497

Update: The Radiographic Features

of Pulmonary Tuberculosis
John H. W oodring1
H. Mac Vandiviere2
Andrew M. Fried1
Marcus L. Dillon3
Terry D. W illiams1
Irene G. Melvin2
Received April 1 5, 1 985; accepted after revision
November 4, 1985.
1 Department of Diagnostic Radiology, Albert B.
Chandler Medical Center, University of Kentucky
College of Medicine, 800 Rose St., Lexington, KY
40536-0084. Address reprint requests to J. H.
W oodnng.
2Dep ment of Pediatrics, Albert B. Chandler
Medical Center, University of Kentucky College of
Medicine, Lexington, KY 40536-0084.
3Department of Cardiovascular and Thoracic
Surgery, Albert B. Chandler Medical Center, Uni-
versity of Kentucky College of Medicine, Lexington,
KY 40536-0084.
AJR 146:497-506, March 1986
0361 -803X/86/1 463-0497
C American Roentgen Ray Society
Pulmonary tuberculosis produces a broad spectrum of radiographic abnormalities.
During the primary phase of the disease these include pulmonary consolidation (50%),
which often involves the middle or lower lobes or the anterior segment of an upper lobe;
cavitation (29%) or pneumatocele formation(12%); segmental orlobar atelectasis(18%);
pleural effusion (24%); hilar and mediastinal lymphadenopathy (35%); disseminated
miliary disease (6%); and a normal chest radiograph (15%). During the postprimary
phase of the disease, common abnormalities include exudative and/or fibroproductive
parenchymal densities (100%), predominantly in the apical and posterior segments of
the upper lobes (91%); cavitation (45%) with bronchogenic spread of disease (21%);
marked fibrotic response in the lungs (29%); and pleural effusion, empyema, and fibrosis
(18%, 4%, and 41%, respectively). Upper-lobe masslike lesions are seen occasionally
(7%); spontaneous pneumothorax and intrathoracic lymphadenopathy are rare (5%
each). Common causes of a missed diagnosis of tuberculosis are (1) failure to recognize
hilar and mediastinal lymphadenopathy as a manifestation of primary disease in adults,
(2) exclusion of tuberculosis because disease predominates in or is limited to the
anterior segment of an upper lobe or the basilar segment of a lower lobe, (3) overlooking
of minimal fibroproductive lesions or reporting them as inactive, (4) failure to recognize
that an upper-lobe mass surrounded by satellite fibroproductive lesions might be
tuberculous, and (5) failure to consider healed sequelae of primary disease or a positive
purified protein derivative skin test as contributory to identifying the patients pulmonary
disease.
During the last decade, various authors have enumerated the unusual manifes-
tations of pulmonary tuberculosis in the adult population [1-6]. These unusual
manifestations usually have been implicated in the frequent failure of both radiolo-
gist and clinician to recognize that tuberculosis could be the cause of an abnormal
chest radiograph in patients who are subsequently, and rather surprisingly, proven
to have tuberculosis. As Choyke et al. [7] indicate, these so-called unusual
manifestations of tuberculosis in adults are actually typical of the disease: W hat is
unusual is that they often represent primary disease occurring in the adult popula-
tion.
Although physicians are more familiar with the radiographic manifestations of
postprimary tuberculosis than with those of primary disease, problems in radi-
ographic diagnosis do occur. Minimal exudative or fibroproductive tuberculosis
may be overlooked or, commonly, fibroproductive lesions may be assumed to be
inactive even though the patient subsequently proves to be sputum-positive for
Mycobacterium tuberculosis [1 , 5, 8]. Miller and MacGregor [1 ] reported several
cases of advanced postprimary tuberculosis with extensive upper-lobe cavitation
in which tuberculosis was not even considered as a diagnostic possibility!
Because of the apparent widespread difficulty in recognizing the radiographic
manifestations of pulmonary tuberculosis, we thought it would be beneficial to
review the spectrum of radiographic abnormalities attributable to M. tuberculosis
in a university medical center. W e emphasize the radiographic features of primary
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498 W OODRING ET AL.
AGE IN YEARS
Fig. 2.-Primary lymphohematogenous dissemination with miliary pattern in
43-year-old man.
AJR:146, March 1986
o PRIMARY TB
POST- PRIMARY TB
Fig. 1.-Prevalence of primary and postprimary tuberculosis by age in 90
patients.
and postprimary disease, similarities and differences between
the two, and the recognition of certain patterns that should
lead to suspicion of pulmonary tuberculosis. The pathogen-
esis of pulmonary tuberculosis is also discussed.
Materials and Methods
The chest radiographs and medical records of patients diagnosed
as having clinically active M. tuberculosis were reviewed. Between
1 974 and 1 984, 1 07 patients with active pulmonary tuberculosis were
documented at the University of Kentucky Medical Center. Of these,
1 7 patients had insufficient information in their medical records to
determine whether they had primary or postprimary disease with M.
tuberculosis. These 1 7 patients were excluded from the study. The
Centers for Disease Control and American Thoracic Society criteria
for confirmation of tuberculosis were met in the 90 remaining cases,
that is, (1) either bacteriologic confirmation of current disease or both
TABLE 1 : Location of Pulmonary Consolidation in 73 Patients
with Pulmonary Tuberculosis
Site of consoldabon
Type of Pul monary Tuberculosis
Primary
(n=17)
Postpnmary
(n=56)
Right upper lobe:
Anterior 4 18
Apical
Posterior
0
1
41
31
Right middle lobe
Right lower lobe:
Superior
Basal
2
1
3
10
13
16
Left upper lobe:
Anterior 2 16
Apical
Posterior
1
2
33
30
Lingula
Left lower lobe:
2 14
Superior
Basal
Totals
2
4
14
10
24 246
a significant skin reaction to the purified protein derivative (PPD) and
clinical and/or radiographic evidence of current disease, and (2)
radiographic improvement after administration of two or more anti-
tuberculous drugs [9, 10].
Primary tuberculosis was documented in 34 (38%) of the 90
patients on the basis ofthe following criteria: (1) recently documented
conversion of the PPD skin test coupled with a positive culture of M.
tuberculosis from tissue or body fluids (24 patients); (2) recently
documented conversion of the PPD skin test coupled with clinical
and radiographic evidence of current disease although subsequent
cultures for M. tuberculosis were negative (seven patients, all chil-
dren); and (3) positive culture for M. tuberculosis with no prior history
of tuberculosis, a previously negative PPD skin test, and a previously
normal chest radiograph (three patients). At the time of illness these
patients were anergic and the PPD skin test was nonreactive. Of the
34 patients with primary tuberculosis, 1 9 were female and 1 5 were
male; the patients were between 6 months and 87 years of age
(average, 24 years) (fig. 1). Of these 34 patients, 1 9 (56%) were 18
years of age or older. These 1 9 adults with primary tuberculosis
comprised 25% of the 75 adults with active pulmonary tuberculosis
in our total study population of 90 individuals. As shown in figure 1,
four of the patients with primary tuberculosis were over 71 years of
age. There was no evidence that these four patients had ever had
tuberculosis or a positive PPD skin test previously to suggest that
the booster effect was the cause of the recent PPD conversion. One
of these four elderly patients was quite debilitated with chronic
lymphocytic leukemia. Two of the other adults with primary tubercu-
losis had diabetes mellitus (one case each ofjuvenile-onset and adult-
onset diabetes).
Postprimary tuberculosis was documented in 56 (62%) of the 90
patients on the basis of the following criteria: (1) positive culture for
M. tuberculosis obtained on one or more admissions to the hospital
(all 56 patients), either from the sputum (53 cases), from material
obtained from fiberoptic bronchoscopy (two), orfrom gastric aspirates
(one); and (2) evidence of previous primary infection with tuberculosis
(all 56 patients) based on a documented positive PPD skin test before
the episode of current disease (39 patients), radiographic evidence
of the previous primary infection (35), and/or a previously positive
culture for M. tuberculosis without antituberculous treatment before
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C..
A
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AJR:146, March 1986 PULMONARY TUBERCULOSIS 499
Fig. 3.-Primary tuberculosis in 26-year-old man. A, Consolidation of the
anterior segment of left-upper-lobe cavitation, left paratracheal lymphadenop-
athy (arrow), and enlarged cardiac silhouette from pericardial effusion. Recently
documented conversion of PPD skin test was believed to be noncontributory,
and patient was treated with erythromycin for presumed Mycoplasma pneu-
monia. B and C, 1 month later: spontaneous clearing of pericardial effusion.
Cavitary disease in anterior segment of left upper lobe and left paratracheal
lymphadenopathy (B, arrow) are more clearly seen. Sputum cultures obtained
at this time grew Mycobacterium tuberculosis.
the time of diagnosis (1 1). Of the 56 patients with postprimary
tuberculosis, 36 were men and 20 were women; the patients were
between 20 and 87 years of age (average, 51) (fig. 1). Five of these
56 patients had associated conditions that may have contributed to
the development of postprimary tuberculosis, including chronic renal
failure (two cases) and acute lymphocytic leukemia, chronic alcohol-
ism, and pregnancy (one case each).
The patients in our study were from central and eastern Kentucky.
Although these patients are similar in many respects to those seen
at other major medical centers, the majority came from small rural
communities (less than 1 0,000 population) rather than urban inner-
city areas. In fact, Kentucky is unique in that the case rate of
tuberculosis is significantly greater in the nonurban population.
The chest radiographs of the 90 patients were reviewed and
evaluated for abnormalities of the lung parenchyma, airways, intra-
thoracic lymph nodes, and pleura. Finally, the initial radiographic
report and clinical diagnosis in each patients medical record was
reviewed with attention directed to the degree of initial suspicion of
tuberculous disease. The initial radiographic interpretations were
prepared in conjunction by a radiology resident and board-certified
diagnostic radiologist in all cases. Specific historical information con-
cerning the status of the PPD skin test or a high degree of clinical
suspicion of active tuberculosis was provided to the initial interpreters
in less than one-half of cases. Potential causes of a nondiagnosis of
tuberculosis were evaluated.
Results
Primary Tuberculosis
A normal chest radiograph coupled with a positive culture
for M. tuberculosis was found in five (15%) of the 34 patients
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________
#{149}1
500 W OODRING ET AL. AJR:146, March 1986
Fig. 5.-Primary tuberculosis in 3-year-old boy. Right hilar lymphadenopathy
and thin-walled pneumatocele (arrows) in right lower lobe.
Fig. 6.-Primary tuberculosis in 4-year-old girl. Right lower-lobe collapse
(black arrow) and shift of upper mediastinum to right (white arrow).
with primary tuberculosis, who were clinically thought to have
endobronchial disease. Two patients presented with a diffuse
miliary pattern (fig. 2). The remaining 27 patients had pulmo-
nary parenchymal consolidation, atelectasis, intrathoracic
Fig. 4.-Primary tuberculosis in 24-year-old female diabetic with recent
conversion of PPD skin test. Multiple cavities with air-fluid levels (arrowheads)
in superior segment of right lower lobe.
lymphadenopathy, pleural effusion, and pericardial effusion as
either isolated or combined findings.
Pulmonary consolidation occurred in 1 7 patients (50%). In
1 3 patients a single area of pulmonary consolidation was
encountered; in four patients multiple areas of parenchymal
consolidation were present. Overall, 24 areas of consolidation
were encountered in these 1 7 patients (table 1). The right and
left lungs were equally affected; the mid and lower parts of
the lungs were involved slightly more often than the upper
lung zones; however, when the upper lobes were involved,
anterior segment involvement was more common than in-
volvement of the apical or posterior segments (table 1 , fig. 3).
Cavitation had developed in five (29%) of the 1 7 patients
with pulmonary consolidation (figs. 3 and 4); in one case air-
fluid levels were noted. In two patients pneumatoceles were
present (fig. 5). In seven of these patients pulmonary consol-
idation was an isolated finding; however, in 1 0 patients con-
solidation was associated with other findings including lymph-
adenopathy, pleural effusion, pericardial effusion, and lobar
atelectasis.
Segmental or lobar atelectasis occurred in six patients
(1 8%) (fig. 6). The anterior segment of the right upper lobe
was involved in one case, the right middle lobe in two cases,
and the right lower lobe in three cases.
Pleural effusion was present in eight (24%) of the 34
patients (fig. 7). Effusion was unilateral in seven cases and
bilateral in one. The size of the effusion was judged to be
small in two cases, medium in one, and large in six according
to the criteria of Roper and W aring [1 1 ]. Three patients
presented with isolated pleural effusions; however, in five
patients effusion was associated with parenchymal consoli-
dation and/or lymphadenopathy. Pericardial effusion was
seen in only one case (fig. 3). Echocardiography was not
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Fig. 7.-Primary tuberculosis in 8-year-old girt. Large pleural effusion on Fig. 8.-Primary tuberculosis in 13-year-old boy. Bilateral hilar, right para-
right. tracheal, and aortic-pulmonic window lymphadenopathy (arrows) resembles
sarcoidosis, lymphoma, or metastatic disease.
AJR:146, March 1986 PULMONARY TUBERCULOSIS 501
performed routinely and therefore was not evaluated in this
retrospective study.
Hilar and/or mediastinal lymphadenopathy was present in
1 2 (35%) of the 34 patients (figs. 3, 5, and 8). Lymphadenop-
athy was present in six of the 1 5 children and six of the 19
adults. Lymphadenopathy was limited to the hilum in six
cases, involved both hilar and mediastinal nodes in three, and
was limited to the mediastinum in three. In two patients
lymphadenopathy was an isolated finding; however, in 10
instances lymphadenopathy was associated with pleural ef-
fusion, consolidation, and/or atelectasis.
The radiographic diagnosis was initially correct in only 11
(34%) of these patients with primary tuberculosis. Radi-
ographic patterns most often diagnosed as tuberculosis in-
cluded a miliary pattern, parenchymal consolidation accom-
panied by lymphadenopathy in a child, and cavitation. Pat-
terns least likely to elicit a diagnosis of tuberculosis included
a normal chest radiograph, hilar and mediastinal lymphade-
nopathy in an adult, and isolated findings of parenchymal
consolidation, atelectasis, or pleural effusion.
The clinical diagnosis was initially correct in 29 cases (85%)
on the basis of the history and physical examination, chest
radiograph report, and knowledge of a recent conversion of
the PPD skin test. However, in five patients, all adults, tuber-
culosis was initially excluded as a possible diagnosis because
the chest radiograph was felt to be incompatible with the
diagnosis of tuberculosis in an adult. Four of these patients
demonstrated hilar and/or mediastinal lymphadenopathy and
the fifth had consolidation of the anterior segment of the right
upper lobe.
Postprimary Tuberculosis
Pulmonary parenchymal disease was present in all 56
patients with postprimary tuberculosis. In seven patients a
single segment of lung was involved; in 49, two or more areas
of the lungs were involved. Overall, 246 areas of pulmonary
disease were present in these 56 patients (table 1). The apical
and posterior segments of the upper lobes were the most
commonly involved parts of the lungs (figs. 9 and 10).
Involvement of unusual parts of the lung was common in
postprimary tuberculosis (fig. 1 1). Twenty-four patients had
disease involving the anterior segment of an upper lobe; 18
patients had involvement of the basilar segments of the lower
lobes. However, in the vast majority of these cases, disease
was present in more typical parts of the lung as well, for
example, the apical and posterior parts of the upper lobes or
superior segment of a lower lobe. In only one case each was
postprimary tuberculosis isolated to the anterior segment of
an upper lobe or basilar segment of a lower lobe.
The pulmonary parenchymal disease was characterized as
being exudative, fibroproductive (fibronodular and/or fibrocal-
cific), and nodular. The most common finding (79%) was that
of a mixture of exudative and fibroproductive lesions. In 18%
the pulmonary disease was purely fibroproductive in nature,
and in 3% the disease was purely exudative in nature. In 11
patients virtually all parts of both lungs were involved, and
the disease was considered to be extensive. Lobar enlarge-
ment was noted in one case. Large nodules or masslike
densities were seen in four patients. These always occurred
in the upper lobes and were always accompanied by other
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.
I . . 4
,, . ....
-.-
,
114
502 W OODRING ET AL. AJR:146, March 1986
9
Fig. 9.-Postprimary tuberculosis. Fibroproductive (fibronodular) densi-
ties in apical segment of left upper lobe (arrows), initially interpreted as old,
inactive scarring. Sputum culture obtained 1 year later grew Mycobacterium
tuberculosis.
Fig. 1 0.-Postprimary tuberculosis in apical and posterior segments of
both upper lobes in 36-year-old man. Blunting of right costophrenic angle
(curved arrow) and calcified Ghon lesion in lingula (straight arrow) were
residual findings from primary infection.
/ p
I r I
Fig. 1 1 .-Postprimary tuberculosis in 77-year-old man. Homogeneous con-
solidation of right middle and lower lobes and mottled consolidation of left lower
lobe. Subtle fibroproductive lesions in apical segment of right upper lobe
(straight arrow) and calcified Ghon lesion in left lower lobe (curved arrow).
Bilateral apical pleural thickening.
Fig. 1 2.-Postprimary tuberculosis in 87-year-old woman. A 2-cm nonneo-
plastic masslike density is seen associated with marked fibrosis of right upper
lobe with upward retraction of right hilum and displacement of trachea to right.
There is marked right apical pleural thickening. Fibroproductive lesions are
present in basilar segments of right lower lobe and apical segment of left upper
lobe. Calcified Ghon lesion in left lower lobe (arrowhead).
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Fig. 13.-Postprimary tuberculosis in 20-year-old man. A 5-cm thick-walled
cavity in posterior segment of right upper lobe contains air-fluid level (black
arrow). Bronchogenic spread with acute tuberculous pneumonia involving
basilar segments of right lower lobe, left upper lobe and lingula, and basilar
segments of left lower lobe. W hite arrow indicates calcified aortic-pulmonic
window node from previous primary infection.
Fig. 1 4.-Postprimary tuberculosis. Extensive fibroproductive and exudative
densities with cavitation in apical and posterior segments of right upper lobe.
Right hilar and paratracheal lymphadenopathy (straight arrows). Curved arrow
indicates calcified Ghon lesion in right lower lobe.
AJR:146, March 1986 PULMONARY TUBERCULOSIS 503
areas of fibroproductive or exudative densities (satellite le-
sions) (fig. 12).
Cavitation was common, being present in 25 (45%) of the
56 patients (fig. 1 3). In six cases a single cavity was present;
in 1 9 cases there were multiple cavities. The cavity walls
ranged from very thin and smooth to very thick and nodular.
Air-fluid levels were present in five cases. Pneumatoceles
were encountered in only one case. Bronchogenic spread of
tuberculous material from upper-lobe cavities to other parts
of the ipsilateral and/or contralateral lung was presumed to
have occurred in 1 2 of the 56 patients (fig. 13) and often
resulted in extensive abnormalities on the chest radiograph.
A marked fibrotic response was evoked in the lungs of 16
patients (29%) (fig. 1 2). This was manifested by lobar atelec-
tasis in nine patients, upward hilar retraction in 1 0, downward
hilar retraction in one, tracheal deviation in seven, and ac-
quired tracheomegaly in four.
Pleural effusion occurred in 1 0 (1 8%) of the 56 patients
with postprimary tuberculosis. Effusion was unilateral in eight
cases and bilateral in two. The size of effusion was small in
seven cases and medium in three. In two cases air-fluid levels
were present in the pleural space, indicating bronchopleural
fistula with empyema formation. Apical pleural thickening was
present in 23 cases (41 %) (figs. 1 1 , 1 2, and 14); it was
unilateral in 14 cases and bilateral in nine. The extent of apical
pleural thickening was usually 1 cm or less; in only three
cases was the apical pleura over 1 cm in thickness. Sponta-
neous pneumothorax was noted in three of 56 patients and
was usually associated with extensive disease with multiple
cavities.
Hilar and/or mediastinal lymphadenopathy was present in
three patients (5%) with postprimary tuberculosis (fig. 14).
Lymph node groups involved included the right hilar, right
paratracheal, and subcarinal nodes. The presence of intra-
thoracic lymphadenopathy in these three cases accompanied
rather extensive parenchymal disease with multiple areas of
cavitation. By comparison with the lung disease, lymphade-
nopathy was not a prominent feature of postprimary tuber-
culosis in these three cases.
Residual evidence of the original primary infection was
apparent in 35 cases (63%). This included calcified or non-
calcified Ghon lesions in 24 patients, calcified hilar and/or
mediastinal lymph nodes in nine, and blunting of the lateral
costophrenic angle in nine (figs. 10-14).
The radiographic diagnosis was initially correct in 33 (59%)
of these 56 patients. In 1 2 patients the radiograph was
interpreted as abnormal but tuberculosis was not considered
as a diagnosis, and in 1 1 patients the chest radiograph was
interpreted as being normal (six cases) or as showing inactive
lung scars (five cases). Common pitfalls in radiographic inter-
pretation included the following: Fibroproductive lesions were
either overlooked entirely or interpreted as being inactive;
involvement of the anterior segments of the upper lobes or
basal parts of the lower lobes was used as evidence against
the diagnosis of tuberculosis; and large nodular or masslike
densities were interpreted as being neoplastic. The clinical
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504 W OODRING ET AL. AJR:146, March 1986
diagnosis was initially correct in only 31 cases (55%). In 12
patients the pulmonary symptoms were mild and nonspecific,
and tuberculosis was not thought to be the cause; in addition,
in several cases the chest radiographic abnormalities and
positive PPD skin test were considered to be noncontributory
to the present illness. In 1 3 patients the pulmonary symptoms
were so slight that pulmonary disease was not clinically
suspected. In all, there were 1 7 patients (30%) in which
neither the radiologist nor clinician initially suspected tuber-
culosis, resulting in a delay of 1 -3 years in the diagnosis.
Discussion
Primary tuberculosis is an airborne infection. The site of
primary tuberculosis in the lungs reflects areas of greatest
ventilation; the most common sites are the middle or lower
lung zones or the anterior segment of an upper lobe [1 2]. The
regional multiplication of organisms is followed by hilar and/
or mediastinal lymphadenopathy and the lymphohematoge-
nous dissemination of organisms diffusely to the lungs and to
numerous extrapulmonary sites [1 2]. During this time, most
patients are either asymptomatic or develop mild to moderate
systemic symptoms [1 2]. Tuberculin conversion occurs in 4-
8 weeks, at which time the patient will demonstrate a positive
PPD skin test [12]. This corresponds to an activation of
macrophage responsiveness, when activated macrophages
become capable of containing the primary infection [1 2]. In
2%-6% of cases, the lymphohematogenous dissemination of
massive numbers of viable organisms results in clinical and
radiographic evidence of miliary tuberculosis [7, 1 2, 1 3]. This
event is life-threatening and is characterized clinically by fever,
weight loss, prostration, and, if untreated, death from respi-
ratory failure and disseminated intravascular coagulation
[12]. In about 10% of primary infections, acquired immunity
is inadequate to contain the primary infection, and regional
multiplication is followed by chronic, progressive parenchymal
disease [1 2]. This phenomenon is distinguishable from post-
primary disease only by documentation of a recent conversion
of the PPD skin test [1 4]. In the remainder of cases the
primary infection is contained but remains a significant risk
for postprimary tuberculosis unless preventive treatment is
given [1 5, 1 6]; memory lymphocytes become immunologically
committed, and patients with primary infection generally retain
both tuberculin reactivity and immunity from primary reinfec-
tion for life [12].
Primary tuberculosis was once thought to be strictly a
disease of childhood. During this century there has been a
marked decrease in the incidence of tuberculosis in the United
States as a result of careful public health measures and the
advent of antituberculous chemotherapy. Because of this,
only a small percentage of American adults have a positive
PPD skin test, indicating that most adults today are suscep-
tible to the development of primary tuberculosis [1 , 7]. W e
can be reasonably certain that 25% of the adults with pul-
monary tuberculosis in our series had the primary form of the
disease. Figure 1 shows three age-related peaks of highest
prevalence. The highest prevalence of primary tuberculosis
was noted in the 0-5-year age group; a second peak was
noted in the 21 -30-year age group; and a third peak was
noted in patients 71 years of age or older. The high prevalence
of primary tuberculosis in young adults may be related to
mobile, healthy, susceptible individuals living or working in
crowded environments or under poor socioeconomic condi-
tions [5]; primary tuberculosis in the elderly may be related to
poor or crowded living conditions in addition to chronic or
debilitating disease and immunosuppression [5]. Because of
the recent increased prevalence of primary tuberculosis in
adults, the term childhood tuberculosis to describe primary
tuberculosis should be abandoned.
Postprimary tuberculosis is the name given to a clinical and
radiographic pattern of disease that correlates pathogeneti-
cally with acquired hypersensitivity and immunity [1 3]. The
careful observations and retrospective analyses of Stead [14,
17] and others [1 2] have led to the understanding that in 90%
of cases, postprimary tuberculosis results from reactivation
of a previously dormant primary i J#{231}n; a minority of cases
represent a continuation of the pnThary disease [13, 14].
Rarely, postprimary tuberculosis is exogenous superinfection
on an inactive or even active original infection-true reinfec-
tion [13].
The early parenchymal infiltrate of postprimary tuberculosis
results from the intensive inflammatory reaction in the hyper-
sensitive host [1 8]. This may lead to caseous necrosis, which
over time is apt to slough into a bronchus, leaving a cavity
[1 8]. The most commonly involved parts of the lungs in
postprimary disease are the apical and posterior segments of
an upper lobe [1 , 5, 8, 1 3, 1 8-20]. Two main factors have
been postulated to explain this common location of postpri-
mary tuberculosis. The higher regional oxygen tensions of the
apical and subapical parts of the upright lung (1 1 4 to 1 32 mm
Hg) have been highly touted as being responsible for apical
localization of postprimary disease. It is suggested that the
demonstrated higher oxygen tensions in the apex of the
upright lung produce increased mycobacterial virulence; the
lower parts of lung where alveolar oxygen tension is 1 08 mm
Hg or less are theorized to be quite resistant to the develop-
ment of postprimary tuberculosis [1 8]. This concept may best
be put to the test by observing populations dwelling at high
altitude. Above 1 0,000 feet (3048 m) of elevation, alveolar
oxygen tension is substantially less than 1 00 mm Hg; above
1 5,000 feet (4570 m), alveolar oxygen tension is well below
80 mm Hg, even in the extreme apex of the lung [181.
Nevertheless, native permanent residents of the Peruvian
highlands (1 0,300-1 4,300 feet [31 38-4357 m]) seem to be
especially disposed to tuberculosis as compared to lowland
natives (sea level) [1 8, 21].
A more likely explanation of the apical localization of post-
primary tuberculosis is related to impaired clearance mech-
anisms from poor lymph flow [1 8]. Pulmonary lymph flow is
related to two factors: microvascular pressure and respiratory
motion. In the erect lung, owing to gravitational effect, pul-
monary perfusion and microvascular pressure are reduced in
the apex relative to the middle and lower lung zones; as a
result, apical lymph flow is also relatively deficient compared
to the more dependent parts of the lung [1 8]. In addition,
lymph flow in small lymphatic channels is directly related to
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AJR:146, March 1986 PULMONARY TUBERCULOSIS 505
respiratory excursion. Since the anterior rib cage moves with
respiration but the posterior rib cage is relatively fixed, lymph
flow is also restricted in the posterior parts of the lung [18].
In primary tuberculosis, lymphohematogenous dissemination
results in the seeding of mycobacterial organisms to many or
all parts of the lungs; the decreased lymph flow in the apical
and posterior parts of the lungs would result in decreased
clearance of organisms from these parts of the lung and
would favor the development of postprimary tuberculosis in
these locations [18].
Our study reveals a broad spectrum of radiographic abnor-
malities in primary and postprimary tuberculosis not unlike
those demonstrated in other reports on this subject. It also
provides helpful insights into common causes for a misdi-
agnosis of tuberculosis.
In children, a clinical diagnosis of primary tuberculosis usu-
ally is made when an abnormal chest radiograph is coupled
with clinical evidence of pulmonary disease and a documented
conversion of the PPD skin test. Certain radiographic pat-
terns, such as parenchymal consolidation associated with
hilar and/or mediastinal lymphadenopathy, or isolated hilar
and/or mediastinal lymphadenopathy, in children elicit a fre-
quent diagnosis of primary tuberculosis on the basis of the
chest radiograph alone.
In adults, these same findings often are viewed as unusual,
atypical, or even incompatible with tuberculosis, and tuber-
culin conversion may be viewed as a coincidental and unre-
lated phenomenon. Four adults in our 34 cases of primary
tuberculosis escaped initial radiographic and clinical diagnosis
because hilar and/or mediastinal lymphadenopathy were con-
sidered by the clinician and radiologist alike to be incompatible
with adult tuberculosis. Hilar and mediastinal lymphadenop-
athy are nonspecific findings that occur in bronchogenic car-
cinoma, metastatic neoplasm, sarcoidosis, lymphoma, and
fungal disease. But if the lymphadenopathy in these adults
had been recognized as a possible manifestation of primary
tuberculosis, the conversion of the PPD skin test might have
been viewed as related to the patients illness, and a correct
diagnosis of primary tuberculosis might have been made. In
another adult patient, tuberculosis was excluded as a possi-
bility because parenchymal consolidation was limited to the
anterior segment of an upper lobe. W hile disease limited to
the anterior segment of an upper lobe or basilar segment of
a lower lobe is rare in postprimary tuberculosis and common
in nontuberculous pneumonia, it should be remembered that
these findings are rather common in primary tuberculosis.
Postprimary disease in adults is often misdiagnosed also.
The clinical symptoms often are minimal and the patient may
report only a nonspecific smokers cough or no symptoms
at all. In our series, 1 7 (30%) of 56 cases of active postprimary
tuberculosis were missed by both the clinician and the radiol-
ogist, resulting in a 1 -3-year delay in diagnosis on one or
more hospital admissions.
Incorrect appraisal of disease activity was the most com-
mon cause of misdiagnosis. In local fibroproductive (fibro-
nodular, fibrocalcific) tuberculosis the exudative lesion is grad-
ually replaced by one or more sharply circumscribed shadows,
which are often irregular and angular in contour [13]. Strand-
ing toward the hilum occurs, and calcification in one or more
of the nodules often appears [1 3]. This pattern of pulmonary
abnormality is characteristic of granulomatous disease and is
seldom, if ever, found in other bacterial infections. However,
we found that it was this characteristic pattern fo parenchymal
tuberculosis that caused the greatest difficulty in diagnosis. It
is this stage of postprimary tuberculosis that is often over-
looked entirely or is reported as old scarring or no active
disease. This is incorrect, since many of these patients may
be sputum-positive. W ithout films dating back at least 6
months, an accurate statement about the stability of a fibro-
productive lesion cannot be made; all of these lesions should
be reported as possible tuberculosis or fungal disease, activ-
ity indeterminant [1 0, 22]. Even in patients with unchanging
tuberculous scars, active tuberculous infection can still be
present on sputum culture [1 ]. Therefore, these patients
should be reported as radiographically stable rather than
inactive [1 0, 22]. The term fibrotic, often used to describe
this pattern of disease, is not recommended [1 0] because it
implies inactivity.
The second most common cause for a misdiagnosis of
postprimary tuberculosis was involvement of an anterior seg-
ment of an upper lobe or basilar segment of a lower lobe by
parenchymal disease. It is a common misconception that
involvement of these areas excludes tuberculosis. This is
certainly not true of primary disease; moreover, in postprimary
disease we found the anterior segments of the upper lobes
to be involved in 46% of cases and the basilar segments of
the lower lobes to be involved in 32% of cases. In most of
these cases cavitary or fibroproductive disease was present
in typical locations; many of these patients also showed
residual radiographic evidence of the previous primary dis-
ease-subtle but helpful adjunctive findings in arriving at a
correct diagnosis.
The third most common cause for misdiagnosis of postpri-
mary disease was the presence of large nodular or masslike
densities that were considered to be neoplastic. Typically,
these were upper-lobe-predominant, rather than basilar, and
were associated with fibroproductive lesions in typical loca-
tions.
As Palmer [1 9] states, pulmonary tuberculosis continues
to keep the physician humble. Since the advent of antituber-
culous chemotherapy 30 years ago, there has been a dramatic
drop in the incidence of tuberculosis in this country. This has
created a generation of American physicians who have little
experience with it. Although the case rate of tuberculosis is
relatively stable in many areas of the country, some areas are
experiencing a marked increase in incidence. In addition, the
recent increased prevalence of primary tuberculosis in adults
has produced a confusing spectrum of disease seldom en-
countered in adults in the past. Because of the infectious
nature of tuberculosis, the morbidity and mortality of the
natural course of the disease, and the excellent therapeutic
results of antituberculous chemotherapy in most cases, there
is good reason for all physicians to be sensitive to the contin-
ued existence of this disease. The presence of healed Se-
quelae of primary disease or a positive PPD should suggest
that almost any radiographic abnormality could represent
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active tuberculosis. The recognition of primary disease in the
adult and close scrutiny for and proper reporting of fibropro-
ductive lesions could further improve the detection and diag-
nosis of active tuberculosis.
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