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To clarify the structure and function of the airways in Mycobacterium avium-intracellulare (MAI) infection, we performed pulmonary function tests and high-resolution computed tomography (HRCT) of
the thorax in female patients 61 ± 9 yr of age (n = 12) with pulmonary MAI infection without predisposing lung disease and compared their data with those of normal female volunteers 54 ± 8 yr of age
(n = 9). We calculated the E/I ratio, i.e., the average ratio of HRCT number at full expiration to that
at full inspiration, as an index for the evaluation of air trapping distal to the small airways. Patients
showed significant increases in residual volume and slope of phase III (
N2) of the single-breath nitrogen test, and significant decreases in flow at 50 and 25% of FVC, suggesting hyperinflation and
obstruction of the small airways. HRCT of patients revealed the small nodules and ectasis of bronchioles and small bronchi located mainly in segments (S) S2, S3, S4, and S5. The E/I ratio was significantly elevated in patients, and especially higher in the upper lung field than in the lower lung field,
suggesting air trapping distal to the small airways. The difference of E/I ratio between the upper and
lower field is probably related to the segmental distribution of CT abnormalities. These findings suggest that MAI infection can lead to air trapping distal to the small airways.
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INTRODUCTION |
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INTRODUCTION
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Pulmonary infection with Mycobacterium avium-intracellulare (MAI), a nontuberculous mycobacteria, usually occurs in subjects with damaged lungs such as those afflicted with pulmonary tuberculosis, chronic obstructive pulmonary disease (COPD), bronchiectasis, and the lungs of heavy smokers (1, 2), or in persons with immunodeficiency such as AIDS (3). Recent reports (4) have demonstrated the existence of pulmonary infection of MAI without predisposing lung disease and with no demonstrable immunodeficiency (primary MAI infection; PMAI). PMAI occurs predominantly in middle-aged or elderly women and is increasing in the United States (1) and in Japan (9). Computed tomographic (CT) findings of the lung revealed that multiple small nodules and bronchiectasis are characteristic of PMAI (9).
Because these small nodules are located in centrilobular regions and are usually accompanied by the ectasis of bronchioles and small bronchi when identified by high-resolution CT (HRCT), we have speculated that patients with PMAI have a dysfunction of the small airways. Therefore, in the present study, we evaluated the structure and function of the small airways, using pulmonary function tests and the E/I ratio in patients with PMAI. The E/I ratio, proposed by us in a previous report (14), is the average ratio of HRCT number at full expiration to that at full inspiration; the ratio reflects air trapping distal to the small airways.
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Subjects
We studied 12 patients with PMAI and nine normal volunteers as controls (Table 1). The patients presented to the Shinshu University Hospital between January 1996 and August 1997 with complaints of cough, sputum, bloody sputum, and chest pain and/or a further examination because of chest radiographic abnormalities. All patients had abnormal findings on chest radiographs and CT scans, and cultured MAI in sputum on at least two separate occasions (one patient) or in samples obtained from the radiographically affected region using a sterilized fiberoptic bronchoscope (11 patients). They had no other distinct lung disease, as judged from past history and previous chest radiographic and/or CT findings. All had no abnormal findings, which suggested immunodeficiency in routine laboratory tests (Table 2), and they were free from HIV infection when judged by the physical diagnosis.
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All patients and normal volunteers were female nonsmokers. They gave written consent to participate in the study after they had been informed of the nature of all procedures.
Pulmonary Function Tests
Spirometry was performed in triplicate using a rolling-seal-type pulmonary function testing system (Chestac-65V; Chest Co. Ltd., Tokyo,
Japan). VC, FEV1, and FEF25
75 were calculated from the spirogram.
FRC was measured by the He dilution method, after which the subjects immediately inspired to TLC and maximally expired to RV, permitting calculation of subdivisions of the lung volumes. RV/TLC was
calculated. These values were also expressed as a percent of the predicted values, which were determined for VC, FEV1, and RV by the
methods of Baldwin and colleagues (15), Berglund and colleagues
(16), and Grimby and Soderholm (17), respectively. The peak expiratory flow rate (PEF) and flow at 50 and 25% of forced vital capacity
(
50 and 25, respectively) were calculated from the maximal expiratory flow-volume curve (MEFV). The nitrogen slope of phase III
(N2) was measured from the single-breath nitrogen washout curve.
To avoid increased variability in the measurement of the phase III
slope derived from the rate of inspiration or expiration (18, 19), all
subjects were instructed to exhale slowly (0.5 L/s) to RV and then to
inhale 100% oxygen at 0.5 L/s to TLC and without breathholding to
slowly exhale at 0.2 to 0.3 L/s back to RV. The ratio of closing volume
(CV) to VC (CV/VC) was calculated. In this system a flow meter that
can detect the exhalation and inhalation rates was attached in front of
the subjects, which enabled them to control their airflow during the
maneuver. DLCO was measured by the single-breath method (Pulmocorder model R1551S; Anima Co., Tokyo, Japan). The ratio of DLCO
to alveolar volume (DLCO/VA) was calculated. We determined the predicted values for DLCO by the method of Nishida and colleagues (20).
An arterial blood sample was drawn from the brachial artery while the
subject breathed room air to measure PaO2, PaCO2, and pH, using a
blood gas analyzer (ABL-3; Radiometer, Copenhagen, Denmark). All
measurements were performed with subjects in the seated position.
High-Resolution Computed Tomographic Scans
We used a helical (spiral) CT scanner (Hi Speed Advantage; GE
Medical Systems, Milwaukee, WI). After conventional 10-mm-thick contiguous scanning for screening of chest abnormalities, HRCT scanning with 1-mm collimation was performed for the affected regions
and was reviewed by two chest radiologists who had no knowledge of
the patients' clinical data. The presence of small nodules (
5 mm)
and ectasis of bronchioles and small bronchi, which are features considered characteristic of PMAI (9), were evaluated in each of the
18 segments of the lung fields depicted in Table 4.
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For the E/I ratio (14), scanning with 3-mm collimation was performed and HRCT images were reconstructed with bone algorithm. Scanning was done at both full inspiration and full expiration at the
two anatomic levels, e.g., at the level of the right upper lobe bronchus
(the level of the upper lung field) and at the level of the right inferior
pulmonary vein (the level of the lower lung field). HRCT images were
photographed using a window setting appropriate for the lungs (window level, 
700 Hounsfield units [HU]; window width, 1,000 HU).
The average HRCT numbers in each lung field were calculated at full
inspiratory (TLC level) and expiratory positions (RV level). The E/I
ratio was obtained by dividing CT number at RV level by that at TLC
level.
Statistics
The values presented in the text and tables are mean ± standard deviation (SD). One-way analysis of variance and Student's t test were used for comparisons between groups; p < 0.05 was considered significant.
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Subjects' Characteristics
As shown in Table 1, the ages of 12 patients with PMAI (61 ± 9 yr of age) and those of nine normal volunteers (54 ± 8 yr of age) were not significantly different. The patients had significantly lower body weights (46.5 ± 5.3 kg) and body mass index values (19.4 ± 1.9 kg/m2) compared with those of 52.2 ± 6.3 kg and 21.8 ± 2.5 kg/m2, respectively, of the normal volunteers. The body height values were not significantly different between the two groups.
Six (50%) of 12 patients had no symptoms, and they were identified by public health screening chest radiographs. Cough, sputum, bloody sputum, and chest pain were observed but were mild. No patients had night sweats, low grade fever, or dyspnea. No rales were audible in any patient. The results of routine laboratory tests (Table 2) were all within normal range.
Pulmonary Function Tests
The results of PFT in patients with PMAI and in normal volunteers are summarized in Table 3. Although within normal
range, VC (% predicted) was significantly lower in the patients than in the normal volunteers, FEF2575 was significantly lower in the patients with PMAI than in the normal volunteers. The patients with PMAI showed significant increases
in RV (%) (% predicted) and RV/TLC (%), suggesting hyperinflation of the lung. Although FEV1 (% predicted) was
not different between the two groups, significantly lower 50
and 25 and higher N2 values were observed in the patients
with PMAI. DLCO (% predicted), DLCO/VA (ml/min/mm Hg/L) PaO2, and PaCO2 were within normal range in both groups.
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HRCT Appearance
The segmental distribution of small nodules and ectasis of bronchioles and small bronchi in 12 patients with PMAI are summarized in Table 4. These findings were predominant in segments (S) S2, S3, S4, and S5, but they were not frequent in the lower lobes. S1, which is usually affected by pulmonary tuberculosis, was completely free from these opacities. None of the patients had changes suggesting emphysematous destruction of the lung parenchyma.
E/I Ratio
HRCT scans at full inspiration and expiration at the upper and lower field of a patient with PMAI and a normal volunteer are shown in Figures 1 and 2. In the patient with PMAI, multiple small nodules, partially fused, and ectasis of small bronchi were found mainly in right S2, S3, and S4. The density of the lung field at full expiration was not increased as much in the patient with PMAI as in the normal volunteer, suggesting the existence of air trapping.
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As shown in Table 5, the E/I ratio of the total lung field was significantly higher in the 12 patients with PMAI than in the nine normal volunteers. The ratio in the upper lung field was significantly higher than that in the lower lung field in the patients with PMAI. There was no significant difference in the lower lung field between the two groups.
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In the present study, patients with PMAI had significantly
lower 50 and 25, higher N2, and similar FEV1 values compared with those of normal volunteers. These results indicate
that the patients with PMAI had an obstruction in the small
airways (21) that was not detected with the spirometric
method. The lowered FEF2575 also suggested small airways
lesions (24) in the patients with PMAI. Because all of the patients were nonsmokers, had chest CT abnormalities (including multiple nodules and bronchiectasis characteristic of MAI
infection) (9), and had no distinct predisposing lung disease, the structural abnormalities caused by MAI infection might be responsible for the pulmonary dysfunction.
An examination of closing volume can also detect a dysfunction in the small airways (25), but the present patients
with PMAI had normal CV/VC value. Although the reason
for the different results between N2 and CV/VC is not
known, there are two possible explanations. One possibility is
that the sensitivity and specificity might be different between
two indices. Using abnormal FEV1/FVC as a reference diagnosis, Dosman and Cotton (25) determined that CV/VC had a
high degree of specificity, but low sensitivity, whereas N2 was
reasonably specific and sensitive. The other possible reason
could be due to the localization of the MAI infected region. Milic-Emili and colleagues (26) have noted that airway closure occurs more easily in the lower lungs than in the upper
lungs during expiration near to RV because of a gravitational
difference between the apex and the base of the lungs. This
phenomenon and an increased collapsibility of peripheral airways lead to an increased CV/VC when the small airways obstruction occurs. However, because it seems that the upper
lung field is predominantly affected by MAI infection, CV/VC
remains normal.
Comroe and Fowler (27) commented that the identification
of N2 could detect an uneven distribution of inspired gas in
the lungs, though it could not enable the diagnosis of specific
types of pulmonary disease. Some studies have mentioned
that N2 is useful for interpretation of early lung dysfunction,
especially peripheral airway obstruction (22, 25, 28). In the
single-breath nitrogen test, the positive phase III slope depends partially on the apex-to-base difference in the preexpiratory N2 concentration and on the degree of interregional
asynchronous lung emptying (29). Peripheral airflow obstruction increases the time constant for the emptying of intraregional lung units distal to the obstruction, and results in a
higher regional RV for these units (30). Thus, the alveolar
units with narrowed peripheral airways have a high N2 concentration after the inhalation of 100% oxygen to TLC. Because MAI infection was found to affect predominantly the
upper lung field, a much larger interregional RV and higher
N2 concentration might occur in the infected region. This phenomenon is probably the reason for the increased N2 in patients with PMAI.
The interpretation of the increased RV in the patients with PMAI is difficult because HRCT scanning showed no apparent emphysematous changes. One possible explanation is the overestimation of the predicted value of RV. We used the equation of Grimby and Soderholm (17). Our subjects were all Japanese women and their body height were short. The normal volunteers exhibited slightly high RV compared with the 100% baseline. The patients with PMAI, even if we take into account an overestimation of the percent predicted RV, showed significantly higher RV values than did the normal volunteers; thus, the patients with PMAI had hyperinflation of the lungs.
The tests mentioned above to detect the earliest functional abnormalities of the small airways can neither express the potential regional heterogeneity of airway dysfunction nor localize the distribution of the airways involved. Recent CT and/or HRCT scans obtained at full expiration (31), including the E/I ratio (14), have provided insights into the relations between the structure and function of the small airways. These methods are useful to detect earlier changes of emphysematous destruction of the lung parenchyma and air trapping distal to the small airways in COPD and emphysema, and they can demonstrate the distribution of the abnormalities in the lung fields involved. We (14) calculated the E/I ratio in patients with emphysema, and examined the relations among the PFT, the E/I ratio, and the visual scoring (VS) for emphysematous changes, and found that the VS showed a much higher correlation with DLCO/VA, whereas the E/I ratio showed a much stronger correlation with RV/TLC. These finding suggest that the E/I ratio reflects air trapping distal to the small airways (14). In the present study, the higher E/I ratio values in the patients with PMAI has demonstrated that this disorder includes air trapping distal to the small airways. The reason for the difference of distribution in the E/I ratio, i.e., why the ratio was higher in the upper lung field than in the lower field, is probably due to the segmental distribution of small nodules and ectasis of bronchioles and small bronchi.
The small nodules seem to be closely related to the formation of epithelioid granuloma caused by MAI infection (9). However, the genesis of bronchiectasis remains unresolved; it may be a result of the chronic inflammation caused by MAI or caused by the existence of preceding bronchiectasis. Because we (36) recently observed increases in neutrophil and lymphocyte accounts and an elevated level of neutrophil elastase in the BAL fluid obtained from the affected region in the patients with PMAI, we suspect that the ectasis of bronchioles and small bronchi is related to the chronic inflammation caused by MAI. However, as shown in Figure 1, the bronchiectasis of MAI infection was not so distinct when compared with the bronchiectasis caused usually by chronic airway infection, and the results of PFT and E/I ratio in the present study showed the diffuse distribution of small airways dysfunction predominantly in the upper lung fields. Therefore, it is impossible to deny that the dysfunction is due to the constitutional abnormality, though we need further studies to elucidate it.
In summary, we performed pulmonary function testing and
examined the E/I ratio using helical CT scanning in pulmonary MAI infection of patients without distinct predisposing
lung disease and with no demonstrable immunodeficiency,
and we compared their data with those of normal volunteers.
Patients showed significant increases in RV and the E/I ratio,
suggesting air trapping distal to their small airways. In addition, the E/I ratio was higher in the patients' upper lung fields,
a finding that is probably related to the segmental distribution
of the ectatic changes caused by MAI infection. The present
findings suggest that a MAI infection leads to air trapping distal to the small airways. It also seems that the parameter N2
is useful for the detection of early lung dysfunction in patients
infected with MAI.
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Footnotes |
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Correspondence and requests for reprints should be addressed to Keishi Kubo, M.D., First Department of Internal Medicine, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto, 390-8621, Japan. E-mail: keishik{at}gipac.shinshu-u.ac.jp
(Received in original form February 11, 1998 and in revised form May 12, 1998).
Acknowledgments: Supported in part by Grant-in-Aid for Scientific Research (B) No. 08457179 from the Ministry of Education, Science and Culture of Japan.
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References |
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1. Miller, W. T. Jr., and W. T. Miller Sr.. 1993. Pulmonary infections with atypical mycobacteria in the normal host. Semin. Roentgenol. 28: 139-149 [Medline].
2. Wallace, R. J. Jr., J. Glassroth, D. Griffith, K. N. Olivier, J. L. Cook, and F. Gordin. 1997. Diagnosis and treatment of disease caused by nontuberculous mycobacteria. Am. J. Respir. Crit. Care Med. 156: S1-S25 .
3. Kalayjian, R. C., Z. Toossi, J. F. Tomashefski Jr., J. T. Carey, J. A. Ross, J. W. Tomford, and R. J. Blinkhorn Jr.. 1995. Pulmonary disease due to infection by Mycobacterium avium complex in patients with AIDS. Clin. Infect. Dis. 20: 1186-1194 [Medline].
4. Prince, D. S., D. D. Peterson, R. M. Steiner, J. E. Gottlieb, R. Scott, H. L. Israel, W. G. Figueroa, and J. E. Fish. 1989. Infection with Mycobacterium avium complex in patients without predisposing conditions. N. Engl. J. Med. 321: 863-868 [Abstract].
5. Iseman, M. D.. 1989. Mycobacterium avium complex and the normal host: the other side of the coin. N. Engl. J. Med. 321: 896-898 [Medline].
6. Reich, J. M., and R. E. Johnson. 1991. Mycobacterium avium complex pulmonary disease: incidence, presentation, and response to therapy in a community setting. Am. Rev. Respir. Dis. 143: 1381-1385 [Medline].
7.
Reich, J. M., and
R. E. Johnson.
1992.
Mycobacterium avium complex
pulmonary disease presenting as an isolated lingular or middle lobe
pattern: the Lady Windermere Syndrome.
Chest
101:
1605-1609
8. Kennedy, T. P., and D. J. Weber. 1994. Nontuberculous mycobacteria: an underappreciated cause of geriatric lung disease. Am. J. Respir. Crit. Care Med. 149: 1654-1658 [Abstract].
9. Tanaka, E., R. Amitani, A. Niimi, K. Suzuki, T. Murayama, and F. Kuze. 1997. Yield of computed tomography and bronchoscopy for the diagnosis of Mycobacterium avium complex pulmonary disease. Am. J. Respir. Crit. Care Med. 155: 2041-2046 [Abstract].
10.
Hartman, T. E.,
S. J. Swenson, and
D. E. Williams.
1993.
Mycobacterium
avium-intracellulare complex: evaluation with CT.
Radiology
187:
23-26
11.
Moore, E. H..
1993.
Atypical mycobacterial infection in the lung: CT appearance.
Radiology
187:
777-782
12.
Swenson, S. J.,
T. E. Hartman, and
D. E. Williams.
1994.
Computed tomographic diagnosis of Mycobacterium avium-intracellulare complex
in patients with bronchiectasis.
Chest
105:
49-52
13.
Primack, S. L.,
P. M. Logan,
T. E. Hartman,
K. S. Lee, and
N. L. Muller.
1995.
Pulmonary tuberculosis and Mycobacterium avium-intracellulare complex: a comparison of CT findings.
Radiology
194:
413-417
14. Eda, S., K. Kubo, K. Fujimoto, Y. Matsuzawa, M. Sekiguchi, and F. Sakai. 1997. The relations between expiratory chest CT using helical CT and pulmonary function tests in emphysema. Am. J. Respir. Crit. Care Med. 155: 1290-1294 [Abstract].
15. Baldwin, E. D., A. Cournand, and D. W. Richards Jr.. 1948. Pulmonary insufficiency: I. Physiological classification, clinical methods of analysis, standard values in normal subjects. Medicine (Baltimore) 27: 243-278 [Medline].
16. Berglund, E., G. Birath, J. Bjure, G. Grimby, I. Kjellmer, L. Sandqvist, and B. Soderholm. 1963. Spirometric studies in normal subjects: I. Forced expirogram in subjects between 7 and 70 yr of age. Acta Med. Scand. 173: 185-191 [Medline].
17. Grimby, G., and B. Soderholm. 1963. Spirometric studies in normal subjects: III. Static lung volumes and maximum voluntary ventilation in adults with a note on physical fitness. Acta Med. Scand. 173: 199-206 .
18.
Robertson, P. C.,
N. R. Anthonisen, and
D. Ross.
1969.
Effect of inspiratory flow rate on regional distribution of inspired gas.
J. Appl. Physiol.
26:
438-443
19.
Hurst, T. S.,
B. L. Graham, and
D. J. Cotton.
1984.
Fast vs. slow exhalation before O2 inhalation alters subsequent phase III slope.
J. Appl.
Physiol.
56:
52-56
20. Nishida, O., M. Kambe, N. Sewake, M. Takano, H. Kawane, Y. Kodomari, K. Arita, H. Nasuno, and Y. Nishimoto. 1976. Pulmonary function in healthy subjects and its prediction: 5. Pulmonary diffusing capacity in adults. Jpn. J. Clin. Pathol. 24: 941-947 .
21. Macklem, P. T.. 1972. Obstruction in small airways: a challenge to medicine. Am. J. Med. 52: 721-724 [Medline].
22. Petty, T. L., G. W. Silvers, R. E. Stanford, M. D. Baird, and R. S. Mitchell. 1980. Small airway pathology is related to increased closing capacity and abnormal sloe of phase III in exercised human lungs. Am. Rev. Respir. Dis. 121: 449-456 [Medline].
23. Wright, J. L., L. M. Lawson, P. D. Pare, S. Kennedy, B. Wiggs, and J. C. Hogg. 1984. The detection of small airway disease. Am. Rev. Respir. Dis. 129: 989-994 [Medline].
24. Wright, J. L., P. Cagle, A. Churg, T. V. Colby, and J. Myers. 1992. Disease of the small airways. Am. Rev. Respir. Dis. 146: 240-262 [Medline].
25.
Dosman, J. A., and
D. J. Cotton.
1981.
Interpretation of tests of early
lung dysfunction.
Chest
79:
261-262
26.
Milic-Emili, J.,
J. A. Henderson,
M. B. Dolovich,
D. Trop, and
K. Kaneko.
1966.
Regional distribution of inspired gas in the lung.
J.
Appl. Physiol.
21:
749-759
27. Comroe, J. H., and W. S. Fowler. 1951. Lung function studies: VI. Detection of uneven alveolar ventilation during a single breath of oxygen. Am. J. Med. 31: 408-413 .
28. Malmberg, R., B. Simonsson, and E. Berglund. 1963. Airways obstruction and uneven gas distribution in the lung. Thorax 18: 168-171 .
29. Engel, L. A., and P. T. Macklem. 1977. Gas mixing and distribution in the lung. In J. G. Widdicombe, editor. Respiratory Physiology II, Vol. 14. University Park, Baltimore, MD. 37-82.
30.
Otis, A. B.,
C. B. McKerrow,
R. A. Bartlett,
J. Mead,
M. B. McIlroy,
N. J. Selverstone, and
E. P. Radford Jr..
1956.
Mechanical factors in distribution of pulmonary ventilation.
J. Appl. Physiol.
8:
427-443
31.
Knudson, R. J.,
J. R. Standen,
W. T. Kaltenborn,
D. E. Knudson,
K. Rehm,
P. Habib, and
J. D. Newell.
1991.
Expiratory computed tomography for assessment of suspected pulmonary emphysema.
Chest
99:
1357-1366
32.
Heremans, A.,
J. A. Verschakelen,
L. Van Fraeyenhoven, and
M. Demedts.
1992.
Measurement of lung density by means of quantitative CT scanning: a study of correlations with pulmonary function
tests.
Chest
102:
805-811
33.
Lamers, R. J.,
G. R. Thelissen,
A. G. Kessels,
E. F. Wouters, and
J. M. van Engelshoven.
1994.
Chronic obstructive pulmonary disease: evaluation with spirometrically controlled CT lung densitometry.
Radiology
193:
109-113
34. Miniati, M., E. Filippi, F. Falaschi, L. Carrozzi, E. N. Milne, H. D. Sostman, and M. Pistolesi. 1995. Radiologic evaluation of emphysema in patients with chronic obstructive puylmonary disease: chest radiography versus high resolution computed tomography. Am. J. Respir. Crit. Care Med. 151: 1359-1367 [Abstract].
35. Goldin, J. G., and D. R. Aberle. 1997. Functional imaging of the airways. J. Thorac. Imaging 12: 29-37 [Medline].
36. Yamazaki, Y., K. Kubo, M. Sekiguchi, and T. Honda. 1998. Analysis of BAL fluid in M. avium-intracellulare infection in individuals without predisposing lung disease. Eur. Respir. J. (In press)
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 M. L. Beggs, R. Stevanova, and K. D. Eisenach Species Identification of Mycobacterium avium Complex Isolates by a Variety of Molecular Techniques J. Clin. Microbiol., February 1, 2000; 38(2): 508 - 512. [Abstract] [Full Text]
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Y. YAMAZAKI, K. KUBO, A. TAKAMIZAWA, H. YAMAMOTO, T. HONDA, and S. SONE Markers Indicating Deterioration of Pulmonary Mycobacterium avium-intracellulare Infection Am. J. Respir. Crit. Care Med., December 1, 1999; 160(6): 1851 - 1855. [Abstract] [Full Text]
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