SYMPOSIUM REVIEW ARTICLE
Radiology of Chronic Cavitary Infections
Loren Ketai, MD,* Bart J. Currie, FRACP,† Michael R. Holt, MBBS,‡§
and Edward D. Chan, MD∥¶#**
Abstract: Chronic cavitary lung disease is an uncommon manifes-
tation of pulmonary infection, and is a pattern which worldwide is
most commonly caused by reactivation tuberculosis. Other organ-
isms, however, can cause similar radiologic patterns. Endemic fungi
have long been recognized as potential causes of this pattern in
North and South America, but the frequency with which these
diseases present with chronic cavities in North America is relatively
Downloaded from http://journals.lww.com/thoracicimaging by BhDMf5ePHKbH4TTImqenVKgR5BWYxyIrzBifDRV4rl4AjaSVRDz+dXegDUMRlyPp on 08/26/2018
small. Nontuberculous mycobacteria and chronic aspergillus infec-
tions are recognized with increasing frequency as causes of this
pattern. Melioidosis, a bacterial infection that can also cause
chronic lung cavities, was previously understood to be relevant
primarily in Southeast Asia, but is now understood to have a wider
geographic range. While cultures, serologies, and other laboratory
methods are key to identifying the infectious causes of chronic lung
cavities, radiologic evaluation can contribute to the diagnosis.
Differentiating the radiologic patterns of these diseases from reac-
tivation tuberculosis depends on subtle differences in imaging
findings and, in some cases, appreciation of underlying lung disease.
Key Words: pneumonia, mycobacterial infections, fungal infections,
melioidosis
(J Thorac Imaging 2018;33:334–343)
C hronic cavitary lung disease is an uncommon manifes-
tation of pulmonary disease that can be accompanied
by high morbidity. Chronic cavities can be caused by pri-
mary lung and metastatic neoplasms and by other non-
infectious diseases such as granulomatosis with polyangiitis
(Fig. 1).1 Infectious agents are well known causes of chronic
cavitary lung disease, the most common responsible
pathogen worldwide being Mycobacterium tuberculosis. As
the prevalence of tuberculosis has fallen in the United States
and in many other nations, the relative likelihood that
chronic cavitary disease is caused by other pathogens in
those countries has risen. In North America, the differential
diagnosis of infectious causes of chronic cavitary lung dis-
ease includes nontuberculous mycobacteria (NTM), Asper-
gillus, and, depending on regional differences, Histoplasma,
Coccidioides, and Blastomyces2–5 (see article by Holt and
Chan6). Melioidosis and Paracoccidioidosis are additional
From the *Department of Radiology, University of New Mexico,
Albuquerque, NM; †Royal Darwin Hospital and Menzies School of
Health Research, Darwin, NT, Australia; §Department of Medicine,
University of Colorado Denver, Aurora; ∥Pulmonary Section, Denver
Veterans Affairs Medical Center; ‡Division of Mycobacterial and Res-
piratory Infections; ¶Department of Medicine; #Program in Cell Biology,
National Jewish Health; and **Division of Pulmonary Sciences and
Critical Care Medicine, University of Colorado Denver Anschutz
Medical Campus, Denver, CO.
The authors declare no conflicts of interest.
Correspondence to: Loren Ketai, MD, Department of Radiology,
MSC10 5530, 1 University of New Mexico, Albuquerque, NM
87131-0001 (e-mail: lketai@salud.unm.edu).
Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
DOI: 10.1097/RTI.0000000000000346
334 | www.thoracicimaging.com J Thorac Imaging  Volume 33, Number 5, September 2018
Copyright r 2018 Wolters Kluwer Health, Inc. All rights reserved.
considerations in patients having resided or traveled outside
North America. For most of these pathogens, cavitation is
only one of several possible morphologic presentations.
In many cases, the cavitary form of these infections is
associated with signs, symptoms, and potential complica-
tions that are different from the other manifestations of the
same infection. Development of the cavitary presentation
may also be associated with specific predisposing morbid-
ities. Radiologists should be aware of the potential com-
plications and underlying morbidities associated with these
infections. Identification of a specific pathogen based on
imaging findings alone, however, will remain elusive. Only
occasionally, when combined with epidemiologic informa-
tion, can imaging findings suggest a specific pathogen.
IMAGING OF CAVITIES
Differentiation of infectious from noninfectious cav-
ities can be difficult. Widely quoted data setting the
threshold for cavity wall thickness for diagnosis of benignity
below 5 mm and the threshold for diagnosis of malignancy
above 15 mm are based on chest radiograph measurements
performed 35 years ago.7 More recent analysis of computed
tomography (CT) images has compared primary and
metastatic cancer to both chronic and acute infections (lung
abscesses, septic emboli). In this heterogenous population,
satellite nodules were approximately twice as common in
benign compared with malignant nodules, regardless of
whether the cavities were solitary or multiple. In contrast, a
notch (focal indentation) in the outer contour of the cavity is
twice as common in malignant compared with benign
nodules. Multiple other findings did not reliably discrim-
inate benign from malignant etiologies when applied to both
solitary and multiple cavities. Wall thickness was not a
useful discriminator in either group.8
This and other studies suggest that higher level analysis
would be necessary to reliably differentiate chronic cavitary
infectious disease from a neoplasm. A variety of textural
analysis approaches are able to efficiently segment cavities
from the surrounding lung on CT scans, but complex image
analysis has not been directed at differentiation of benign
from malignant cavities.9 This would likely require analysis
performed with multilayered convolutional neural networks
(deep learning) that could identify discriminant features of
cavities and adjacent lung parenchyma that may not be
apparent to human observers.10
NTM
Although NTM are an important cause of chronic
cavitary infections, the signature radiologic finding asso-
ciated with these organisms is bronchiectasis, which can
occur in conjunction with cavities or without them. Bron-
chiectasis may be caused by these pathogens, or, conversely,
preexisting bronchiectasis may predispose to colonization
and establishment of infection with NTM. The latter occurs
J Thorac Imaging  Volume 33, Number 5, September 2018 Radiology Chronic Cavitary Infections

FIGURE 1. A and B, Imaging of a patient with granulomatosis with polyangiitis. Coronal CT reconstructions demonstrate multiple cavities
of differing wall thickness.

in patients with cystic fibrosis, and even individuals with Most NTM infections are due to Mycobacterium avium
cystic fibrosis transmembrane conductance regulator gene complex (MAC)—a group that is comprised of several dis-
heterozygosity may be predisposed to NTM lung disease.11 tinct NTM species. A minority of NTM infections are

FIGURE 2. A and B, Middle-aged woman with MAC infection, initially manifesting with mild bronchiectasis in the middle lobe, and
normal right lung apex. C and D, Follow-up CT 2 years later shows increased extent of bronchiectasis in addition to interval development
of a right apical cavity. This patient demonstrates findings of both the nodular bronchiectatic (nonclassic) and cavitary (classic) form of
MAC infection. MAC indicates Mycobacterium avium complex.

Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved. www.thoracicimaging.com | 335
Copyright r 2018 Wolters Kluwer Health, Inc. All rights reserved.
Ketai et al J Thorac Imaging  Volume 33, Number 5, September 2018

FIGURE 3. A and B, Radiograph and CT in a middle-aged woman demonstrating classic thin-walled cavity seen with MAC, with relatively
little adjacent parenchymal disease. Nodules are also seen in the lower lobe. MAC indicates Mycobacterium avium complex.

caused by mycobacteria classified as rapid growers, princi-
pally the Mycobacterium abscessus complex. Although less
common than MAC, these organisms cause significant
morbidity due to their characteristic antibiotic resistance
and poor response to treatment.12
Classically, MAC pulmonary infections may be classified
into an (upper lobe) fibrocavitary lung disease seen mostly in
male individuals with underlying chronic obstructive pulmo-
nary disease (COPD) and a bronchiectatic form most com-
monly seen in women with slender body habitus and chest
wall deformities.2,13 There are, however, overlaps between
these syndromes such that features of both may be seen in any
one patient (Fig. 2). When compared with patients with
cavitary tuberculosis, patients with NTM cavitary lung dis-
ease are more likely to have widespread bronchiectasis.14
Some investigators have suggested that at least some of the
apparent cavities that develop in NTM actually represent
progression of cylindrical to cystic bronchiectasis.
The presence of a cavitary component to the disease has
important clinical implications. These patients have a much a
higher 5-year mortality than patients whose manifestations of
infection are confined to bronchiectasis and nodules. Accord-
ingly, the presence of cavitary disease generally warrants the
initiation of treatment and necessitates a more intensive treat-
ment regimen than that used in noncavitary disease.13,15–17
The radiologic manifestations of cavitary MAC are
similar to tuberculosis, but do have subtle distinctions.
Compared with tuberculous cavities, MAC-infected cavities
have thinner walls with less surrounding parenchymal
opacities and tend to develop pleural thickening adjacent to
the cavity (Fig. 3). In one study, pleural thickening adjacent
to the cavity, right upper lobe bronchiectasis, and ill-defined
tree-in-bud nodules all carried odds ratios > 5 for predicting
NTM over tuberculous infection (Fig. 4).14 There is con-
siderable overlap in appearance of different NMTs, but one
series showed M. abscessus more likely than MAC to
manifest as the bronchiectatic nodular rather than cavitary
disease. When cavities were present in M. abscessus infec-
tions, they were less likely to be thin walled (Fig. 5).18
Extrapulmonary findings on CT scan may also suggest
NTM over tuberculous cavitary lung disease. NTM infection, in
general, and especially that due to Mycobacterium fortuitum has

FIGURE 4. A and B, Radiograph and CT showing advanced cavitary MAC infection in a patient with underlying COPD. Marked focal
pleural thickening is present (arrows). COPD indicates Chronic Obstructive Pulmonary Disease.

336 | www.thoracicimaging.com Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
Copyright r 2018 Wolters Kluwer Health, Inc. All rights reserved.
J Thorac Imaging  Volume 33, Number 5, September 2018
FIGURE 5. Patient who acquired mycobacterium abscessus
infection while being treated with infliximab. CT shows several
thick-walled cavities (courtesy of D. Lynch MD, Denver, CO).
been associated with achalasia.19 The definitive pathophysiology
is speculative, that is, the predilection of mycobacteria to grow in
lipid substrates has raised the possibility of lipoid aspiration as a
prelude to NTM infection in patients with achalasia.
CAVITARY HISTOPLASMOSIS
Similar to NTM, histoplasmosis can cause cavitary
disease that is morphologically similar to reactivation
tuberculosis. Although acute histoplasmosis can cause lung
cavities de novo, the classic description of cavitary histo-
plasmosis is that of upper lobe inflammation originating
FIGURE 6. A–D, Chronic histoplasmosis. A and B, Detail from chest radiograph of a patient with emphysema, initially with thin-walled
apical bulla. Follow-up radiograph shows development of apical cavities due to chronic histoplasmosis infection. C and D, Coronal and
axial CT show multiple cavities superimposed upon bullous emphysema (courtesy of D. Conces MD, Indianapolis, IN).
Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
Copyright r 2018 Wolters Kluwer Health, Inc. All rights reserved.
Radiology Chronic Cavitary Infections
adjacent to a preexisting bullae. This is followed by thick-
ening of the bullae walls, due to local necrosis and fibrosis,
which ultimately leads to volume loss (Fig. 6). Fibrotic
change may also occur in the lower lobes discontiguous
from upper lobe cavities, but its pathogenesis there remains
speculative.3,20
The aforementioned fibrocavitary lung disease is epi-
demiologically linked to men with COPD, much like cavitary
NTM infections. This presentation was initially recognized
when evidence of histoplasmosis infection was sought among
patients in tuberculosis sanatoriums and among patients
presenting with chronic lung cavities. A more recent study of
chronic histoplasmosis, which used culture or serologic evi-
dence of histoplasmosis infection accompanied by symptoms
for > 6 weeks as its inclusion criteria, identified a different
presentation that was more common in women and occurred
in the absence of COPD. This presentation is manifest by
imaging findings of nodules, adenopathy, and noncavitary
parenchymal opacities. While both this presentation and chronic
cavitary histoplasmosis commonly have positive serology due
to chronic antigenic stimulation, the noncavitary form is much
less likely to have sputum cultures positive for Histoplasma
capsulatum.21
CHRONIC PULMONARY ASPERGILLOSIS
Aspergillus is a more common cause of cavitary lung
disease than any of the other pathogens discussed in this
review save NMT. It has long been recognized as causing
angioinvasive infections in neutropenic patients and allergic
bronchopulmonary disease in asthmatic patients, but the
description of its intermediate chronic manifestation is still
www.thoracicimaging.com | 337
Ketai et al J Thorac Imaging  Volume 33, Number 5, September 2018

FIGURE 7. A–C, Middle-aged man with chronic pulmonary aspergillosis. A, Chest radiograph shows a relatively thin-walled cavity in the
left upper lobe. B, Follow-up chest radiograph demonstrates progression of the infection manifest as thickening of the cavity wall and
associated pleural thickening along the superior margin of the cavity. C, CT demonstrates necrotic lung parenchyma within the cavity.

FIGURE 8. A and B, Chest radiograph and CT of middle-aged patient with chronic pulmonary aspergillosis and extensive upper lobe
cavities superimposed on underlying emphysema. An aspergilloma is present in the left upper lobe cavity (black arrow on radiograph,
white arrow on CT), much smaller than the air-filled cavity that contains it. No Monod sign is seen.

338 | www.thoracicimaging.com Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
Copyright r 2018 Wolters Kluwer Health, Inc. All rights reserved.
J Thorac Imaging  Volume 33, Number 5, September 2018
FIGURE 9. Monod sign in a patient with underlying cavitary (classic
pattern) MAC infection. A crescent of air (black arrows) outlines a
right upper lobe aspergilloma. MAC indicates Mycobacterium avium
complex.
in evolution. Chronic pulmonary aspergillosis is an accepted
umbrella term that some experts divide into (1) subacute
invasive aspergillosis (when the disease develops rapidly, in
<3 mo), (2) chronic cavitary pulmonary aspergillosis (when
then disease develops more slowly), and (3) fibrosing
aspergillosis (when extensive fibrosis, often asymmetric, is
present)22,23 (see article by Holt and Chan6). As these dis-
tinctions can be difficult to make radiologically, radiologists
may prefer the more general term.24
Worldwide, chronic pulmonary aspergillosis most
often occurs in lung damaged from tuberculosis, occurring
in 20% or more of patients with prior cavitary tuberculous
disease. The resulting progression of cavities and adjacent
parenchymal opacities can be very difficult to differentiate
from failure of tuberculosis treatment or recurrent infec-
tion. In areas wherein the prevalence of tuberculosis is
low, COPD becomes the major risk factor for the disease,
likely due to associated bullous emphysema as well as the
use of inhaled and/or systemic corticosteroids to treat
exacerbations.25 Chronic pulmonary aspergillosis can also
occur in conjunction with cavitary or bronchiectatic NTM
FIGURE 10. A and B, Chest radiograph and CT of a 32-year-old man with chronic thin-walled coccidioidomycosis cavity in the left
upper lobe.
Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
Copyright r 2018 Wolters Kluwer Health, Inc. All rights reserved.
Radiology Chronic Cavitary Infections
infection. The production of bronchiectasis and cavities by
either one of these pathogens may increase susceptibility
to the other.22
As a whole, patients with chronic pulmonary asper-
gillosis manifest clinical and imaging findings similar to
chronic histoplasmosis and classic NTM infection. The
disease most commonly occurs in middle-aged men, with
complaints of respiratory symptoms, anorexia, and weight
loss. Radiologically, this disease can present as persistent
consolidation in the upper lobes that develops cavitation or
can involve a preexisting cavity. In either case, progressive
disease results in single or multiple thick or thin-walled
upper lobe cavities that slowly increase in size (Fig. 7).
Progression of upper lobe cavitary disease is associated with
local architectural distortion, but extensive fibrosis can also
occur into the adjacent lobes, often asymmetrically. Pleural
thickening is often conspicuous, adjacent to the areas of
consolidation or cavitation, and may presage the develop-
ment of an aspergilloma.
Aspergillomas have been reported in up to 50% of
cases of chronic pulmonary aspergillus infections, and,
when present, they may or may not manifest a “Monod
sign” (Fig. 8). This sign is caused by soft tissue attenu-
ation material separated from the cavity wall by a cres-
cent of air.26 Its presence suggests the presence of an
intracavity mycetoma, a diagnosis confirmed by demon-
strating that the soft tissue mass is mobile within the
cavity. Thoracic radiologists often differentiate a
“Monod sign” from the crescent of air formed by necrotic
tissue that has partially retracted from the cavity wall,
terming the latter an “air crescent” sign. (Fig. 9). Either
sign can be seen in the setting of chronic pulmonary
aspergillosis, the Monod sign caused by simple aspergil-
lomas (without infection in the adjacent parenchyma)
and the air-crescent sign in the setting of chronic
pulmonary aspergillosis that has a necrotizing
component.24,27 Neither the air-crescent sign nor the
Monod sign is entirely specific for presence of Aspergil-
lus, and can occasionally be seen in other infections or in
noninfectious diseases, such as granulomatosis with pol-
yangiitis or a cavitating malignancy.28
www.thoracicimaging.com | 339
Ketai et al J Thorac Imaging  Volume 33, Number 5, September 2018

FIGURE 11. A and B, CT coronal reconstructions showing rupture of thin-walled cavities into the pleural space with resulting pneu-
mothoraces. A, Small upper lobe cavity communicates with the pleural space (arrow). Chest tube (not seen) had already evacuated much
of the pneumothorax. B, Thin-walled cavity has ruptured into the left pleural space and then collapsed (arrow), causing a large
pneumothorax.

COCCIDIOIDOMYCOSIS histoplasmosis, or chronic cavitary aspergillous. Rather than

Cavitary lung disease caused by coccicioidomycosis usu- presenting as fibrocavitary disease, most cavities are single, seen
ally presents differently than that seen with NTM, chronic on CT in up to 11% of patients.4 These cavities may be thin

FIGURE 12. A–C, Middle-aged man who presented with chronic coccidioidomycosis and hemoptysis. A, Coronal CT demonstrates right
upper lobe cavitary infection with marked volume loss. Intracavitary material (arrow) could represent mycetoma or blood. B and C,
Bronchial arteriogram shows intense vascular blush in the area of the cavity.

340 | www.thoracicimaging.com Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
Copyright r 2018 Wolters Kluwer Health, Inc. All rights reserved.
J Thorac Imaging  Volume 33, Number 5, September 2018 Radiology Chronic Cavitary Infections

walled, developing in an area of prior consolidation, or they
may be thick walled, caused by cavitation of a nodule (Fig. 10).
In the absence of prior imaging, isolated thin-walled cysts can
be mistaken for an intrapulmonary bronchogenic cyst. These
solitary cavities are asymptomatic in most patients but can
become superinfected or be associated with hemoptysis.29 The
cavities resolve spontaneously in up to 50% of patients. Rarely,
a peripheral cavity can rupture into the pleural space, causing
pneumothorax or pyopneumothorax (Fig. 11). Progression of
chronic coccidioidomycosis infection to fibrocavitary disease is
much less common than are single cavities, occurring in > 1%
of infections, the rate possibly higher in certain ethnic groups
such as African Americans or Filipinos.
Differences between the appearance of this form of coc-
cidioidomycosis and reactivation tuberculosis can be subtle.
Calcifications may occur within lymph nodes and lung paren-
chyma, but, in general, they are less common than seen with
tuberculosis or histoplasmosis.4,30 While coccidioidomas may
show a greater predilection for the anterior segments of
the upper lobes than tuberculomas, the distribution of
disease in chronic cavitary coccidioidomycosis is commonly
indistinguishable from reactivation tuberculosis. This disease
manifestation requires long-term antifungal treatment. Patients
developing hemoptysis due to bronchial artery hypertrophy
driven by chronic inflammation may require bronchial artery
embolization (Fig. 12).
PARACOCCIDIOIDOMYCOSIS
Paracoccidioimycosis is the most common systemic
mycosis in South America, most cases occurring in Brazil
(see article by Holt and Chan6). The infection can occur in
the absence of preexisting lung disease, but may cooccur
with tuberculosis in 10% to 15% of cases. Radiographic
findings of the chronic form of paracoccidioidomycosis
include peribronchovascular thickening and nodules of
varying sizes.31 Necrosis in these nodules and in areas of
consolidation can form irregular shaped cavities, but the
prevalence of cavitation is less than that seen in reactivation
tuberculosis. The disease involvement is often bilateral and
symmetric resulting in fibrosis that manifests as architectural
distortion, traction bronchiectasis, and cicatricial emphy-
sema with basilar bullae. Parenchymal calcifications, even in
this chronic form are rare. This pattern of “butterfly wing”
perihilar opacities without parenchymal calcification differs
from the typical appearance of reactivation tuberculosis in

FIGURE 13. A–C, Chronic paracoccidioidomycosis. A and B, Chest radiograph and coronal reconstruction of CT show cavites and
extensive peribronchial opacities in a parahilar distribution. Unlike the typical pattern of reactivation tuberculosis, the apices of both lungs
are relatively spared. C, Axial CT section does not demonstrate parenchymal or nodal calcifications despite extensive disease. No pleural
effusion seen (courtesy of A. Soares Souza Jr, MD, PhD, São José do Rio Preto—SP, Brazil).

Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved. www.thoracicimaging.com | 341
Copyright r 2018 Wolters Kluwer Health, Inc. All rights reserved.
Ketai et al J Thorac Imaging  Volume 33, Number 5, September 2018

The disease can be acquired by inhalation or inoculation.

FIGURE 14. A patient with recurrent infectious symptoms of
4 months duration due to cavitary melioidosis. Chest radiograph
demonstrates large thin-walled left upper lobe cavity but no evi-
dence of apical fibrosis or left upper lobe volume loss.
which parenchymal calcifications are often present and
apical fibrosis is most conspicuous (Fig. 13). As in the case
with tuberculosis, these fibrotic changes frequently persist
despite adequate treatment of the infection.32,33
MELIOIDOSIS
Anomalous to most infectious chronic cavitary lung
disease, melioidosis is caused by neither mycobacterium nor
fungus, but by the environmental bacterium Burkholderia
pseudomallei. The organism is endemic to the tropics and
subtropics. The highest incidence occurs in northern Australia
and Southeast Asia, but improved surveillance has recently
substantially expanded the known melioidosis-endemic
regions globally, now including many locations in the
Americas.34 The most common presentation of melioidosis is
community-acquired pneumonia with a wide diversity of
severity. The vast majority of cases have an acute pre-
sentation, but, in around 10% of patients, the infection can
cause chronic disease (defined as symptoms being present for
> 2 mo), of which the majority manifest as chronic pulmonary
infection.35 Even less common is presentation as a relapsing
or delayed onset infection, likely reflecting the ability of
B. pseudomallei to survive and multiply within macrophages
and other phagocytes, analogous to tuberculosis. Some surgical
specimens have demonstrated granulomatous inflammation.36
The former is linked to severe weather events in endemic
regions with aerosolisation of B. pseudomallei, and to pre-
sentation with acute bacteremic pneumonia, which can be
severe and rapidly progress to multilobar disease and shock.37
Melioidosis is being increasingly recognized as an opportun-
istic pathogen, with diabetes being the most common risk
factor and severe disease being uncommon in healthy hosts.38
Chronic melioidosis can occur after either inhalation or fol-
lowing infection by inoculation through the skin. It is more
likely than acute disease to affect the upper lobes, wherein it
can cause multiple cavities, nodules, and fibrosis. In countries
where tuberculous is endemic, its appearance may often be
mistaken for reactivation tuberculosis.39 Meldioidosis cavities
are often thin walled, and compared with reactivation tuber-
culosis, are less likely to be associated with persistent apical
fibrosis or calcifications40,41 (Figure 14).
CONCLUSIONS
The infectious causes of chronic cavitary pulmonary
disease are changing, as is our understanding of their scope
and epidemiology. Differentiating radiologic patterns of these
diseases from reactivation tuberculosis depends on subtle
differences in imaging findings and, in some cases, apprecia-
tion of underlying lung disease (Table 1). The rising NTM
prevalence, in general, increases the likelihood of it being the
cause of chronic cavitary lung disease. As the division between
classic (cavitary) disease and nonclassic bronchiectatic nod-
ular disease is often breached, the presence of conspicuous
bronchiectasis and nodules accompanying cavitary disease of
limited extent should suggest the possibility of NTM infection.
The other major cause of cavitary disease is chronic
pulmonary aspergillosis. Large numbers of patients live with
chronic lung and/or mild immunologic disorders that can abet
this infection, suggesting that it is underdiagnosed. Progressive
enlargement of preexisting upper lobe cavities or bullae with
associated pleural thickening warrants laboratory evaluation
for this disease.
Several of the other diseases are less prevalent.
Endemic fungi, which have long been recognized as a
potential cause for chronic cavitary disease in North
America, are probably less important causes of progressive
disease. Coccidioidomycosis is much more likely to present
as a solitary, relatively stable cavity, while the prevalence of
chronic cavitation in chronic histoplasmosis may have been
overreported. Paracoccidioidomycosis is an important cause
of chronic fibrocavitary disease in South America. While it
can mimic tuberculosis, parenchymal disease is more likely

TABLE 1. Key Imaging Findings of Pathogens Causing Chronic Cavities

Imaging Findings Differing from Tuberculosis Underlying Lung Disease
NTM Greater extent of coexisting bronchiectasis, Thinner cavity Bronchiectasis from numerous causes,
walls, greater adjacent pleural thickening COPD
Cavitary Histoplasmosis Can appear very similar to tuberculosis. Non-cavitary Emphysema with bullae
chronic disease also occurs
Chronic pulmonary aspergillus May be superimposed on tuberculosis. Frequent co- Emphysema with bullae, tuberculosis
occurring aspergilloma
Chronic Coccidioidomycosis Solitary thin walled cavities more common than complex No close association
fibrocavitary disease
Chronic Paracoccidioidomycosis Parahilar > than apical upper lobe fibrocavitary disease. Not a prerequisite for infection but minority
Pleural involvement uncommon. Calcifications of cases co-occur with tuberculosis
uncommon
Chronic Melioidosis Apical fibrosis less common. Calcifications less common No close association (predilection for
patients with diabetes)

342 | www.thoracicimaging.com Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
Copyright r 2018 Wolters Kluwer Health, Inc. All rights reserved.
J Thorac Imaging  Volume 33, Number 5, September 2018
to be symmetric, perihilar, and unaccompanied by calcifi-
cations. Melioidosis is an important regional pathogen but
with an endemic footprint that is expanding substantially
with improved surveillance. The incidence of melioidosis has
risen dramatically with improved diagnostics. The rising
incidence may also be fueled by the increasing number of
diabetic patients globally and potentially by the occurrence
of extreme weather events. The latter are likely to drive
increased numbers of acute infections; their impact on the
incidence of chronic disease is unknown.
REFERENCES
1. Martinez F, Chung JH, Digumarthy SR, et al. Common and
uncommon manifestations of Wegener granulomatosis at chest CT:
radiologic-pathologic correlation. Radiographics. 2012;32:51–56.
2. Martinez S, McAdams HP, Batchu CS. The many faces of
pulmonary non-tuberculous mycobacterial infection. AJR Am J
Roentgenol. 2007;189:177–186.
3. Kaufman C. Histoplasmosis: a clinical and laboratory update.
Clin Microbiol Rev. 2007;20:115–132.
4. Jude CM, Nayak NB, Patel MK, et al. Pulmonary Coccidioi-
domycosis: pictorial review of chest radiographic and CT
findings. Radiographics. 2014;34:912–925.
5. Fang W, Washington L, Kumar N. Imaging manifestations of
blastomycosis: a pulmonary infection with potential dissem-
ination. Radiographics. 2007;27:641–655.
6. Holt MR, Chan ED. Chronic cavitary infections other than
tuberculosis. J Thorac Imaging. 2018;33:322–333.
7. Woodring JH, Fried AM, Chuang VP. Solitary cavities of the
lung: diagnostic implications of cavity wall thickness. AJR Am
J Roentgenol. 1980;135:1269–1270.
8. Honda O, Tsubamoto M, Inoue A, et al. Pulmonary cavitary
nodules on computed tomography: differentiation of malignancy
and benignancy. J Comput Assist Tomogr. 2007;31:943–949.
9. Mansoor A, Bagci U, Foster B, et al. Segmentation and image
analysis of abnormal lungs at CT: current approaches, challenges,
and future trends. Radiographics. 2015;35:1056–1076.
10. Chartrand G, Cheng PM, Vorontsov E, et al. Deep learning: a
primer for radiologists. Radiographics. 2017;37:2113–2131.
11. Szymanski EP, Leung JM, Fowler CJ, et al. Pulmonary
nontuberculous mycobacterial infection. A multisystem, multi-
genic disease. Am J Respir Crit Care Med. 2015;192:618–28.
12. Lee M-R, Sheng W-H, Hung C-C, et al. Mycobacterium
abscessus complex infections in humans. Emerg Infect Dis.
2015;21:1638–1646.
13. Aksamit TR, Philley JV, Griffith DE. Nontuberculous
mycobacterial (NTM) lung disease: the top ten essentials.
Respir Med. 2014;108:417–425.
14. Kim C, Park SH, Oh SY, et al. Comparison of chest CT
findings in nontuberculous mycobacterial diseases vs. Myco-
bacterium tuberculosis lung disease in HIV-negative patients
with cavities. PLoS One. 2017;12:3.
15. Lam PK, Griffith DE, Aksamit TR, et al. Factors related to
response to intermittent treatment of Mycobacterium avium complex
lung disease. Am J Respir Crit Care Med. 2006;173:1283–1289.
16. Wallace RJ Jr, Brown-Elliott BA, McNulty S, et al. Macrolide/
Azalide therapy for nodular/bronchiectatic mycobacterium
avium complex lung disease. Chest. 2014;146:276–282.
17. Ito Y, Hirai T, Maekawa K, et al. Predictors of 5-year
mortality in pulmonary Mycobacterium avium-intracellulare
complex disease. Int J Tuberc Lung Dis. 2012;16:408–414.
18. Chung MJ, Lee KS, Koh WJ, et al. Thin section CT findings of
nontuberculous mycobacterial pulmonary diseases: comparison
Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
Copyright r 2018 Wolters Kluwer Health, Inc. All rights reserved.
Radiology Chronic Cavitary Infections
between Mycobacterium avium-intracellulare complex and
Mycobacterium abscessus infection. J Korean Med Sci. 2005;20:
777–783.
19. Church AC, Watkin S. Non-tuberculous mycobacteria mas-
querading as aspiration pneumonia in patients with gastro-
intestinal problems. Respir Med. 2006;100:1663–1665.
20. Knox KS, Hage CA. Histoplasmosis. Proc Am Thorac Soc.
2010;7:169–172.
21. Kennedy CC, Limper AH. Redefining the clinical spectrum of
chronic pulmonary histoplasmosis: a retrospective case series of
46 patients. Medicine. 2007;86:252–258.
22. Denning DW, Cadranel J, Beigelman-Aubry C, et al. Chronic
pulmonary aspergillosis: rationale and clinical guidelines for
diagnosis and management. Eur Respir J. 2016;47:45–68.
23. Kosmidis C, Denning DW. The clinical spectrum of pulmonary
aspergillosis. Thorax. 2015;70:270–277.
24. Desai SR, Hedayati, Patel K, et al. Chronic aspergillosis of the
lungs: unravelling the terminology and radiology. Eur Radiol.
2015;25:3100–3107.
25. Hayes GE, Novak-Frazer L. Chronic pulmonary aspergillosis
—where are we? and where are we going? J Fungi. 2016;2:1–34.
26. Nitschke A, Sachs P, Suby-Long T, et al. Monod sign. J Thorac
Imaging. 2013;28:W120.
27. Marshall GB, Farnquist BA, MacGregor JH, et al. Signs in
thoracic imaging. J Thorac Imaging. 2006;21:76–90.
28. Walker CM, Abbott GF, Greene RE, et al. Imaging pulmonary
infection: classic signs and patterns. AJR Am J Roentgenol.
2014;202:479–492.
29. Stockamp NW, Thompson GR. Coccidioidomycosis. Infect Dis
Clin North Am. 2016;30:229–246.
30. Malo J, Luraschi-Monjagatta C, Wolk DM, et al. Update on
the diagnosis of pulmonary coccidioidomycosis. Ann Am
Thorac Soc. 2014;11:243–253.
31. Funari M, Kavakama J, Shikanai-Yasuda MA, et al. Chronic
pulmonary paracoccidioidomycosis (South American blasto-
mycosis): high-resolution CT findings in 41 patients. AJR Am J
Roentgenol. 1999;173:59–64.
32. Barreto MM, Marchiori E, Viviane B, et al. Thoracic
paracoccidioidomycosis: radiographic and CT findings. Radio-
graphics. 2012;32:71.
33. Marchiori E, Valiante PM, Zanetti G, et al. Paracoccidioido-
mycosis: high-resolution computed tomography–pathologic
correlation. Eur J Radiol. 2011;77:80–84.
34. Chewapreecha C, Holden MTG, Vehkala M, et al. Global and
regional dissemination and evolution of Burkholderia pseudo-
mallei. Nature Microbiol. 2017;2:1–8.
35. Meumann EM, Cheng AC, Ward L, et al. Clinical features and
epidemiology of melioidosis pneumonia: results from a 21-year
study and review of the literature. Clin Infect Dis.
2012;54:362–369.
36. Wong KT, Puthucheary SD, VadiVelu J. The histopathology of
human melioidosis. Histopathology. 1995;26:51–55.
37. Ketai L, Currie BJ, Alva Lopez LF. Thoracic radiology of
infections emerging after natural disasters. J Thorac Imaging.
2006;21:265–275.
38. Currie BJ. Melioidosis: evolving concepts in epidemiology,
pathogenesis and treatment. Semin Respir Crit Care Med.
2015;36:111–125.
39. Vidyalakshmi K, Chakrapani M, Shrikala B, et al. Tuberculosis
mimicked by melioidosis. Int J Tuberc Lung Dis. 2008;12:1209–1215.
40. Burivong W, Wu X, Saenkote W, et al. Thoracic radiologic
manifestations of melioidosis. Curr Probl Diagn Radiol. 2012;41:
199–209.
41. Alsaif HS, Venkatesh SK. Melioidosis: spectrum of radiological
manifestations. Saudi J Med Med Sci. 2016;4:74–78.
www.thoracicimaging.com | 343