumb R, Bastian I. Tuberculosis in Australia: bacteriologically confirmed cases and drug resistance, 2000: Report of the Australian Mycobacterium Laboratory Reference Network. Commun Dis Intell 2002;26:226-233.

3. Badak FZ, Kiska DL, Setterquist S, Hartley C, O'Connell MA, Hopfer RL. Comparison of mycobacteria growth indicator tube with BACTEC 460 for detection and recovery of mycobacteria from clinical specimens. J Clin Microbiol 1996;34:2236-2239.

4. Casal M, Gutierrez J, Vaquero M. Comparative evaluation of the mycobacteria growth indicator tube with the BACTEC 460 TB system and Lowenstein-Jensen medium for isolation of mycobacteria from clinical specimens. Int J Tuberc Lung Dis 1997;1:81-84.

5. Cornfield D B, Beavis KG, Greene JA, Bojak M, Bondi J. Mycobacterial growth and bacterial contamination in the mycobacteria growth indicator tube and BACTEC 460 culture systems. J Clin Microbiol 1997;35:2068-2071.

6. Pfyffer G E, Welcher HM, Kissling P, Cieslak C, Casal MJ, Gutierrez J, et al. Comparison of the mycobacteria growth indicator tube (MGIT) with radiometric and solid culture for recovery of acid-fast bacilli. J Clin Microbiol 1997;35:364-368.

7. Kubica GP, Wayne LG. The mycobacteria: a sourcebook (Part A and B). Marcel Dekker, Inc; 1984

8. Wayne GW, Sramek HA. Agents of newly recognised or infrequently encountered mycobacterial diseases. Clin Microbiol Rev 1992;5:1-25.

9. Wallace RJ, et al. Diagnosis and treatment of disease caused by nontuberculosis mycobacteria (Official statement of the American Thoracic Society). Am Rev Respir Dis 1990;142:940-53.

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Author affiliations

Correspondence: Dr Frank Haverkort, Senior Medical Scientist, Mycobacterium Reference Laboratory, Western Australian Centre for Pathology and Medical Research (PathCentre), Locked Bag 2009, Nedlands WA 6909. Telephone: +61 8 9346 2162. Facsimile: +61 8 9346 3354. Email: frank.haverkort@health.wa.gov.au


This article was published in Communicable Diseases Intelligence Volume 27, No 2, June 2003.